Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GIR Test 1 > B5.017 - Hepatic and Gallbladder Physiology > Flashcards

B5.017 - Hepatic and Gallbladder Physiology Flashcards

1
Q

what makes up the portal triad

A

bile duct portal venule portal arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are liver sinusoids

A

large capillaries between plates of hepatocytes that drain blood into central vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the central vein

A

drains filtered blood to hepatic vein and IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

liver cell types

A

hepatocytes sinusodal endothelial cells kupffer cells stellate cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are kupffer cells

A

Kupffer cells are the monocyte/macrophage cells of the liver. They are the first line against infection or toxins in the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are stellate cells

A

Stellate (Ito) cells store lipid soluble vitamins (most notably Vitamin A) and fat. They secrete extracellular matrix components and contract, causing hepatic fibrosis in cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe flow of bile compared to central vein

A

they flow in opposite directions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are chonlangiocytes

A

cells lining the bile dictule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what does the gall bladder do

A

stores bile and concentrates bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the sphincter of oddi

A

high pressure zone of resistance to bile flow from the common bile duct into duodenum. Prevents reflux of duodenal contents into the pancreatic and bile ducts and promote sifting of the gallbladder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

functions of the liver

A

production of bile regulation of cholesterol synthesis regulation of blood sugar production of urea detox of blood production of blood proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

composition of bile

A

water proteins Na Bile salts bilirubinfatty acids lecithin K Ca Cl HCO3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what cells produce water to go into bile

A

hepatocytes cholangiocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what proteins are there in bile

A

IgA, IgM, IgG Mucin Albumin Apolipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is mucin

A

glycosylated protein, forming gel, lubrication, barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does bile become more concentrated

A

the longer bile sits in the gall bladder the more concentrated it gets. It continuously pumps Na out of the gall bladder lumen and water follows

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

factors promoting biliary cholesterol secretion

A

increased uptake from blood increased de novo cholesterol synthesis decreased bile acid synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where does majority of our cholesterol come from

A

de novo synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

describe de novo synthesis of cholesterol

A

HMGCoA Reductase is the major enzyme creating cholesterol pool. CYP7A1 then converts cholesterol to bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the types of bile in the bile acid pool and what are their %

A

CA - 50% - CYP7A1, CYP8B1 CDCA - 30% - CYP7A1 DCA - 15% - bacterial 7alpha dehydroxylase LCA - <5% - bacterial 7alpha dehydroxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

why is bile made by the liver

A

the liver is the only organ with all the enzymes necessary to make bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what does conjugation of bile acids do

A

makes the bile acids into bile salts that then are water soluble and can transport fats to the cells lining the duodenum to take up the nutrients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what amino acids are bile acids combined with

A

glycine and taurine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is MRP2

A

transports bilirubin into bile from hepatocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is CYP7A1

A

converts cholesterol into bile acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is MDR3

A

transports phospholipids into bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is ABCG5 and ABCG8

A

transports cholesterol into bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is BSEP

A

transports bile acids into bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is NTCP

A

transports bile acids from the enterocyte –> portal circulation back to the hepatocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is Ostalpha and beta

A

transport bile acids into portal circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is ASBT

A

bile acid transporter into the enterocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is ABCG5 and 8

A

pumps cholseterol out of the enterocyte back into the lumen to be excreted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what percentage of bile do you lose in feces

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is FXR

A

farsenoid x receptor a nuclear receptor that is a ligand activated transcriptional factor, bile acid binds to it and it inhibits CYP7A1 to decrease bile acid synthesis Key in feedback inhibition of bile acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does bile acid activated FXR do

A

inhibits CYP7A1 to decrease bile acid synthesis induces BSEP to increase biliary acid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what do bile acid sequestrants do

A

bind negatively charged bile salts in the intestine and prevent their reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are bile acid sequestrants

A

cholestyramine colesevelam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how much ingested cholesterol is kept

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is CCK

A

peptide hormone secreted by enteroendocrine cells (I cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what stimulates CCK secretion

A

dietary fat and amino acids

41
Q

what does CCK do

A

stimulates gallbadder contraction causes relaxation of the sphincter of Oddi stimulates pancreatic acinar cells to secretive digestive juice inhibits gastric emptying and promotes digestion

42
Q

what are micelles

A

formed from bile salts formed in the gut containing dietary lipids and bile salts

43
Q

describe the structure of micelles

A

bile salts form the edge whereas lipids exist in a bilayer on the inside of the micelle providing a large surface area for action of pancreatic lipase

44
Q

what do micelles do

A

facilitate the absorption of digested lipid by gut enterocytes and provide a large surface area for the action of pancreatic lipase

45
Q

what is progressive familial intrahepatic cholestasis (PFIC)

A

progressive liver disease leading to liver failure genetic defects in bile secretion autosomal recessive

46
Q

presentation of PFIC

A

itching, jaundice, growth failure, cirrhosis, portal hypertension, hepatomegaly

47
Q

progressive familial intrahepatic cholestasis type 1 genetic disorder

A

byler disease ATP8B1 mutation - phospholipid flippase

48
Q

PFIC1 mechanism

A

not well understood, but may be associated with altered apical membrane structure that impairs biliary bile salt secretion with normal phospholipids in bile

49
Q

labs for PFIC1

A

mildly elevated AST/ALT Normal GGT not associated with gallstone risk

50
Q

symptoms of PFIC1

A

early infancy onset, cirrhosis in first decade of life, elevated serum bile acids, severe pruritis diarrhea, pancreatitis, short stature

51
Q

PFIC2 mutation

A

BSEP - BSEP is integral in bile acid movement out of hepatocyte to move to enterocyte biliary acid secretion deficit, normal biliary phospholipids

52
Q

PFIC2 progression

A

fast, cirrhosis in 1 year of life giant cell hepatitis, hepatocellular necrosis, portal fibrosis

53
Q

PFIC2 labs

A

higher AST/ALT than PFIC1

Generally normal GGT

serum bile acid elevation,

severe pruritis

1/3 develop gallstones

portal hypertension

more severe than hepatobiliary disease than PFIC1 and higher risk than HCC and cholangiocarcinoma

54
Q

PFIC3 mutation

A

MDR3 mutation

ABCB4 transporter

55
Q

describe PFIC3

A

exposure of cholangiocytes to normal levels of detergent bile acids causes chilangiopathy

decreased phospholipid secretion resulting in unstable micelles, crystallization of cholesterol and small bile duct obstruction

late infancy onset, slow progression, cirrhosis in young adult life

56
Q

labs for PFIC3

A

more severe elevation of AST/ALT than PFIC1 and 2

higher GGT distinguishes PFIC3 from PFIC1 and PFIC2

pruritis

57
Q

treatment for PFIC

A

UDCA - more effective in PFIC3

bile acid sequestrants for pruritis

srugical before cirrhosis in PIFC1 and PFIC2

liver transplant only effective treatment for PFIC3

58
Q

biliary atresia

A

progressive idiopathic disease of extrahepatic biliary tree

most common cause of neonatal cholestasis

59
Q

labs of biliary atresia

A

elevated conjugated bilirubin causing jaundice in first 8 weeks of life and pale stool

elevated AST/ALT and GGT

60
Q

treatment for biliary atresia

A

early surgical intervention (Kasai procedure)

improves transplant free outcome

most common indication of liver transplantation in children

61
Q

what is dubin johnson syndrome

A

Mrp2 (ABCC2 mutation) which transports bilirubin into bile

jaundice usually only symptom

normal liver enzymes

black liver due to impaire excretion of epinephrine metabolites

liver usually functionally normal

good prognosis

62
Q

what is crigler najjar syndrome

A

complete loss of enzyme activity (elevated unconjugated bilirubin, bilirubin encephalopathy)

63
Q

gilbert syndrome

A

partial loss of enzyme activity due to mutation or genetic variation. Generally healthy. get a little yellow under stress

64
Q

PBC

A

primary biliary cholangitis

autoimmune destruction of small bile ducts in portal triad

65
Q

what causes PBC

A

anti mitochondrial antibody AMA in ~95% PBC

female dominant

middle aged

66
Q

clinical presentation of PBC

A

pruritis, dry mouth/eye and fatigue appear first, jaundice usually appears later

hypercholesterolemia, xanthomas

elevated ALP, GGT

liver biopsy to confirm

67
Q

what is UDCA

A

increases bile acid pool hydrophilicity

promotes biliary bicarbonate secretion

anti apoptosis

decreases pruritis

60% responders have normal life span

40% do not have adequate response

68
Q

what deo FXR agonists do

A

inhibit bile acid synthesis

inhibit inflammation

reduces liver enzymes in PBC patients

increases pruritis

69
Q

what is treatment for pruritis

A

bile acid sequestrant

cholestyramine

70
Q

what are FXR agonists

A

obeticholic acid

OCA

ocaliva

71
Q

what is PSC

A

affects both intra and extrahepatic duct (fibrosis around bile duct)

male dominant

autoimmune mediated destruction of bile duct (most patients have elevated IgM and pANCA)

up to 80% have IBD

72
Q

labs for PSC and symptoms

A

pruritis, elevated ALP, GGT, hyperbilirubinemia

narrowing of bile duct

portal hypertension, cirrhosis, hepatosplenomegaly

73
Q

ICP - intrahepatic cholestasis of pregnancy

A

common pregnancy related liver disease

reversible, rapidly resolves after pregnancy

usually presents in 3rd trimester, jaundice may follow

74
Q

labs and treatment for ICP

A

elevated AST/ALT, bile acids, mild jaundice

UDCA, cholestyramine, symptoms resolve quickly after delivery

75
Q

cholelithiasis epidemiology

A

~95% of all biliary tract diseases

Native americans > hispanics > caucasians > africans > asians

more common after 3rd decade, increases with age

F>M

76
Q

modifiablie risk factors for cholelithiasis

A

obesity, dyslipidemia, T2DM, metabolic syndrome, pregnancy, rapid weight loss, TPN

77
Q

drugs that may lead to cholelithiasis

A

octreotide - long lasting analogue of somatostatin that inhibits CCK release

clofibrate - lipid lowering drug that increases biliary cholesterol and decreased bile acid secretion

78
Q

what are the types of gallstones and their risk factors

A

cholesterol stones - >80%

risk factors: obesity, gender, race, estrogen, age

pigment stones - <20%

79
Q

what are the types of pigment stones

A
  1. black pigment stones - calcium bilirubinate polymer, formed in gallbladder,
    1. chronic hemolysis (sickle cell), chrons disease
  2. brown pigment stone - various amounts of cholestrol/fatty soap/ calcium bilirubinate
    1. formed in bile duct, chronic biliary tract infection, bacterial beta glucuronidase deconjugates bilirubin, biliary stasis
80
Q

pathogenesis of cholelithiasis

A

supersaturation of cholesterol or bilirubin salt in bile

81
Q

what are pathogenic factors of cholelithiasis

A

hypersecretion of cholesterol or bilirubin

decreased secretion of bile salts and phospholipids

imbalance of nucleation/antinucleation proteins

decreased gallbladder motility

biliary stasis

82
Q

what is biliary sludge

A

microscopic gallstones

suspension of cholesterol monohydrate crystal or calcium bilirubin particulates in mucin gel, can vanish or progress to gallstone

83
Q

what is nucleation

A

altered balance of pronucleating vs antinucleating agnents in the bile

pronucleating agents: mucin gel, a hydrophobic molecule that promotes nucleation of crystals, a scaffold that allows gallstone to grow

anti nucleating agents - apolipoprotein A, UDCA

84
Q

clinical stages of cholelithiasis

A
  1. lithogenic state - conditions favor gallstone formation
  2. asymptomatic gallstones
  3. symptomatic - episodes of biliary colic after a fatty meal
  4. complicated, gallbladder attack
85
Q

complications of gallstones

A

asymptomatic stones do not requrie treatment

biliary colic

acute cholecystitis

empyema

gangrene

perforation

choledocholithiasis

ascendign cholangitis

pancreatitis

gallladder cancer

86
Q

acute cholecystitis

what is it and presentation

A

inflammation of the gall bladder

acute calculous cholecystitis - 90%

acute acalculous cholecystitis - 10%

RUQ paint, mild fever, murphys sign

87
Q

labs and dx for cholecystitis

A

mild elevation of liver enzymes, leukocytosis, mild elevation of ALP, bilirubin, amylase and lipase, tachycardia

dx is with US, gallstone lodged in neck or cystic duct, GB wall thickening, distene GB

88
Q

what is gallbladder empyema

A

accumulation of infected fluid, mostly associated iwht acute cholecystitis and infected bile, Risk of sepsis, perforation

89
Q

what is gallbladder hydrops

A

prolonged cystic duct obstruction

90
Q

treatment of acute cholecystitis

A

IV fluid, antibiotics, pain meds

91
Q

what is

A
92
Q

acute acalculous cholecystitis causes and symptoms, treatment

A

distended gallbladder without stone

critically ill patients

major cause: bile stasis resulted from fever, dehydration, lithogenic bile, absence of feeding

higher risk of gangrene and perforation

treatment is supportive care, cholecystectomy, cholecystostomy

93
Q

how does bile stay sterile

A

bile is sterile bc of constant bile flow, bacteriostatic activity of bile salts, IgA, Oddi,

94
Q

predisposing factors of ascending cholangitis

A

biliary obstruction and stasis

Oddi disrupted

95
Q

mechanism of ascending cholangitis

A

bacteria migrate into biliary system from the intestine

usually E coli, Klebsiella, enterobacter

high biliary pressure reduces antibacterial defense, increased bile ductular permeability permitting bacteria to enter the systemic circulation

presence of stomes promotes bacterial colonization

96
Q

clinical presentation of ascending cholangitis

A

charcots triat: rever, RUQ, jaundice

reynolds pentad - fever, RUQ pain, jaundice, hypotension, altered mental status

97
Q

treatment of ascending cholangitis

A

supportive care, antibiotics, pain medicine

removal of stone (ERCP)

98
Q

what does UDCA in gallstone treatment

A

decreases biliary cholesterol saturation

promotes bile secretion and flow

gallstone dissolution

doesnt treat pigment stones

preventative use: PFIC3, rapid weight loss, recurring choledocholithiases

GIR Test 1 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions