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Pharm Exam 3 (Sab) > Module 7 > Flashcards

Module 7 Flashcards

1
Q

When a chemical is absorbed and gets into blood this means it has?

A

100% bioavailability

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2
Q

If a chemical compound comes into the blood and it is hydrophilic it can be excreted by the _______

A

Kidneys

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3
Q

The liver transforms compounds by _______ to detoxify or activate them

A

Biotransformation

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4
Q

Why does the liver need to biotransform chemical compounds?

A

The liver needs to modify them to make them lipophobic/hydrophilic

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5
Q

Lipophoic and a hydrophillic compound means that is it

A

water-soluble

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6
Q

Once the liver completes biotransformation and it does detoxicatican the non-toxic metabolic can be?

A

excreted by the kidney

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7
Q

In the liver once biotransformation occurs and the compound is activated into a toxic metabolite it can now do what?

A
  • Pharmacologic effects
  • pathologic effect
  • DNA injury
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8
Q

what is involved with biotransformation in the liver and is a hemoprotein?

A

Cytochrome P450

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9
Q

Compounds from outside the body getting into the body (exogenous compound)

A

Xenobiotics

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10
Q

Xenobiotic: which is this?
Horrible, DNA damage, produced by distillery using petroleum

A

PCB

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11
Q

Xenobiotic: Which is this?
Liver cannot handle this

A

PAH

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12
Q

Chemical/biochemical modification of degradation, usually through specialized _______ (primary hepatic) systems.

A

Enzymatic

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13
Q

Enzymatic systems power ?

A

Biotransformation

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14
Q

why do we need to have drug metabolism? Excretion of metabolites . We need them polarized and turned into?

A

Lipophobic and hypophilic

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15
Q

In Phase 1, the liver introduces or uncovers functional groups on molecules (e.g., -OH, -NH₂, -SH) through _______

A
  • oxidation
  • reduction
  • hydrolysis.
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16
Q

Phase 1 can convert certain _______ into active forms, as seen with drugs that require bioactivation

A

nontoxic metabolites

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17
Q

Phase 1 and Phase II reactions are biotransformation of chemicals that occur during _______

A

drug metabolism

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18
Q

MFOs (mixed function oxidases) help during Phase 1. These include?

A
  • Cytochrome P450 mono-oxygenase
  • MAOs (Monoamine oxidase)
  • Peroxidases
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19
Q

The MFOs are a oxidation-reduction reaction to turn lipophilic to lipophobic this is a non-synthetic _______

A

Redox reaction

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20
Q

Liver preps Xenobiotics to prepare compound for the next step which is _______

A

Redox

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21
Q

Phase 1 does oxidation and reduction which is a redox reaction. Reduction: cytochrome P450 reductases include

A
  • Esterases
  • Amidases
  • Hydrolases
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22
Q

Phase 1 metabolites: Are not necessarily cleared _______

A

rapidly

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23
Q

Phase 1 metabolies: May undergo a subsequent reaction in which an endogenous substrate combines with the newly incorporated functional group to form a _______

A

highly polar conjugate

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24
Q

Phase 1 reaction preps compounds to allow a potential _______ for something new

A

binding site

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25
Q

what happens after phase I reactions?

A

Phase II

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26
Q

Phase II reactions usually known as _______ and are addition rxns

A

Conjugation reactions

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27
Q

Phase 1 reactions are non-synthetic and phase II reactions are

A

synthetic

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28
Q

In Phase 2, the liver conjugates (links) the substance to another compound, such as _______ making it more water-soluble and less active

A

Glucuronic acid, sulfates, glutathione, amino acid

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29
Q

During phase 2 the conjugated compounds can be excreted more easily in

A

urine or bile

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30
Q

Phase 2 generally _______ and detoxifies metabolites, preparing them for excretion

A

inactivates

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31
Q

What can be attached to products of phase 1 and conjugate to make compound water soluble

A
  • -COOH
  • -OH
  • NH2
  • -SH
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32
Q

Phase II reactions can make

A

endogenous substrates

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33
Q

After conjugation in Phase 2 the compounds can go to the kidney and be excreted in urine or can get recycled in the liver multiple times and create bile salts and bile pigments. These compounds can then be excreted in?

A

Feces

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34
Q

if a xenobiotic compound comes in already hydrophilic it can do directly to _______

A

plasma circulation and be excreted by the kidneys

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35
Q

For Nontoxic Metabolites: The liver may convert inactive compounds into _______ or prepare them for excretion

A

active metabolites

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36
Q

For Toxic Metabolites: The liver _______ potentially harmful metabolites, often rendering them harmless and facilitating their elimination from the body

A

detoxifies

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37
Q

Reductase and oxidase don’t affect polar compounds because they?

A

Already have charge that can conjugate

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38
Q

Lipophilic Xenobiotics go to phase 1 (bioactivation or inactivation) which makes the compound?

A

Polar

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39
Q

Once the lipophilic xenobiotic goes through phase 1 and becomes polar it goes to phase 2 for

A

Bioinactivation/ conjugation

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40
Q

Once the lipophilic xenobiotic goes through phase 1 and becomes polar it goes to phase 2 for conjugation. Once it is conjugated in phase 2 it becomes _______ and can then go to extracellular mobilization

A

Hydrophilic

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41
Q

Xenobiotics that are accumulated (storage in body,fat, bone) are highly lipophilic and metabolically stable. Can they go through Phase 1 alone to get to extracellular mobilization or do they have to go through phase 2 as well?

A

Phase 1 only

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42
Q

Common signs of hepatic insufficiency

A

Depression, Anorexia, GI upset, Hepatic encephalopathy, Weight loss, Icterus

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43
Q

The liver takes non-polar substances and make them

A

polar

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44
Q

Ammonia is lipohilic and is made by the body. Ammonia turns into ammonium. The liver then converts ammonium into _______ to be excreted

A

Urea

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45
Q

Hepatocellular damage (Leakage enzyme) is _______ when the dog in WNL

A

undetectable

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46
Q

Leakage enzymes are cycosolic that was bound on the liver because of

A

liver damage

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47
Q

what enzymes are included in hepatocellular damage

A

AST, ALT, ALP, LDH, GGT

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48
Q

Biliary stoppage is little to no bile flow (what is this)

A

Cholestasis

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49
Q

Increase in bilirubin in blood (jaundice)

A

Hyperbilirubinemia

50
Q

T/F: Oxidative stress, steroids, NSAIDS have an effect on the liver

A

F

51
Q

Altered synthesis of clotting factors and albumin is a liver problem/disfunction that causes a decrease in?

A

Albumin and clotting factors

52
Q

what creates bile?

A

hepatocytes and cholangiocytes

53
Q

Inflammation of biliary system

A

Cholangitis

54
Q

Flow of bile

A

Choleresis

55
Q

Bile is an _______

A

exocrine aqueous mixture (organic and inorganics)

56
Q

The excretion of bile is not directly excreted into _______

A

bloodstream

57
Q

Starting place for bile formation is the _______

A

Canaliculi

58
Q

Starting place for bile formation is the canaliculi which is a canal of bile flow into path of becoming?

A

adult bile

59
Q

What is not a vital tissue

A

Gall bladder

60
Q

what stimulates pancreatic and biliary secretions. This contracts the ball bladder abd relaxes the sphincter of Oddi

A

CCK (PKZ)

61
Q

This is soluble in water meaning it is hydrophobic and lipophilic. It is needed to make bile

A

Cholesterol

62
Q

_______ causes cholesterol to gain an OH group to become cholic and chenodeoxycholic acid.

A

7 alpha hydroxylase

63
Q

What are the “primary” bile acids?

A

Cholic acid and Chenodeoxycholic acid

64
Q

Once cholic acid is formed _______ turn it into deoxycholic acid by removing the OH group

A

7 alpha dehydroxylase

65
Q

7 alpha dehydroxylase converts chenodeoxycholic acid into _______ by removing the OH group

A

Lithocholic acid

66
Q

What are the “secondary bile salts”

A

Deoxycholic acid and lithocholic acid

67
Q

Secondary bile salts become less lipophilic by being conjugated to form

A

Bile salts

68
Q

When deoxycholic acid is conjugated it becomes?

A

Glycine

69
Q

When lithocholic acid is conjugated it becomes _______ which is a bile salt

A

Taurine

70
Q

What are the two major proteins in bile salts

A

Glycine and taurine

71
Q

Bile acids are _______ meaning they have polar and nonpolar ends

A

amphipathic

72
Q

Bile acids preform _______ which prevents lipids in the GI from coming back together (break them down and keep them small)

A

Emulsification

73
Q

What stimulates Bile acids and what do bile acids help to do?

A
  • Induction of bile flow
  • Detoxification (xenobiotics)
  • Protection against bacterial overgrowth
  • Signaling (farsenoid)
  • Glucose metabolism (GLUT 4)
74
Q

Adaptive function of bile acids decompensates in pathology that affects secretion

A
  • Plasma membrane damage (Cholangiocytes)
  • Mitochondrial damage
  • Apoptosis
75
Q

Oily, foul smelling shit

A

Steatorrhea

76
Q

what can cause steatorrhea

A

Resuccution of the SI or A LOT of fatty foods

77
Q

when could you expect to see steatorrhea?

A
  • pancreatic/hepatic disease
  • Hypersecretion or hyposecretion of bile acids/salts
  • Failure to synthesize Apoprotein B
78
Q

What are lipids transported and bound to in the SI once they are absorbed in the SI?

A

Apoprotein B

79
Q

When Apoprotein B synthesis fails we expect to see steatorrhea because?

A

rate of reabsorption of lipids is decreased so poop is “fatty”

80
Q

What are bile pigments comprised of?

A

Dead RBC

81
Q

Biliverdin bile pigment is what color?

A

Green

82
Q

Bilirubin bile pigment is what color?

A

Yellow (jaudice/icterus)

83
Q

What is the substrate of bile pigments

A

Tetrapyrroles (hemoglobin)

84
Q

Bilverdin is the _______ form of bilirubin

A

oxidized

85
Q

In the gut bile pigments are metabolized by gut bacteria to _______ pigements. which then get excreted in feces

A

Brown

86
Q

RBC get old and after their lifespan is over they become _______

A

Senescent

87
Q

Senescent is used by the reticular endothelial system (RES) in the

A

liver and spleen

88
Q

Hemoglobin is usually metabolized to biliverdin and bilirubin; normally conjugated with _______

A

sugar residue (glucuronic acid)

89
Q

what in the spleen is the rate limiting steps to make biliverdin. This substance in the spleen breaks open hemoglobin and turns it into biliverdin

A

Hemeoxigenase

90
Q

Biliverdin has a partial reduction to be turned into this lipophilic substance

A

Bilirubin

91
Q

why can we see jaundice?

A

Bilirubin (yellow) is lipophilic so it is in fats

92
Q

Ligandin has a receptor for bilirubin-albumin conjugate and then puts on hepatocytes to become?

A

Bilirubin diglucuronide (can be excreted in urine or bile)

93
Q

Insol Br requires _______ for transport into spleen

A

albumin

94
Q

Bile pigments can be modified in the GI tract to become?

A

Urobilinogens or stercobilinogen

95
Q

In the GIT bilirubin is reabsorbed and secreted into urine

A

Urobilinogens (when exposed to air it becomes brown)

96
Q

In the GIT bilirubins are oxidized to stercobilins bacteria. They are then excreted as?

A

Stercobilinogen (gives feces brown color)

97
Q

Hyperbilirubinemia can cause?

A
  • Excessive hemolysis
  • Hepatic/bile obstruction
  • Ineffective erythropoiesis
  • hepatic overproduction
  • Hepatic defects
98
Q

when there is too much RBC death the liver gets overwhelmed so there is an overflow of?

A

Bilirubin

99
Q

more _______ in the SI causes urobilinogen to increase

A

Bilirubin diglucuronide

100
Q

When there is more RBC cell death the liver is overwhelmed so there is an overflow of bilirubin. this increases bilirubin diglucuronide in the SI and causes stercobilin (BLACK/TAR poo)

A

Excessive hemolysis

101
Q

what is the cause of clay colored stools?

A

Extrahepatic obstruction (mass outside bile duct)

102
Q

During an energetic crysis like starvation the liver helps the body form carbs from non carbs (sugars, proteins)

A

negative energy balance

103
Q

How can the liver make new carbs during negative energy balance

A

Gluconeogenesis, ketogenesis and glycogenolysis

104
Q

Liver can take FA and AA and use B-oxidation to convert FFA to Acetyl Coa . Acetyl CoA can use oxidative phosphorylation to make?

A

Acetoacetate and B-hydroxybutyric acid

105
Q

Alanine is used in the liver during negative energy balance to concert it to sugar

A

Gluconeogeneisis

106
Q

what are derived from NEFAs?

A

Ketones

107
Q

when insulin is LOW and glucagon is HIGH it increases cAMP in adipose and increases the activity of?

A

Hormone-sensitive lipase (HSL)

108
Q

HSL breaks down triglycerides into?

A

NEFAs

109
Q

During starvation NEFAs can be used in?

A

Hepatocytes

110
Q

the hepatocytes use NEFAs to start ketogenosis to create ketones for?

A

energy

111
Q

Ketones are a _______ acid

A

volatile and fixed

112
Q

Ketones can be used by all organs but vital organs require _______ to break down ketones to use for energy

A

Transverase

113
Q

Acetoacetate plus succinylCoA make what

A

3 ketoacid CoA

114
Q

A polyaromatic hydrocarbon entered the blood stream of a cat and became a threat. How might the hepatic system help to minimize the T 1/2 of these compounds before they lead to potentially disastrous pathology?

A

The liver has the capability to transform these compounds via enzymatic pathways that will attenuate their toxicity

115
Q

what is the expected change in ALT, AST, ALP and LDH due to cholestatsis?

A

They increase

116
Q

what is the best index of hepatocellular damage?

A

Elevated ALT and ALP

117
Q

The primary effect of bile secretion int the GI tract during/after a meal?

A

Emulsification

118
Q

Which expression best reflects the adaptive significance of Phase 1 hepatic reactions linked specifically to MFOs

A

MFOs prime compounds for conjugation with polar compounds during phase 2

119
Q

T/F: endogenous compounds like catecholamines, aldosterone and thyroid hormones are subject to hepatic biotransformation by the same enzymatic machinery that processes xenobiotics

A

T

120
Q

T/F: An animal with hepatic disease that is showing signs might be linked to the inability of the liver to process ammonia

A

T

121
Q

conjugation of bilirubin with glucuronate occurs?

A

Hepatocytes

122
Q

Increases HSL, NEFAs and ketogenesis are stimulated by _______ rather than insulin

A

Glucagon

Pharm Exam 3 (Sab) (3 decks)

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