Exam 1: Liver Flashcards

(57 cards)

1
Q

what is a lobule

A

functional unit of the liver

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2
Q

what are hepatocytes

A

liver cells that produce and secrete bile

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3
Q

what does bile do

A

bile stimulates peristalsis and breaks down fats in the intestine

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4
Q

what are canaliculus

A

channels between hepatocytes that drain bile into the common bile duct into the duodenum and gal bladder

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5
Q

hepatic artery

A

carries oxygenated blood into the liver

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6
Q

portal vein

A

carries unoxygenated blood high in nutrients from GI tract into the liver

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7
Q

what is the portal vein’s main responsibility

A

provides energy for the liver

NUTRIENTS TO LIVER

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8
Q

where do all visceral veins drain

A

into the portal vein

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9
Q

sinusoids

A

venous caps of the liver between hepatocytes which carry blood to hepatic vein

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10
Q

where are kupffer cells found

A

line sinusoids

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11
Q

what do kupffer cells do

A

act as macrophages to destroy old WBC’s, RBC’s and bacteria

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12
Q

hepatic vein

A

carries blood from sinusoids to the inferior vena cava

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13
Q

what is the metabolism of bilirubin chain

A

old RBCs break down in blood stream->
heme breakdown produces unconjugated bilirubin in blood->
bilirubin circulates through liver and is conjugated in the hepatocytes->
bilirubin leaves liver in bile via the hepatic duct->
excreted into duodenum->
excreted via feces

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14
Q

what does bile contain

A

h2o, electrolytes, bile acids, cholesterol, bilirubin

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15
Q

where does bile drain into

A

small intestine (duodenum)

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16
Q

most acids that are secreted into the duodenum are what

A

reabsorbed back into the blood

400-800ml is produced a day in an adult

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17
Q

bilirubin must be what to exit the blood

A

Conjugated… water soluble

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18
Q

what is jaundice

A

symptom of liver disease caused by hyperbilirubinemia (excess bilirubin in blood)

Leads to deposition of bile pigment in skin and sclera

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19
Q

what are the 3 types of jaundice

A
  1. hemolytic jaundice
  2. intrahepatic obstructive jaundice
  3. extrahepatic obstructive jaundice
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20
Q

hemolytic jaundice

A

excessive lysis of RBC

liver cannot keep up conjugating which leads to increased unconjugated bilirubin buildup in blood

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21
Q

intrahepatic jaundice

A

(damage to liver)
hepatocellular damage, so liver cannot conjugate or excrete bilirubin

increased unconjugated bilirubin buildup in blood

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22
Q

extrahepatic obstructive jaundice

A

(outside liver)
bile duct obstruction (galstone) so bile cannot get through

leads to increased CONJUGATED bilirubin to accumulate in liver and bloodstream

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23
Q

extrahepatic jaundicce can lead to what

A

intrahepatic obstructive jaundice due to backup

24
Q

hepatitis

A

inflammation of liver

can lead to degeneration and scarring, necrosis of hepatocytes

25
onset of hep A
acute, sudden
26
onset of hep B
insidious, gradual
27
source of infection for hep a
contaminated food/water | poor sanitation
28
source of infection for hep b
blood- needles, sexual contact
29
mode of transmission hep A
fecal-oral route and blood
30
mode of transmission hep b
body fluids- blood, semen, saliva
31
chronic state hep A
none, self-limiting
32
chronic state hep B
yes- clinical mani for 6+ months
33
diagnosis of hep ABC
HAV antigen and antibodies
34
clinical mani of hep A
``` Fever malaise anorexia nausea jaundice ```
35
clinical mani of hep B
``` anorexia malaise joint aching abdominal pain jaundice may lead to liver failure ```
36
onset of hep C
insidious
37
what are the mani of hep C
fatigue, can progress to permanent liver damage
38
who is at risk for hep C
those with history of snorting/injecting drugs and receiving blood before 1992
39
mode of transmission hep C
blood only
40
biliary atresia definition
CONGENITAL malformation (incorrect development in utero) absence or obstruction of common bile duct (ends in pouch)
41
what is the patho of biliary atresia
atresia leads to plugging, inflammation, fibrosis of bile canaliculi no drainage of bile-> backs up-> damages hepatocytes
42
diagnosis of biliary atresia
increased serum direct bilirubin increased serum liver enzymes
43
clinical mani of biliary atresia
jaundice hepatomegaly acholic (clay colored stools)
44
Cirrhosis of liver
chronic liver disease (failure) marked by degeneration of hepatocytes (inflammation, fibrosis, and scarring)
45
etiology of chrrhosis
1. alcholism : breaks down to acetaldehyde which damages hepatocytes 2. hepatitis
46
decreased amino acids because hepatocytes cant keep up leads to
wasting of body tissues
47
decreased albumin synthesis and decreased levels in the blood stream leads to
edema, ascites (enlarged abdomen), and pleural effusion
48
decreased synthesis of blood clotting compounds (fibrinogen and prothrombin) leads to
``` bleeding: ecchymosis epistaxis blood in urine and stool gums bleeding petachiae ```
49
decreased conversion of glycogen fats and amino acids to glucose leads to
hypoglycemia weightloss fatigue confusion
50
decreased detox of drugs leads to
drowsiness, coma
51
decreased conversion of ammonia to urea leads to
(ammonia cant leave body and screws with brain) | hepatic encephalopathy= personality changes, confusion and coma
52
increased bilirubin leads
jaundice dark red/brown urine acholic stools pruritis
53
portal hyper tension leads to
blood back up: | ascites, splenomegaly, caput medusa, esophageal varicies
54
why does esophageal varicies happen with liver failure
increased pressure builds up in esophageal blood vessels so it ruptures easily, massive hemorrhage and you bleed into airway
55
liver enzymes in chronic liver failure
``` increased: LDH ALT AST ALP these are released from damaged hepatocytes ```
56
what proteins are decreased in liver failure
albumin and pre-albumin
57
which two products build up in blood in liver failure
ammonia and bilirubin