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Patho II > Exam 1: Liver > Flashcards

Exam 1: Liver Flashcards

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
Q

onset of hep A

A

acute, sudden

26
Q

onset of hep B

A

insidious, gradual

27
Q

source of infection for hep a

A

contaminated food/water

poor sanitation

28
Q

source of infection for hep b

A

blood- needles, sexual contact

29
Q

mode of transmission hep A

A

fecal-oral route and blood

30
Q

mode of transmission hep b

A

body fluids- blood, semen, saliva

31
Q

chronic state hep A

A

none, self-limiting

32
Q

chronic state hep B

A

yes- clinical mani for 6+ months

33
Q

diagnosis of hep ABC

A

HAV antigen and antibodies

34
Q

clinical mani of hep A

A 
Fever
malaise
anorexia
nausea
jaundice
35
Q

clinical mani of hep B

A 
anorexia
malaise
joint aching
abdominal pain
jaundice 
may lead to liver failure
36
Q

onset of hep C

A

insidious

37
Q

what are the mani of hep C

A

fatigue, can progress to permanent liver damage

38
Q

who is at risk for hep C

A

those with history of snorting/injecting drugs and receiving blood before 1992

39
Q

mode of transmission hep C

A

blood only

40
Q

biliary atresia definition

A

CONGENITAL malformation (incorrect development in utero)

absence or obstruction of common bile duct (ends in pouch)

41
Q

what is the patho of biliary atresia

A

atresia leads to plugging, inflammation, fibrosis of bile canaliculi

no drainage of bile-> backs up-> damages hepatocytes

42
Q

diagnosis of biliary atresia

A

increased serum direct bilirubin

increased serum liver enzymes

43
Q

clinical mani of biliary atresia

A

jaundice
hepatomegaly
acholic (clay colored stools)

44
Q

Cirrhosis of liver

A

chronic liver disease (failure) marked by degeneration of hepatocytes

(inflammation, fibrosis, and scarring)

45
Q

etiology of chrrhosis

A
  1. alcholism : breaks down to acetaldehyde which damages hepatocytes
  2. hepatitis
46
Q

decreased amino acids because hepatocytes cant keep up leads to

A

wasting of body tissues

47
Q

decreased albumin synthesis and decreased levels in the blood stream leads to

A

edema, ascites (enlarged abdomen), and pleural effusion

48
Q

decreased synthesis of blood clotting compounds (fibrinogen and prothrombin) leads to

A 
bleeding: 
ecchymosis
epistaxis
blood in urine and stool
gums bleeding
petachiae
49
Q

decreased conversion of glycogen fats and amino acids to glucose leads to

A

hypoglycemia
weightloss
fatigue
confusion

50
Q

decreased detox of drugs leads to

A

drowsiness, coma

51
Q

decreased conversion of ammonia to urea leads to

A

(ammonia cant leave body and screws with brain)

hepatic encephalopathy= personality changes, confusion and coma

52
Q

increased bilirubin leads

A

jaundice
dark red/brown urine
acholic stools
pruritis

53
Q

portal hyper tension leads to

A

blood back up:

ascites, splenomegaly, caput medusa, esophageal varicies

54
Q

why does esophageal varicies happen with liver failure

A

increased pressure builds up in esophageal blood vessels so it ruptures easily, massive hemorrhage and you bleed into airway

55
Q

liver enzymes in chronic liver failure

A 
increased:
LDH
ALT
AST
ALP
these are released from damaged hepatocytes
56
Q

what proteins are decreased in liver failure

A

albumin and pre-albumin

57
Q

which two products build up in blood in liver failure

A

ammonia and bilirubin

Patho II (23 decks)

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