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N935 Pathophysiology > Basic Hepatic Physiology > Flashcards

Basic Hepatic Physiology Flashcards

1
Q

Liver Functions (7)

A
  1. removes potentially toxic byproducts of certain medications
  2. metabolizes nutrients from food to produce energy when needed
  3. helps your body fight infection by removing bacteria from the blood (macrophages)
  4. produces most of the substances that regulate blood clotting
  5. produces bile and bile salts, a compound needed to digest fat and to absorb vitamins A, D, E, K
  6. produces most proteins needed by the body
  7. prevents shortages of nutrients by storing vitamins, minerals, and sugar
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2
Q

xenobiotic

A

anything not natural to the body. ex) dust, meds

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3
Q

basic functional unit of liver

A

lobule

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4
Q

how many lobules in the liver

A

50,000-100,000

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5
Q

basic structures of a liver lobule (9)

A
  1. portal vein
  2. sinusoids (capillaries)
  3. central vein
  4. hepatic artery
  5. bile canniculi (capillaries that transport bile) and bile duct
  6. space of dissent and lymphatic duct
  7. hepatic cellular plates (liver cells)
  8. kupffer cells (macrophages)
  9. interlobular septa (holds everything together)
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6
Q

2 things that feed blood to liver

A

portal vein and hepatic artery

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7
Q

how thick is the hepatic plate

A

one to two cells thick

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8
Q

sinusoids function

A

remove bacteria, inside capillaries and move around

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9
Q

what supplies blood pressure to the hepatic artery

A

aorta to celiac trunk to hepatic artery

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10
Q

what % of O2 comes from portal vein and what % of O2 comes from hepatic artery

A

50% and 50%

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11
Q

Portal Vein SvO2

A

85%

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12
Q

Hepatic Artery SaO2

A

98-100%

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13
Q

normal hepatic BF (and % CO)

A

1500ml/minute or 25-30% CO

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14
Q

how many ml/min (and %) of blood is supplied via the portal vein

A

1100ml/min or 75%

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15
Q

how many ml/min (and %) of blood is supplied via the hepatic artery

A

400ml/min or 25%

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16
Q

average portal vein pressure

A

9mmHg

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17
Q

what is hepatic portal vein blood flow dependent upon

A

dependent upon blood flow to the GI tact and spleen

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18
Q

what 3 organs and 1 artery does the celiac artery (branched from the aorta) feed before the blood supply gets to the liver?

A

artery: hepatic artery branches from celiac artery
organs: stomach, spleen, pancreas

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19
Q

what 3 anatomical landmarks does the superior mesenteric artery (branched from the aorta) feed before the blood supply gets to the portal vein?

A

pancreas, small intestines, colon

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20
Q

bridging fibrosis

A

destruction of liver parenchymal cells results in replacement with fibrous tissue that contracts around the vessels. greatly impedes portal vein flow.
“cell plates replaced by fibrosis and chokes sinusoids it surrounds”

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21
Q

fatty liver pathophysiology

A

fat deposited inside liver cell. starts to crowd intracellular organelles

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22
Q

liver fibrosis pathophysiology

A

crowded intracellular organelles begins to die. fibrotic tissue replacing dead tissue

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23
Q

cirrhosis pathophysiology

A

constriction of sinusoids and capillaries. irreversible damage.

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24
Q

stages of alcohol induced liver damage

A
  1. fatty liver
  2. liver fibrosis
  3. cirrhosis
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25
Q

what constitutes metabolic syndrome

A

HTN, increased triglycerides, increased BG

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26
Q

3 most common reasons for NAFLD

A

obesity
DMII
metabolic syndrome

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27
Q

NAFLD

A

steatotosis

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28
Q

NASH

A

what NAFLD progresses to, inflammation. progresses to cirrhosis

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29
Q

what type of receptors does the hepatic artery have

A 
alpha receptors (vasoconstriction)
beta receptors (vasodilation)
dopaminergic receptors (vasodilation)
cholinergic receptors (vasodilation)
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30
Q

what type of receptors does the portal vein have

A 
alpha receptors (vasoconstriction)
dopaminergic receptors (vasodilation)
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31
Q

normal liver blood volume including what is in hepatic veins and sinusoids

A

450mL

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32
Q

how much blood can be stored in the hepatic veins and sinusoids

A

.5-1L (commonly occurs in CHF)

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33
Q

how liver compensates for a hemorrhage

A

blood shifts from hepatic veins and sinusoids into central circulation (as much as 300mL)

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34
Q

kupffer cells function (3)

A
  1. line hepatic venous sinusoids and cleanse blood as it passes through these sinuses. bacterium that passes into these cells is then digested
  2. also phagocytose cellular debris, viruses, proteins, particulate matter
  3. release various enzymes, cytokines, other chemical mediators
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35
Q

what system are the kupffer cells a part of

A

monocyte macrophage system aka reticuloendothelial system

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36
Q

how does fluid and protein get into the spaces of disse

A

pores in sinusoids are very permeable and therefore permit passage of the fluid and protein into spaces of disse and that is the creation of lymph fluid

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37
Q

a 10-15mmHg increase in hepatic venous pressure does what?

A

can increase lymph flow to 20x normal, produces “sweating” from the liver surface with large amounts of free fluid entering the abdominal cavity aka ascites

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38
Q

what happens with blockage of the portal vein

A

produces high pressure in the GI tract with transudation of fluid through the gut into the abdominal cavity which can also cause ascites

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39
Q

metabolic functions of the liver include (5)

A
  1. carbohydrate metabolism
  2. fat metabolism
  3. protein metabolism
  4. drug metabolism
  5. miscellaneous metabolic functions
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40
Q

final products of carbohydrate metabolism

A

glucose, fructose, galactose. (glucose is final common pathway for most CHO)

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41
Q

specific liver functions associated with CHO metabolism (4)

A
  1. conversion of galactose and fructose to glucose
  2. storage of large amounts of glycogen (glycogenesis)
  3. gluconeogenesis (used from proteins and fats after you’ve used carbs)
  4. formation of many chemical compounds from intermediate products of CHO metabolism
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42
Q

chemical formula of glucose, fructose, galactose

A

C6H12O6

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43
Q

how is most glucose stored after a meal

A

stored as glycogen

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44
Q

glucose buffer function

A

storage of glycogen allows liver to remove excess glucose from the blood, store it, and return it to the blood when BG concentration decreases

45
Q

does glycogen contribute to osmolality

A

no

46
Q

2 parts of the body able to store significant amounts of glycogen

A

liver and muscles

47
Q

what enhances glycogen storage

A

insulin

48
Q

what enhances glycogenolysis

A

epinephrine and glucagon

49
Q

how many hours of fasting before hepatic glycogen steers are depleted

A

24 hours. after that, gluconeogenesis uses fat first to compensate.

50
Q

the liver and kidney are unique in that they can convert these 4 things to glucose

A

amino acids
glycerol
pyruvate
lactate

51
Q

agents that increase gluconeogenesis

A

glucocorticoids
catecholamines
glucagon
thyroid hormone

52
Q

agents that decrease gluconeogenesis

A

insulin

53
Q

specific liver functions associated with fat metabolism (3)

A
  1. oxidation of fatty acids to supply energy for other body functions (beta oxidation)
  2. synthesis of large amounts of cholesterol, phospholipids, and lipoproteins
  3. synthesis of fat from CHO and proteins
54
Q

triglycerides chemical makeup

A

glycerol and 3 fatty acids

55
Q

what is the goal of the oxidation of fatty acids

A

to take out of storage and make glucose aka to derive energy from fat (triglycerides)

56
Q

how is energy derived from fat (triglycerides)

A
  • they must be split into glycerol and fatty acids
  • fatty acids are then split by beta oxidation into 2 carbon acetyl radicals that form acetyl coenzyme A
  • acetyl coA enters the citric acid cycle and is oxidized to liberate tremendous amounts of energy
57
Q

where can beta oxidation occur

A

in all body cells, but occurs especially rapidly in hepatic cells

58
Q

since the liver cannot use all of the acetyl Co-A it produces, this is what happens

A
  • converted to acetoacetic acid (combination of 2 acetyl Co-A molecules)
  • acetoacetic acid is highly soluble and leaves the hepatocytes, enters the blood, and is absorbed by other tissues
  • the tissues reconvert the acetoacetic acid back into the acetyl Co-A which enters the citric acid cycle and is oxidized to produce energy
  • in the way liver is responsible for a major part of fat metabolism
59
Q

acetyl Co-A is used by the liver to synthesize these 2 things

A

cholesterol and phospholipids

60
Q

both cholesterol and phospholipids are used by body cells to form these 3 things

A
  1. cell membranes
  2. intracellular structures
  3. chemical substances important to cell function ex) hormones
61
Q

specific liver functions associated with protein metabolism (4)

A
  1. deamination of proteins (removal of nitrogen)
  2. formation of urea for removal of ammonia (NH3) from the body fluids
  3. formation of plasma proteins
  4. synthesis of amino acids and synthesis of other compounds from amino acids
62
Q

3 branch chain amino acids

A

leucine
isoleucine
valine

63
Q

deamination

A

enzymatic process which converts amino acids into their respective keto acids and results in production of ammonia as a byproduct (cleaves off nitrogen and converts back to carbonyl group). liver is principle site

64
Q

formation of urea from ammonia and purpose

A

removes ammonia from the body fluids
large amounts of ammonia are formed by deamination process. bacteria in the gut with subsequent absorption into the blood

65
Q

how can excessive ammonia happen

A

if the liver does not perform deamination or if there is greatly reduced blood flow

66
Q

porta caval shunt

A

shunts portal blood into IVC to bypass liver. increased ammonia and hepatic encephalopathy can develop.

67
Q

how many plasma proteins (g) can hepatocytes form per day

A

15-50g/day

68
Q

most important plasma proteins (quantitatively)

A

albumin

a1 antitrypsin

69
Q

what does a1 antitypsin do

A

trypsin breaks down proteins. ex)emphysema has lack of antitrypsin so lung tissue is degraded

70
Q

transamination process

A

a keto acid is formed that has the same chemical composition as the AA to be formed except at the keto oxygen. next an amino radical is transferred from an available AA to the veto acid to take the place of the keto oxygen. this process takes many steps.

71
Q

phase 1 reaction in the liver

A

modify substances through CYP450 through oxidation or reduction

72
Q

oxidation

A

90% of all reactions
primarily via CYP450 enzymes and secondarily by mixed function oxidases
often generates reactive oxygen species because carboxyl, epoxy, and hydroxyl groups are introduced into the parent compound

73
Q

reduction

A

mainly catalyzed by CYP450 enzymes

74
Q

examples of CYP450 inducers

A

ethanol
barbiturates
ketamine
benzos

75
Q

examples of CYP450 inhibitors

A

ranitidine
amiodarone
ciprofloxacin

76
Q

drugs with very high rate of hepatic extraction from circulation

A 
lidocaine
morphine
verapamil
labetalol
propanolol
77
Q

drugs that have products of phase 1 reactions that are more active than the parent compound or considered cytotoxic

A

acetaminophen- glutathione is a free radical scavenger

isoniazid: metabolite that causes cells to activate their programmed cell death
halothane: hepatitis

78
Q

drugs efficiently extracted from the blood by the liver

A 
(efficiently extracted because fairly lipid soluble at baseline)
lidocaine
meperidine
morphine
nortrriptyline
pentazocine
propoxyphene
propanolol
labetalol
verapamil
79
Q

drugs poorly extracted from the blood by the liver

A 
acetaminophen
clindamycin
diazepam
digoxin
phenytoin
theophylline
warfarin
80
Q

phase II drug reactions

A

may or may not follow a phase 1 reaction, involves conjugation of a substance with a water soluble metabolite

81
Q

conjugation and most common added proteins

A

taking something small and adding something large and charged to make it water soluble so it can be excreted in the urine or bile
glucoronide is most common, then sulfate
taurine and glycine can also be utilized by the body

82
Q

the liver stores large quantities of these fat soluble vitamins

A

A, B12, D, E, K

83
Q

iron is stored in the liver as

A

ferritin

84
Q

apoferritin

A

protein produced by hepatic cells, excreted in large amounts to bind to excess iron in body fluids. apoferritin+iron=ferritin which is then stored in hepatocytes until the iron is needed elsewhere in the body

85
Q

transferrin

A

binds to iron and carries it in the blood for transport so iron does not travel in its free radical form and oxidize everything

86
Q

vitamin K is a required co factors for the synthesis of these 4 factors

A

2 (prothrombin), 7, 9, 10

87
Q

vitamin K deficiency manifests as a

A

coagulopathy due to impaired formation of factors 2, 7, 9, 10

88
Q

2 factors not produced by the liver

A

factor 8 and vWF

89
Q

liver is the primary site of degradation for (5)

A 
thyroid hormone
insulin
steroid hormones including cortisol, aldosterone, estrogen
glucagon
ADH
90
Q

hepatocytes continually secrete these 4 things into the bile canniculi

A

bile salts
cholesterol
phospholipids
conjugated bilirubin

91
Q

bile ducts from the hepatic lobules eventually form what?

A

the left and right hepatic ducts

92
Q

what two ducts form the common bile duct

A

cystic duct and hepatic duct

93
Q

flow of bile from common bile duct is controlled by

A

sphincter of oddi

94
Q

cholecystokinin

A

hormone released from intestinal mucosa in response to fat and protein that causes contraction of the gallbladder, relaxation of the sphincter of odd, and ejection of bile into the small intestine. also called the “cystic system”

95
Q

bilirubin

A

major end product of hgb degradation. provides valuable tool for diagnosing blood diseases and various types of liver disease

96
Q

how many days do RBC’s recycle

A

120 days

97
Q

Order of events for RBC degradation (5)

A
  1. HGB is split into globin and heme
  2. heme ring is opened and Fe is released and is transported in blood by transferrin
  3. 4 pyrrole rings of the porphyrin structure are converted to biliverdin
  4. biliverdin is rapidly converted to free bilirubin and is released from the macrophages
  5. free bilirubin immediately combines with plasma albumin
98
Q

how to drive carbon monoxide off of iron

A

increase in partial pressure O2

99
Q

what does CO2 combine to

A

nitrogen

100
Q

unconjugated or indirect bilirubin

A

free bilirubin or bilirubin bound to plasma protein. absorbed by hepatocytes, released from albumin, and then conjugated.

101
Q

conjugated or direct bilirubin

A

bilirubin conjugated with either glucoronide (80%) or sulfate (20%) then excreted from hepatocytes by an active transport process into bile canaliculi and then into the intestines

102
Q

urobilinogen

A

in the intestine, about 1/2 of conjugated bilirubin is then converted by bacteria to urobilinogen which is reabsorbed back into the blood. some of it is excreted into urine, majority is excreted back into intestines and eliminated by feces

103
Q

jaundice

A

excess unconjugated OR conjugated bilirubin in the ECF

104
Q

common 2 causes of jaundice

A

hemolytic

obstructive

105
Q

hemolytic jaundice

A

increased destruction/hemolyzation of RBC’s.

  • increased production of bilirubin by macrophages
  • increased unconjugated (free/indirect) bilirubin in blood. hepatocytes cannot process or conjugate all of this bilirubin
  • so while this results in a primarily increased unconjugated bilirubin, you will aolso see a secondary increased in conjugated bilirubin as well
  • rate of urobilinogen in intestine and urinary excretion increases but
  • excretory function of liver is not impaired
106
Q

obstructive jaundice

A

obstruction of bile ducts or damage to hepatocytes (hepatitis) preventing usual amounts of bilirubin from being excreted into GI tract.

  • unconjugated bilirubin enters hepatocytes and is conjugated the usual way. however, now cannot pass from liver into intestine
  • conjugated bilirubin enters blood probably either by rupture of cannaliculi or direct emptying of bile into lymph system
  • therefore, will see most bilirubin in conjugated form
107
Q

2 main causes of bile duct obstruction

A

gallstones, malignancies

108
Q

total obstruction of bile flow clinical finding

A

no conjugated bilirubin can reach the intestines to be converted to urobilinogen and therefore no urobilinogen is reabsorbed into the blood and excreted by kidneys. the urobilinogen test is COMPLETELY negative

N935 Pathophysiology (12 decks)

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