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Pathophys Exam I > GI Mod 4 > Flashcards

GI Mod 4 Flashcards

1
Q

what divides R/L lobes of liver

A

Cantlie’s line

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2
Q

top and bottom borders of liver

A

IVC

gallbladder

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3
Q

connective tissue of liver

A
  1. falciform ligament

2. Glisson’s capsule-surrounds liver, invaginates at hilum of the liver

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4
Q

what is the functional unit of the liver

A
  1. hexagonal arrangement of hepatocytes and microvasculature
  2. at center of the hexagon is the central vein
  3. at each outer corner of hexagon is a portal triad
  4. microvasculature consists of sinusoids and bile canaliculi
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5
Q

what does the portal triad of liver consist of

A
  1. terminal branch of hepatic artery
  2. terminal branch of portal vein
  3. terminal bile duct
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6
Q

bile canaliculi drain into

A

terminal bile ducts

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7
Q

terminal bile ducts eventually drain into

A

R/L hepatic ducts

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8
Q

R/L hepatic ducts merge to form

A

common hepatic duct

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9
Q

common hepatic duct eventually divides into

A
  1. cystic duct which connects to gallbladder

2. common bile duct which descends to merge with pancreatic duct and drain into duodenum

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10
Q

t/f hepatocytes have ability to regenerate

A

true

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11
Q

what are 3 signaling mechanisms for liver regeneration

A

TGF - transforming growth factor
HGF - hepatocyte growth factor
EGF - epidermal growth factor

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12
Q

there is a critical ratio bw _______ _________ mass and ________ mass

A

funcational hepatocyte mass and body mass

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13
Q

fluctuations in the ratio of functional hepatocyte mass vs body mass signal what

A

regeneration or apoptosis

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14
Q

what is the duration of liver regeneration if 50-60% of liver is damaged from 4 days of tylenol overdose

A

completely regenerates in 30 days

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15
Q

hepatic circulation

A
  1. afferent pathways to liver
  2. sinusoids
  3. efferent pathway from liver
  4. lymphatic circulation of lymph - large production of lymph
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16
Q

what are the afferent pathways to the liver

A
  1. portal pathway - 75% from hepatic portal vein

2. arterial pathway - 25% from hepatic artery

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17
Q

what are sinusoids in liver

A

microvasculature within liver

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18
Q

what are the efferent pathway from liver

A
  1. central veins drain into hepatic veins

2. hepatic veins eventually drain into IVC

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19
Q

avg weight of the liver

A

2-3 lbs

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20
Q

portal pathway - hepatic portal vein

A
  1. receives blood from GI tract, spleen and pancreas
  2. contains large amount of nutrients from GI tract
  3. relatively small amount of oxygen
  4. divides into R/L branches and then further divides until it finally delivers blood to portal vein
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21
Q

portal pathway - hepatic portal anastomosis

-4 veins

A

collateral venous circulation with numerous veins of abdominopelvic region

  1. gastroesophageal vein
  2. rectal vein
  3. paraumbilical vein
  4. portorenal vein
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22
Q

portal pathway - portal HTN

A

portal circulation congested and reverse portal blood flow towards portal anastomoses
-occurs when cirrhosis develops

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23
Q

liver arterial pathway - hepatic artery

A

delivers oxygenated blood to liver
accounts for approx 25% of blood flow to liver
originates from celiac trunk

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24
Q

arterial pathway of liver - hepatic artery and portal HTN

A

blood flow to liver from hepatic artery is not impaired

the relative high amount of O2 delivered to hepatocytes is synergistic with regeneration

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25
Q

sinusoids act as what for hepatocytes

A

capillary bed

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26
Q

sinusoids receive blood from

A

2 or 3 portal triad vessels

  • terminal branches of hepatic portal veins and hepatic artery
  • merges nutrient rich blood and O2 rich blood
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27
Q

sinusoids are lined with what

A

hepatocytes - expose hepatocytes to hepatic blood flow

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28
Q

sinsuoids drain into

A

central vein

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29
Q

structure of sinusoid/hepatocyte interface

A
  1. Kupffer cells
  2. fenestrated endothelium
  3. space of Disse - stellate cells
  4. pit cells
  5. microvilli of hepatocytes
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30
Q

what are Kupffer cells

A

monocyte/macrophage origin
located along surface of endothelium
function: phagocytic removal immune complexes, cell debris, etc; and removal of damaged RBC
serves as early or front line defense against liver injury

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31
Q

what is fenestrated endothelium

A
  • large holes in endothelial lining of sinusoid vessel
  • allows nutrients/lipids to travel thru sinusoidal wall and flow to microvilli of hepatocyte
  • endothelium also has pinocytosis function to active transport molecules to microvilli of hepatocyte
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32
Q

what are stellate cells

A

location: Disse Space
function: store vit A, produce/secrete hepatic growth factors for liver regeneration

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33
Q

what happens if stellate cells are stimulated via pathology/disruption of environment homeostasis

A

transform into fibroblastic function (produce collagen) and myblastic function (contractile)
-role in fibrosis

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34
Q

what are pit cells

A

aka granular lymphocytes or NK cells (natural killer)
location: surface of endothelium
function: front line immune defense against tumor formation, viruses, etc (attacks tumor/virus)
also plays role in liver regeneration

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35
Q

lymph system of liver - hepatic lymphatics

  • what % of total lymph fluid
  • drain fluid from where
  • function
A
  • liver produces largest amount of lymph fluid in body
  • approx 20% of total lymph fluid
  • drain fluid from Disse space, glisson’s capsule and other interstitial spaces of liver
  • play critical defensive role in protecting against intestinal bacteria/antigens
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36
Q

what are the two regional zones of hepatocytes in the lobule zone circulation

A

periportal hepatocytes

centrilobular hepatocytes

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37
Q

what is the third regional zone sometimes described in the lobule zone circulation

A

mid way bw periportal and centrilobule zones

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38
Q

what are periportal hepatocytes

A
  • first to receive blood
  • O2 and nutrient rich
  • functional: last to experience necrosis; first to regenerate
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39
Q

what are centrilobular hepatocytes

A

last to receive blood
less O2 and nutrient availability
functional: susceptible to ischemia/necrosis; region of drug metabolism (biotransformation)

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40
Q

liver metabolizes what macromolecules

A

carbs, fats, proteins

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41
Q

liver stores what

A

fat soluble and some water soluble vitamins

  • vitA
  • vitK (critical for clotting cascades)
  • vitD (precuresor involved in conversion of inactive D to active D)
  • vit B12 (water soluble)
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42
Q

liver as endocrine function

A

vit D conversion & T4 to T3 conversion

remove some circulating hormones: insulin, glucagon, GI hormones

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43
Q

liver role in drug metabolism/biotransformation

A

liver serves as intermediate step
drugs ingested in hydrophobic form
liver converts to hydrophilic form to allow excretion

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44
Q

function of liver in carb metabolism

A

regulate blood glucose

inital mechanism to reduce blood glucose - insulin mediated

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45
Q

synthesis of glycogen (glycogenesis)

A

liver stores glucose for future energy needs
glycogen is approx 10% of total liver weight
glycogen synthesized from glucose, amino acids, and pyruvate

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46
Q

gluconeogenesis

A
  • production of glucose from non carb sources
  • glucose can be produced from fatty acids, amino acids, and lactate (rate limiting step is the amount of available substrate NOT liver enzymes)
  • important role to maintain blood glucose during fasting
  • stimulated by glucagon and sympathetics (inhibited by insulin)
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47
Q

what removes FFA and lipoproteins from plasma

A

liver

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48
Q

what is the fasting state of fat metabolism with liver

A 
released into plasma from adipose tissue
FFA are removed from plasma by liver
FFA in liver have two fates:
1. used in energy production - B oxidation, ketone body formation
2. used to synthesize VLDL
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49
Q

feeding state of fat metabolism with liver

A

chylomicron remnants are removed from plasma by liver

  • TGs from chylomicron remnants can be used from energy production (FFA formation) or to synthesize VLDL
  • cholesterol from chylomicron remnants used to synthesize VLDL
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50
Q

lipoprotein synthesis in liver

A

the liver plays impt role in synthesizing lipoproteins needed for lipid transport in plasma

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51
Q

classes of lipoproteins

A
  1. chylomicrons
  2. VLDL
  3. LDL
  4. HDL
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52
Q

what are chylomicrons

A

largest diameter, most lipid, least concentration of proteins
lipids - 99% lipids, TG rich
-synthesized in intestines, transport TGs (digested fats)

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53
Q

what is VLDL

A

very low density lipoprotein
smaller diameter than chylomicron
lipids-90%, TG rich not as much as chylomicron
-synthesized in liver (small amnt in intestines)
-transport TGs to periphery

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54
Q

what is LDL

A

low density lipoprotein
small diameter than VLDL
lipids - 80% lipids, cholesterol rich
-synthesized in plasma (small amnt in liver)
-transport cholesterol from liver to peripheral tissue

55
Q

what is HDL

A

high density lipoprotein
smallest diameter, least lipid, largest concentration of proteins
lipids - 40-60% lipids, cholesterol rich
-synthesized in plasma (small amount in liver)
-remove/transport cholesterol from periphery to liver

56
Q

lipoprotein removal

A

liver plays important role in removal (catabolism) of lipoproteins

57
Q

LDL removal

A

LDL receptors on the liver bind LDL and remove from circulation
ex. familial hypercholesterolemia = LDL receptor deficiency

58
Q

hepatic cholesterol production

A
  1. B oxidation of FFA in the liver creates acetyl CoA
  2. acetyl CoA can be used for energy or can be used to synthesize cholesterol
  3. rate limiting step in cholesterol synthesis is conversion HMG CoA to mevalonate
  4. HMG CoA reductase is enzyme needed for rate limiting step
59
Q

hepatic cholesterol has four possible fates

A

contribute to formation of VLDL
formation of bile acids
formation of cell membranes in liver
excreted from body

60
Q

statins MOA

A

inhibit HMG-CoA reductase

  • this is necessary for cholesterol formation
  • this is the rate limiting step of cholesterol formation in the liver
61
Q

result of statin use

A

decrease cholesterol synthesis by liver
increased production of LDL receptors on liver
increased uptake of LDL by liver
decreased plasma LDL cholesterol levels

62
Q

protein metabolism in the liver

A

involved in many different pathways of amino acid metabolism

  • synthesis of plasma proteins and tissue proteins
  • utilized as fuel source (glucose, ketone bodies, acetyl CoA)
  • pathway to remove nitrogenous wastes from body (urea cycle)
63
Q

synthesis of plasma proteins - albumin

A
  • synthesizes 9-12 grams/day
  • critical role in maintaing fluid homeostasis
  • pathology: ascites/edema
64
Q

synthesis of plasma proteins - proteins of clotting cascade

A

prothrombin and fibrinogen

65
Q

syntehsis of plasma proteins - a1 antitrypsin

A

protect against protein destruction

66
Q

what 4 plasma proteins does the liver synthesize

A
  1. albumin
  2. blood clotting cascade factors
  3. a1 antitrypsin
  4. iron transport proteins
67
Q

amino acids utilized as _____ source by liver

A

fuel

  • formation of glucose
  • formation of ketone bodies
  • transamination of amino acids to form Acetyl CoA - substrate for Kreb’s cycle
68
Q

amino acids remove what from body

A

nitrogenous wastes

69
Q

what is produced from amino acid/nucleic acid breakdown

A

ammonia

  • highly toxic
  • level is 10xs higher in liver vs plasma
70
Q

ammonia is converted to what to be excreted

A

urea

71
Q

urea cycle in liver

A

forms urea from ammonia by products

-liver accounts for 90% of nitrogenous waste excreted in urine

72
Q

transamination of amino acids in liver for

A

glutamate/aspartate

73
Q

two necessary enzymes needed for transamination of amino acids in liver

A

ALT - alkaline transaminase

AST - aspartate transaminase

74
Q

which liver enzyme is more specific to liver than the other

A

AST more than ALT

75
Q

bile fluid is composed of

A
  1. bile acids
  2. phospholipids
  3. cholesterol
76
Q

bile fluid contains/transports via what

A

micelle complex

77
Q

what does bile fluid contain/transport

A
  1. bile pigments - bilirubin
  2. inorganic ions - NA+, K+, Ca++, Cl-, HCO3-
  3. drug metabolites
  4. fat soluble vitamines
78
Q

bile function

A
  1. assist in intestinal fat digestion - emulsfication of lipids in intestines
  2. excretion of hydrophobic substances - cholesterol, bilirubin, hormones, drugs, fat soluble vitamins
79
Q

bile is produced in and secreted from

A

hepatocytes

80
Q
  1. hepatocytes synthesize bile acids from
A

cholesterol

81
Q
  1. hepatocytes secrete bile into
A

canaliculi
(bile acids, phospholipids, cholesterol, bilirubin, drug metabolites all flow into canaliculi) - specific transporters required for each, flow transports componenets via micell comples

82
Q

what stimulates bile production and secretion

A

CCK, secretin

83
Q

bile pathway

A

secreted in bile canaliculi and flow thru biliary tree

  1. during fasting - 75% flows into gall bladder - gallbladder will concentrate bile; 25% continue on and flow into duodenum
  2. during feeding - gall bladder contract via CCK and vagal stimuli
    - bile reaches duodenum and enters enterohepatic circulation
84
Q

enterohepatic circulation of bile - duodenum

A
  • bile acids secreted into duodenum

- bile acids emulsify intestinal fats and form micelles to assist in fat digestion/absorption

85
Q

enterohepatic circulation of bile - jejunum/ileum

A

some of the bile acids interact with intestinal bacteria

form secondary bile acids

86
Q

enterohepatic circulation of bile - terminal ileum

A

99% of intestinal bile acids (primary and secondary) are reabsorbed in the terminal ileum
1% excreted in feces

87
Q

enterohepatic circulation of bile - liver

A

reabsorbed bile acids return to liver (recycled)

88
Q

RBC degredation

A

lifespan 120 days

breakdown in spleen, liver (Kupffer cells) and thruout vascular system

89
Q

bilirubin is a by product of what

A

RBC breakdown

90
Q

pathophys of bilirubin from RBC

A

RBC broken down and hemoglobin is further divided

  • globin: broken down into amino acids
  • heme: broken down into iron and biliverdin
  • iron is stored in liver and recycled into RBC formation in the bone marrow
  • biliverdin is broken down into bilirubin and released in the plasma
91
Q

bilirubin released into plasma is _____soluble

A

fat

92
Q

because bilirubin is fat soluble, it needs a what for transport?

A

protein carrier

93
Q

what does plasma bilirubin attach to

A

albumin

94
Q

the plasma bilirubin is ______ and travels to the liver

A

unconjugated - can’t be excreted in this form

95
Q

bilirubin in the liver

A

plasma unconjugated bilirubin flows into hepatic circulation
becomes conjugated in hepatocytes = water soluble and can be excreted
the newly formed conjugated bilirubin mixes with the bile in the canaliculi
bile is secreted into intestines

96
Q

bilirubin in the intestines

A

conjugated bilirbuin secreted into the duodenum

bacteria in the intestines convert the bilirubin into urobilinogen

97
Q

intestinal urobilinogen will do one of two things

A
  1. remain in colon and be excreted in stool (darker color) 80% of urobilinogen is excreted in feces
  2. be reabsorbed into blood stream - 20% is reabsorbed
    - the reabosrbed urobilinogen is recycled in liver or excreted in urine
98
Q

what is jaundice

A

hyperbilirubinemia
aka icterus
bilirubin pigment causes yellowing (eyes, bruising)
-yellowing of skin and conjunctival membranes d/t excessive bilirubin in blood stream

99
Q

jaundice is a s/s of what

A

dz/pathology that affects bilirubin metabolism/excretion pathways
-not specific to one dz

100
Q

jaundice can be classified as what

A

pre hepatic or post hepatic

101
Q

lab measurements of hyperbilirubinemia

A
  1. total bili - measured directly in blood (if elevated = hyperbilirubinemia)
  2. direct bili - measure directly in blood (if elevated = consistent with post hepatic pathology that impairs conjugated bilirubin secretion into GI
  3. indirect bili - calculated from total and direct measurements (if elevated, consistent with pre hepatic pathology that impairs hepatocyte conversion of unconjugated bilirubin to conjugated bilirubin or increases amount of circulating unconjugated bilirubin
102
Q

urobilinogen in urine

A

nl:0-4mg/24hrs
increased values = pre hepatic jaundice
nl or decreased values = post hepatic jaundice (if normal is 0, hard to have decreased)

103
Q

what does pale stool indicate

A

decreased urobilinogen in intestines

104
Q

what does dark urine mean

A

increased conjugated bilirubin excreted by kidney

105
Q

classification of hyperbilirubinemia described by what

A

location of pathology that disrupts bilirbuin metabolism

106
Q

what is pre hepatic jaundice

A

pathology before bilirubin is conjugated by the hepatocytes

ex. RBC breakdown, genetic dz (GIlbert’s syndrome, sickle cell anemia, thalassemia), kidney dz
- sometimes referred to as hemolytic jaundice

107
Q

what is post hepatic jaundice

A

pathology located after bilirubin is conjugated by hepatocyte and secreted (impaired transport of conjugated bilirubin to GI tract)
decreased secretion or transport of conjugated bilirubin from liver
-can occur anywhere from within canaliculi to sphincter of Oddi
-ex gallstones or pancreatic pathology that blocks the bile ducts
-sometimes referred to as obstructive jaundice

108
Q

what is the result of hemolysis of RBCs

A

increased production of unconjugated bilirubin

109
Q

labs for prehepatic jaundice pathology

A 
total bili - elevated
indirect bili - elecated
direct bili - nml/potential elevated (d/t increased production of elevated conjugated bili)
urine - elevated urobilinogen
urine and stool color - nml
110
Q

examples of what would cause post hepatic jaundice pathology

-impaired secretion from hepatocytes vs biliary duct system

A
  1. impaired secretion from hepatocytes: pregnancy, cancer, hepatitis, cirrhosis, infiltrative dz (amyloidosis, sarcoidosis, TB), meds
  2. biliary duct system: gallstones, strictures, pancreatitis,cancer/tumor
111
Q

labs for post hepatic pathology

A

total bili - elevated
direct bili - elevated (d/t congestive back up)
indirect bili - nml
urine - elevated conjugated bili = dark color, decreased urobilinogen
stool - loss of dark color due to decrease in urobilinogen in feces

112
Q

direct bili vs indirect bili

A

direct bili measures conjugated bili

indirect bili - measures unconjugated bili

113
Q

neonatal jaundice onset and duration

A

onset- 1-2 days after birth

duration - 1-3 weeks

114
Q

neonatal jaundice - result of neonatal physiology

A

increased rate of fetal RBC breakdown
low capacity of liver (hepatocytes) to conjugate bilirubin
decreased GGT and ligandin which impairs conjugation of bilirubin

115
Q

treatment of neonatal jaundice

A

phototherapy - light creates isomers of bilirubin that are water soluble and can be excreted

severe: blood transfusion

116
Q

complications of neonatal jaundice

A
  1. hyperbilirubinemia neurotoxicity

2. monitor neuro

117
Q

what is viruses cause hepatitis

A

viral - Hep A, B, C, D, E, G

118
Q

what is the pathology of hepatitis

A
  1. hepatic cell death/scarring
  2. kupffer cell hyperplasia
  3. inflammation may disrupt canaliculi
119
Q

hepatic cell damage is more severe with what viruses

A

hepatic cell damage more severe in hepatitis B and C

120
Q

what is fulminating hepatitis

A

rare complication in which massive hepatic cell death and liver failure

121
Q

what is cirrhosis of the liver

A

irreversible inflammatory condition

  • considered one of the leading causes of death in US
  • many different disorders cause cirrhosis
122
Q

what is the pathology of cirrhosis of the liver

A

hepatic tissue becomes nodular and fibrotic

size of liver may expand or shrink

123
Q

initial phase of alcoholic cirrhosis

A

fatty accumulation develops within hepatocytes

124
Q

chronic alcohol metabolism and alcoholic cirrhosis

A
  • metabolism of alcohol produces acetaldehyde which disrupts hepatocyte function/metabolism
  • cell damage initiates an inflammatory response and necrosis
  • promotes excessive collagen synthesis and fibrotic accumulation/scarring
125
Q

alcoholic cirrhosis - fibrosis eventually alters what

A

biliary and vascular drainage

-effects: liver functino declines, portal HTN, GI bleeding, caricose veins, ascities, hepatomegaly, splenomegaly

126
Q

which stages of alcoholic cirrhosis are reversible and irreversible

  • fatty liver
  • fibrosis
  • cirrhosis
A

fatty: reversible
fibrosis: reversible with scarring
cirrhosis: irreversible

127
Q

2 types of biliary cirrhosis

A

primary and secondary

128
Q

what is primary biliary cirrhosis

A

autoimmune dz that attacks small intrahepatic bile ducts (canaliculi)
inflammation of duct system leads to fibrotic changes

129
Q

what is secondary biliary cirrhosis

A

develops as a result of chronic obstruction of biliary flow
obstruction leads to inflammation which leads to fibrotic changes
tx: address the cause of obstruction

130
Q

2 types of gallstones

A

cholesterol stones

pigment stones

131
Q

what are cholesterol stones

A
  1. most common
    80% of cases
    yellowish/green
132
Q

what are pigment stones

A 
15%+ of cases
subtypes
black pigment (bili + calcium and other componenets
brown pigment (bilirubin + bacteria)
133
Q

gall bladder and storage of bile

A

concentrates bile that is stored in gallbladder
-5x increase in concentration
-absorbs water and small electrolytes
leaves behind all of the organic substances in bile (cholesterol, bile salts, bilirubin, lecithin)
-stores approx 1-2 oz of concentrated bile

134
Q

cholesterol stone formation

A

supersaturation of cholesterol in gallbladder

incomplete emptying of gallbladder, excess cholesterol formation

Pathophys Exam I (9 decks)

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