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Cells are bathed in an extracellular fl uid (ECF)

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Flashcard 4715009412364

Question
Cells are bathed in an [...]
Answer
extracellular fl uid (ECF)


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Cells are bathed in an extracellular fl uid (ECF)

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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Flashcard 4715014393100

Question
[...] is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF
Answer
ICF


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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Flashcard 4715015965964

Question
ICF is characterized by [...] , Na+ , and Cl-concentrations compared with ECF
Answer
low Ca2+


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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Flashcard 4715017538828

Question
ICF is characterized by low Ca2+ , [...] , and Cl-concentrations compared with ECF
Answer
Na+


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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Flashcard 4715019111692

Question
ICF is characterized by low Ca2+ , Na+ , and [...]concentrations compared with ECF
Answer
Cl-


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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Flashcard 4715034316044

Question
ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with [...]
Answer
ECF


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ICF is characterized by low Ca2+ , Na+ , and Cl-concentrations compared with ECF

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Lipids are ideally suited to a barrier function because they are hydrophobic

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Flashcard 4715107716364

Question
Lipids are ideally suited to a barrier function because they are [...]
Answer
hydrophobic


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Lipids are ideally suited to a barrier function because they are hydrophobic

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Proteins allow cells to interact with and communicate with each other

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Flashcard 4715182165260

Question
Proteins allow cells to [...] with and commu- nicate with each other
Answer
interact


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Proteins allow cells to interact with and commu- nicate with each other

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Flashcard 4715245341964

Question
Proteins allow cells to interact with and [...] with each other
Answer
communicate


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Proteins allow cells to interact with and communicate with each other

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Membranes contain three predominant types of lipid: phospholipids, cholesterol, and glycolipids

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Flashcard 4715350985996

Question
Membranes contain three predominant types of lipid: [...], cholesterol, and glycolipids
Answer
phospholipids


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Membranes contain three predominant types of lipid: phospholipids, cholesterol, and glycolipids

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Flashcard 4715375627532

Question
Membranes contain three predominant types of lipid: phospholipids, [...], and glycolipids
Answer
cholesterol


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Membranes contain three predominant types of lipid: phospholipids, cholesterol, and glycolipids

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Flashcard 4715399220492

Question
Membranes contain three predominant types of lipid: phospholipids, cholesterol, and [...]
Answer
glycolipids


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Membranes contain three predominant types of lipid: phospholipids, cholesterol, and glycolipids

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hydrophobic region is usually composed of fatty acid “tails”

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Flashcard 4715517709580

Question
hydrophobic region is usually composed of [...]
Answer
fatty acid “tails”


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hydrophobic region is usually composed of fatty acid “tails”

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Phospholipids comprise a fatty acid tail coupled via glycerol to a head group that contains phosphate and an attached alcohol

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Flashcard 4715659791628

Question
Phospholipids comprise a [...] coupled via glycerol to a head group that contains phosphate and an attached alcohol
Answer
fatty acid tail


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Phospholipids comprise a fatty acid tail coupled via glycerol to a head group that contains phosphate and an attached alcohol

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Flashcard 4715729521932

Question
Phospholipids comprise a fatty acid tail coupled via [...]l to a head group that contains phosphate and an attached alcohol
Answer
glycerol


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Phospholipids comprise a fatty acid tail coupled via glycerol to a head group that contains phosphate and an attached alcohol

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Flashcard 4716064804108

Question
Phospholipids comprise a fatty acid tail coupled via glycerol to a head group that contains [...]
Answer
phosphate and an attached alcohol


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Phospholipids comprise a fatty acid tail coupled via glycerol to a head group that contains phosphate and an attached alcohol

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Sphingo- myelin is a related phospholipid in which glycerol has been re- placed by sphingosine. The alcohol group in sphingomyelin is choline

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Flashcard 4716372823308

Question
Sphingo- myelin is a related phospholipid in which glycerol has been re- placed by [...]. The alcohol group in sphingomyelin is choline
Answer
sphingosine


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Sphingo- myelin is a related phospholipid in which glycerol has been re- placed by sphingosine. The alcohol group in sphingomyelin is choline

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Flashcard 4716430494988

Question
Sphingo- myelin is a related phospholipid in which glycerol has been re- placed by sphingosine. The alcohol group in sphingomyelin is [...]
Answer
choline


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Sphingo- myelin is a related phospholipid in which glycerol has been re- placed by sphingosine. The alcohol group in sphingomyelin is choline

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adding cholesterol to a membrane reduces its fluidity and makes it stronger and more rigid.

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Flashcard 4717755370764

Question
adding cholesterol to a membrane reduces its [...] and makes it stronger and more rigid.
Answer
fluidity


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adding cholesterol to a membrane reduces its fluidity and makes it stronger and more rigid.

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Flashcard 4717756943628

Question
adding cholesterol to a membrane reduces its fluidity and makes it [...] and more rigid.
Answer
stronger


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adding cholesterol to a membrane reduces its fluidity and makes it stronger and more rigid.

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Flashcard 4717758516492

Question
adding cholesterol to a membrane reduces its fluidity and makes it stronger and more [...].
Answer
rigid


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adding cholesterol to a membrane reduces its fluidity and makes it stronger and more rigid.

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glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via sphingosine to a carbohydrate head group

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Flashcard 4717762448652

Question
glycolipids, a minor but physiologically significant lipid type comprising a [...] coupled via sphingosine to a carbohydrate head group
Answer
fatty acid tail


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glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via sphingosine to a carbohydrate head group

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Flashcard 4717764021516

Question
glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via [...] to a carbohydrate head group
Answer
sphingosine


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glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via sphingosine to a carbohydrate head group

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Flashcard 4717765594380

Question
glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via sphingosine to a [...]
Answer
carbohydrate head group


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glycolipids, a minor but physiologically significant lipid type comprising a fatty acid tail coupled via sphingosine to a carbohydrate head group

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glycolipids create a carbohydrate cell coat that is involved in cell-to-cell interactions and that conveys antigenicity

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Flashcard 4717768740108

Question
glycolipids create a [...] that is involved in cell-to-cell interactions and that conveys antigenicity
Answer
carbohydrate cell coat


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glycolipids create a carbohydrate cell coat that is involved in cell-to-cell interactions and that conveys antigenicity

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Flashcard 4717770312972

Question
glycolipids create a carbohydrate cell coat that is involved in [...] and that conveys antigenicity
Answer
cell-to-cell interactions


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glycolipids create a carbohydrate cell coat that is involved in cell-to-cell interactions and that conveys antigenicity

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Flashcard 4717771885836

Question
glycolipids create a carbohydrate cell coat that is involved in cell-to-cell interactions and that conveys [...]
Answer
antigenicity


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glycolipids create a carbohydrate cell coat that is involved in cell-to-cell interactions and that conveys antigenicity

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Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces

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Flashcard 4717775817996

Question
Peripheral proteins are found on the [...]. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces
Answer
membrane surface


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Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extra

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Flashcard 4717777390860

Question
Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively [...] and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces
Answer
weak


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Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces

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Flashcard 4717778963724

Question
Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using [...]. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces
Answer
simple salt solutions


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Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the intracellular and extracellular plasma membrane surfaces

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Flashcard 4717780536588

Question
Peripheral proteins are found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the [...]
Answer
intracellular and extracellular plasma membrane surfaces


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e found on the membrane surface. Their link to the membrane is relatively weak and, thus, they can easily be washed free using simple salt solutions. Peripheral proteins associate with both the <span>intracellular and extracellular plasma membrane surfaces <span>

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Intracellular: Proteins that localize to the intracellular surface

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Flashcard 4717783682316

Question
Intracellular: Proteins that localize to the [...]
Answer
intracellular surface


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Intracellular: Proteins that localize to the intracellular surface

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Extracellular: Proteins located on the extracellular surface

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Flashcard 4717786828044

Question
Extracellular: Proteins located on the [...]
Answer
extracellular surface


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Extracellular: Proteins located on the extracellular surface

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Integral membrane proteins penetrate the lipid core. They are anchored by covalent bonds to surrounding structures

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Flashcard 4717789973772

Question
Integral membrane proteins penetrate the [...]. They are anchored by covalent bonds to surrounding structures
Answer
lipid core


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Integral membrane proteins penetrate the lipid core. They are anchored by covalent bonds to surrounding structures

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Flashcard 4717791546636

Question
Integral membrane proteins penetrate the lipid core. They are anchored by [...] to surrounding structures
Answer
covalent bonds


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Integral membrane proteins penetrate the lipid core. They are anchored by covalent bonds to surrounding structures

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Fick law: J ⫽ P ⫻ A (C 1 ⫺ C 2 )

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Diffusion rates increase when a molecule’s velocity increases

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Flashcard 4717805702412

Question
Diffusion rates increase when a molecule’s [...] increases
Answer
velocity


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Diffusion rates increase when a molecule’s velocity increases

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diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to molecular radius and the viscosity of the medium through which it diffuses

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Flashcard 4717808848140

Question
diffusion coeffi cient. The coeffi cient is proportional to [...] and in- versely proportional to molecular radius and the viscosity of the medium through which it diffuses
Answer
temperature


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diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to molecular radius and the viscosity of the medium through which it diffuses

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Flashcard 4717810421004

Question
diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to [...] and the viscosity of the medium through which it diffuses
Answer
molecular radius


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diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to molecular radius and the viscosity of the medium through which it diffuses

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Flashcard 4717811993868

Question
diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to molecular radius and the [...] of the medium through which it diffuses
Answer
viscosity


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diffusion coeffi cient. The coeffi cient is proportional to temperature and in- versely proportional to molecular radius and the viscosity of the medium through which it diffuses

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A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with water.

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Flashcard 4717815926028

Question
A molecule’s [...] is determined by measuring its solubility in oil compared with water.
Answer
partition coeffcient


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A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with water.

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Flashcard 4717817498892

Question
A molecule’s partition coeffcient is determined by measuring its [...] in oil compared with water.
Answer
solubility


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A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with water.

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Flashcard 4717819071756

Question
A molecule’s partition coeffcient is determined by measuring its solubility in [...] compared with water.
Answer
oil


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A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with water.

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Flashcard 4717820644620

Question
A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with [...]
Answer
water.


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A molecule’s partition coeffcient is determined by measuring its solubility in oil compared with water.

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Net diffusion rate slows when molecules have to traverse thick membranes compared with thin ones

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Flashcard 4717824576780

Question
Net diffusion rate slows when molecules have to traverse [...] compared with thin ones
Answer
thick membranes


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Net diffusion rate slows when molecules have to traverse thick membranes compared with thin ones

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Flashcard 4717826149644

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[...] slows when molecules have to traverse thick membranes compared with thin ones
Answer
Net diffusion rate


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Increasing the surface area available for diffusion also increases the rate of diffusion

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Flashcard 4717830081804

Question
[...] the surface area available for diffusion also increases the rate of diffusion
Answer
Increasing


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Flashcard 4717831654668

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Increasing the [...] available for diffusion also increases the rate of diffusion
Answer
surface area


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Flashcard 4717833227532

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Increasing the surface area available for diffusion also increases the [...]
Answer
rate of diffusion


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The rate at which molecules diffuse across a membrane is directly proportional to the concentration difference between the two sides of the membrane

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Flashcard 4717836373260

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The rate at which molecules diffuse across a membrane is directly [...] to the concentration difference between the two sides of the membrane
Answer
proportional


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Flashcard 4717837946124

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The rate at which molecules diffuse across a membrane is directly proportional to the [...] between the two sides of the membrane
Answer
concentration difference


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Flashcard 4717839518988

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The rate at which [...] across a membrane is directly proportional to the concentration difference between the two sides of the membrane
Answer
molecules diffuse


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Pores are integral membrane proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support very high transit rates

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Flashcard 4717843451148

Question
Pores are [...] proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support very high transit rates
Answer
integral membrane


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Pores are integral membrane proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they a

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Flashcard 4717845024012

Question
Pores are integral membrane proteins containing [...], water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support very high transit rates
Answer
unregulated


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Pores are integral membrane proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support v

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Flashcard 4717846596876

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Pores are integral membrane proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always [...] and can support very high transit rates
Answer
open


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roteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always <span>open and can support very high transit rates <span>

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Flashcard 4717848169740

Question
Pores are integral membrane proteins containing unregulated, water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support very high [...]
Answer
transit rates


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water- filled passages that allow ions and other small molecules to cross the membrane. Pores are relatively uncommon in higher organisms because they are always open and can support very high <span>transit rates <span>

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Ions (sodium [Na+], potassium [K+], chloride [Cl-], and calcium [Ca2+]) flow through cardiac membrane channels with pores formed by proteins, with these ion channels encoded by specific genes [3]. The pore-forming protein is called the alpha subunit, which also contains the voltage-dependent sensors and gates. For many ion channels, one or more secondary regulatory subunit proteins are present (usually named beta, gamma, delta, and so on) in association with the alpha subunit, and many ion channel proteins have subunit isoforms adding to their complexity

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Pathophysiology and genetics" and "Brugada syndrome: Epidemiology and pathogenesis" and "Etiology of atrioventricular block", section on 'Familial disease'.) Cardiac ion channels and currents — <span>Ions (sodium [Na+], potassium [K+], chloride [Cl-], and calcium [Ca2+]) flow through cardiac membrane channels with pores formed by proteins, with these ion channels encoded by specific genes [3]. The pore-forming protein is called the alpha subunit, which also contains the voltage-dependent sensors and gates. For many ion channels, one or more secondary regulatory subunit proteins are present (usually named beta, gamma, delta, and so on) in association with the alpha subunit, and many ion channel proteins have subunit isoforms adding to their complexity. The encoding genes, amino acid sequences, and structure-function relationships for many ion channels have been described and are now reasonably well understood (figure 1) [4]. Ion chan




The dominant channel types in heart cells are Na+ channels (INa), L-type and T-type Ca2+ channels (ICa-L, ICa-T), and several K+ channels (IK1, Ito1, Ito2, IKr, IKs). The sodium-potassium pump and the sodium-calcium exchanger are not considered channels because they require energy to drive ions across the membrane against their gradients, however they do generate currents (figure 1).

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ng kinetics, or pharmacology (figure 1). For example, the voltage-dependent sodium current (INa) flows through the protein NaV1.5 encoded by the gene SCN5A and similarly for other ion channels. <span>The dominant channel types in heart cells are Na+ channels (INa), L-type and T-type Ca2+ channels (ICa-L, ICa-T), and several K+ channels (IK1, Ito1, Ito2, IKr, IKs). The sodium-potassium pump and the sodium-calcium exchanger are not considered channels because they require energy to drive ions across the membrane against their gradients, however they do generate currents (figure 1). Resting membrane potential — The resting cardiac cell membrane potential is normally polarized between -80 and -95 mV, with the cell interior negative relative to the extracellular spac




The resting cardiac cell membrane potential is normally polarized between -80 and -95 mV, with the cell interior negative relative to the extracellular space. The resting membrane potential is determined by the balance of inward (Na+ and Ca2+) and outward (K+) currents and the corresponding equilibrium potentials of these currents

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ger are not considered channels because they require energy to drive ions across the membrane against their gradients, however they do generate currents (figure 1). Resting membrane potential — <span>The resting cardiac cell membrane potential is normally polarized between -80 and -95 mV, with the cell interior negative relative to the extracellular space. The resting membrane potential is determined by the balance of inward (Na+ and Ca2+) and outward (K+) currents and the corresponding equilibrium potentials of these currents. In turn, the equilibrium potential for a given ion is determined by the concentrations of that ion inside and outside the cell. Using these concentrations, the equilibrium potential is




In the heart, the resting membrane potential is generated by the inward rectifier current (IK1), which is the predominant open channel at rest. Potassium current IK1 flowing through this channel continues until the interior negative potential is at the same magnitude as the equilibrium potential for potassium. Only small amounts of actual potassium flow are required to maintain this potential. The equilibrium potentials for sodium and calcium are positive (approximately +40 mV and approximately +80 mV, respectively) so that when these channels are open, they tend to depolarize the membrane.

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-95 mV. When potassium channels open, potassium ions flow down their gradient as an outward current, carrying positive ions outside the cell and taking the cell toward more negative potentials. <span>In the heart, the resting membrane potential is generated by the inward rectifier current (IK1), which is the predominant open channel at rest. Potassium current IK1 flowing through this channel continues until the interior negative potential is at the same magnitude as the equilibrium potential for potassium. Only small amounts of actual potassium flow are required to maintain this potential. The equilibrium potentials for sodium and calcium are positive (approximately +40 mV and approximately +80 mV, respectively) so that when these channels are open, they tend to depolarize the membrane. Voltage-sensitive sodium, calcium, and potassium channels play only a small role in the resting state since most of these channels are closed [5,6]. The Na-K-ATPase pump maintains the p




Voltage-sensitive sodium, calcium, and potassium channels play only a small role in the resting state since most of these channels are closed [5,6]. The Na-K-ATPase pump maintains the potassium and sodium gradients by pumping potassium into and sodium out of the cells. The Na-Ca exchanger uses the power of the Na gradient to pump Ca out of the cell

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ilibrium potentials for sodium and calcium are positive (approximately +40 mV and approximately +80 mV, respectively) so that when these channels are open, they tend to depolarize the membrane. <span>Voltage-sensitive sodium, calcium, and potassium channels play only a small role in the resting state since most of these channels are closed [5,6]. The Na-K-ATPase pump maintains the potassium and sodium gradients by pumping potassium into and sodium out of the cells. The Na-Ca exchanger uses the power of the Na gradient to pump Ca out of the cell. These and other pumps maintain the ion channel gradient that is important for both excitability and contraction. Action potential in fast response tissues — Tissues that depend upon th




#Cardiologie #Médecine #Physiologie #Rythmologie

Action potential in fast response tissues —

Tissues that depend upon the opening of voltage-sensitive, kinetically rapid (opening in less than a millisecond) sodium channels to initiate depolarization are called fast response tissues [7].

Fast response tissues include the atria, the specialized infranodal conducting system (bundle of His, fascicles and bundle branches, and terminal Purkinje fibers), and the ventricles (figure 2), while the sinoatrial (SA) and atrioventricular (AV) nodes represent slow response tissues.

It is important to recognize that accessory AV pathways (ie, bypass tracts) associated with Wolff-Parkinson-White syndrome are derived from the atria and are thus also fast response tissues dependent upon sodium current for depolarization.

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he Na-Ca exchanger uses the power of the Na gradient to pump Ca out of the cell. These and other pumps maintain the ion channel gradient that is important for both excitability and contraction. <span>Action potential in fast response tissues — Tissues that depend upon the opening of voltage-sensitive, kinetically rapid (opening in less than a millisecond) sodium channels to initiate depolarization are called fast response tissues [7]. Fast response tissues include the atria, the specialized infranodal conducting system (bundle of His, fascicles and bundle branches, and terminal Purkinje fibers), and the ventricles (figure 2), while the sinoatrial (SA) and atrioventricular (AV) nodes represent slow response tissues. It is important to recognize that accessory AV pathways (ie, bypass tracts) associated with Wolff-Parkinson-White syndrome are derived from the atria and are thus also fast response tissues dependent upon sodium current for depolarization. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis".) The following is a simplified description of the steps involved in the generation




Phase 0 — Rapid depolarization (phase 0) occurs when the resting cell is brought to threshold, leading sequentially to activation or opening of voltage-dependent sodium channels, rapid sodium entry into the cells down a favorable concentration gradient, and a cell interior positive potential that can approach +45 mV. The marked depolarization initiates voltage-dependent inactivation of the sodium channels. Calcium channels also open during depolarization, but the inward calcium flux is much slower.

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on of the action potentials also vary in the right and left ventricle, and transmurally across the wall of the heart [9], again depending upon differences in ion channel and current densities. ●<span>Phase 0 — Rapid depolarization (phase 0) occurs when the resting cell is brought to threshold, leading sequentially to activation or opening of voltage-dependent sodium channels, rapid sodium entry into the cells down a favorable concentration gradient, and a cell interior positive potential that can approach +45 mV. The marked depolarization initiates voltage-dependent inactivation of the sodium channels. Calcium channels also open during depolarization, but the inward calcium flux is much slower. ●Phase 1 — Phase 1 repolarization often inscribes a "notch" and is primarily caused by activation of the transient outward potassium currents (Ito) combined with a corresponding rapid d




Phase 1 — Phase 1 repolarization often inscribes a "notch" and is primarily caused by activation of the transient outward potassium currents (Ito) combined with a corresponding rapid decay of the sodium current. The degree of repolarization in phase 1 is dependent on the density of Ito and varies between cardiac chambers and regions within chambers.

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+45 mV. The marked depolarization initiates voltage-dependent inactivation of the sodium channels. Calcium channels also open during depolarization, but the inward calcium flux is much slower. ●<span>Phase 1 — Phase 1 repolarization often inscribes a "notch" and is primarily caused by activation of the transient outward potassium currents (Ito) combined with a corresponding rapid decay of the sodium current. The degree of repolarization in phase 1 is dependent on the density of Ito and varies between cardiac chambers and regions within chambers. ●Phase 2 — Following initial repolarization in phase 1, phase 2 represents a plateau that lasts for hundreds of milliseconds and distinguishes the cardiac action potential from nerve an




#Cardiologie #Médecine #Physiologie #Rythmologie
Phase 2 — Following initial repolarization in phase 1, phase 2 represents a plateau that lasts for hundreds of milliseconds and distinguishes the cardiac action potential from nerve and skeletal muscle action potentials, which are significantly shorter. Late inactivating depolarizing calcium and sodium currents are balanced by activating repolarizing potassium currents to maintain the plateau, which is often down-sloping as repolarizing currents begin to dominate.

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h a corresponding rapid decay of the sodium current. The degree of repolarization in phase 1 is dependent on the density of Ito and varies between cardiac chambers and regions within chambers. ●<span>Phase 2 — Following initial repolarization in phase 1, phase 2 represents a plateau that lasts for hundreds of milliseconds and distinguishes the cardiac action potential from nerve and skeletal muscle action potentials, which are significantly shorter. Late inactivating depolarizing calcium and sodium currents are balanced by activating repolarizing potassium currents to maintain the plateau, which is often down-sloping as repolarizing currents begin to dominate. ●Phases 3 and 4 — The final rapid repolarizing phase 3 is driven by the decay of the calcium current and progressive activation of repolarizing potassium currents (IKr, IKs). Terminal r




Phases 3 and 4 — The final rapid repolarizing phase 3 is driven by the decay of the calcium current and progressive activation of repolarizing potassium currents (IKr, IKs). Terminal repolarization toward the potassium equilibrium potential is dominated in phase 3 by IK1, which then maintains the resting membrane potential (phase 4).

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larizing calcium and sodium currents are balanced by activating repolarizing potassium currents to maintain the plateau, which is often down-sloping as repolarizing currents begin to dominate. ●<span>Phases 3 and 4 — The final rapid repolarizing phase 3 is driven by the decay of the calcium current and progressive activation of repolarizing potassium currents (IKr, IKs). Terminal repolarization toward the potassium equilibrium potential is dominated in phase 3 by IK1, which then maintains the resting membrane potential (phase 4). During one cycle of depolarization and repolarization, the voltage-dependent channels cycle through three different kinetic or gating states: ●Resting. ●Open, as the channels open durin




In the resting state, the channels can be opened positive to the threshold potential. In comparison, the inactivated channel cannot be activated until it cycles or "recovers" to the resting state. These different states are important clinically, since, for example, some antiarrhythmic drugs (such as the class I antiarrhythmic drugs) preferentially bind to open and inactivated sodium channels

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y in diastole, the channel returns to the resting state. The resting and inactivated states are different physiologically, even though the channel is effectively nonconducting in both settings. <span>In the resting state, the channels can be opened positive to the threshold potential. In comparison, the inactivated channel cannot be activated until it cycles or "recovers" to the resting state. These different states are important clinically, since, for example, some antiarrhythmic drugs (such as the class I antiarrhythmic drugs) preferentially bind to open and inactivated sodium channels. Action potential in slow response tissues — The SA and AV nodes represent slow response tissues, which have different properties from the fast response tissues (table 1). Phase 0 depol




Action potential in slow response tissues — The SA and AV nodes represent slow response tissues, which have different properties from the fast response tissues (table 1). Phase 0 depolarization depends on an inward calcium (not sodium) current via L-type calcium channels [10]. These channels are selective for calcium, have a slower conduction velocity than the sodium channels, and take longer to reactivate.

In some cases, as with tissue damage or changes in the extracellular milieu, fast response tissues can be converted to slow response tissues. In this setting, sodium channels become inactivated and depolarization is dependent upon the slow calcium channels.

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different states are important clinically, since, for example, some antiarrhythmic drugs (such as the class I antiarrhythmic drugs) preferentially bind to open and inactivated sodium channels. <span>Action potential in slow response tissues — The SA and AV nodes represent slow response tissues, which have different properties from the fast response tissues (table 1). Phase 0 depolarization depends on an inward calcium (not sodium) current via L-type calcium channels [10]. These channels are selective for calcium, have a slower conduction velocity than the sodium channels, and take longer to reactivate. In some cases, as with tissue damage or changes in the extracellular milieu, fast response tissues can be converted to slow response tissues. In this setting, sodium channels become inactivated and depolarization is dependent upon the slow calcium channels. Impulse propagation — When an action potential forms in a patch of membrane (the source), current flows from this patch to neighboring patches (the sink). Gap junctions are the low resi




The gap junctions are actually active, opening and closing in response to changes in pH, calcium, and, at times, voltage.

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). Gap junctions are the low resistance structures that allow ions to flow from one cell to another and, if the current flow is sufficient, to cause sequential depolarization from cell to cell. <span>The gap junctions are actually active, opening and closing in response to changes in pH, calcium, and, at times, voltage. In addition to ion flow and gap junction resistance, impulse propagation can also be affected by the orientation of fibers and of the collagen matrix in which the fibers reside. "Fast"




In addition to ion flow and gap junction resistance, impulse propagation can also be affected by the orientation of fibers and of the collagen matrix in which the fibers reside

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ow is sufficient, to cause sequential depolarization from cell to cell. The gap junctions are actually active, opening and closing in response to changes in pH, calcium, and, at times, voltage. <span>In addition to ion flow and gap junction resistance, impulse propagation can also be affected by the orientation of fibers and of the collagen matrix in which the fibers reside. "Fast" tissues may conduct very slowly (declining from meters/second to millimeters/second) in a number of circumstances, resulting in prolongation of the QRS and QT intervals on the s




In 1812, the British ophthalmologist James Ware relayed a curious finding to the members of the Royal Society in London

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The gene-based hack that is revolutionizing epidemiology
author in: Pub Med Nature.com Google Scholar Share on Twitter Share on Twitter Share on Facebook Share on Facebook Share via E-Mail Share via E-Mail Illustration by Acapulco Studio PDF version <span>In 1812, the British ophthalmologist James Ware relayed a curious finding to the members of the Royal Society in London. Of thousands of young men recruited to regiments of the British army, only six had been turned away for poor vision in 20 years. But up to one-quarter of students about the same age go




#Infectiologie #Médecine #Pharmacologie #Physiologie
L’efficacité des anti-infectieux résulte en général du rapport entre la concentration de la molécule active obtenue au niveau du site d’action et la sensibilité du micro-organisme à cette molécule.

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#Infectiologie #Médecine #Pharmacologie #Physiologie
t MB $.* FTU MB QMVT QFUJUF DPODFOUSBUJPO QFS- mettant d’inhiber la multiplication du micro- organisme ; t MB $.& T BQQMJRVF Ë DFSUBJOT BOUJGPOHJRVFT vis-à-vis des champignons filamenteux, et est la plus petite concentration permettant d’obtenir une altération morphologique du champignon ; t M *$ 50 , qui s’applique essentiellement aux anti- viraux, est la plus petite concentration permet- tant d’inhiber 50 % de la réplication virale.

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#Infectiologie #Médecine #Pharmacologie #Physiologie
Les molécules dont l’activité est essentiellement bactério-/fongistatique néces- siteront donc l’apport du système immunitaire pour éradiquer le micro-organisme. À l’inverse, les molécules fongicides/bactéricides ne néces- sitent pas l’action du système immunitaire et seront donc privilégiées dans toutes situations d’immunosuppression, qu’elles soient systé- miques (neutropénie, etc.) ou limitées au foyer infectieux (endocardite, méningite, etc.).

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#Infectiologie #Médecine #Pharmacologie #Physiologie
L’acti- vité fongicide/bactéricide sera d’autant plus mar- quée que les concentrations minimales fongicides et bactéricides (CMF et CMB : concentrations qui réduisent un inoculum d’au moins 99,9 %) seront peu différentes des CMI.

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#Infectiologie #Médecine #Pharmacologie #Physiologie
Les critères PK/PD prédictifs de l’efficacité sont les rapports C max /CMI et AUC/CMI

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Degrees of freedom is a critical core concept within the field of statistics

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#Infectiologie #Médecine #Pharmacologie #Physiologie
Le paramètre PK/PD prédicitif de l’efficacité est donc le pourcentage de temps entre deux administrations ou sur 24 heures pendant lequel la concentration en antibiotique est supérieure à la CMI ou à un multiple de la CMI (T > CMI ou le fT > CMI si l’on considère la fraction libre)

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#Infectiologie #Médecine #Pharmacologie #Physiologie
Parmi les antibiotiques et les antifongiques, cer- tains seront également sensibles à l’effet inocu- lum. Cet effet se traduit par une augmentation de la CMI en présence d’un inoculum bactérien ou fongique important. Les molécules sensibles à cet effet, comme les bêtalactamines et l’amphotéricine B, verront donc leur efficacité diminuer dans les infections sévères à fort inoculum.

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#Infectiologie #Médecine #Pharmacologie #Physiologie
Dans le cas des antiviraux, l’efficacité serait cor- rélée au maintien de la concentration au-dessus d’un certain seuil d’efficacité, lequel pourrait correspondre à l’IC 50 , sans que cela ait été for- mellement démontré.

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#meta
That bothered me increasingly until I bought a Kindle which had 'highlight' functionality and virtual keyboard; and I had discovered it to help a lot with recalling.

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How to annotate literally everything | Mildly entertainingᵝ
n At some point in my life I realized I didn't remember most of the books/papers/posts/videos I had consumed few years before. For brevity I'll just refer to all of this as 'content' further on <span>That bothered me increasingly until I bought a Kindle which had 'highlight' functionality and virtual keyboard; and I had discovered it to help a lot with recalling. I've become increasingly obsessed with this and these days ability to highlight when I read serves multiple purposes for me: the very act of spending conscious effort on highlighting an




#Infectiologie #Médecine #Pharmacologie #Physiologie
L’importance du mode d’administration vis-à-vis de l’efficacité a été démontrée dans de nombreuses études. Par exemple, l’efficacité des aminosides dans les infections à bacilles à Gram négatif, qui est liée au rapport C max /CMI, est meilleure lorsqu’ils sont administrés en dose unique journalière que lorsque la dose journalière est divisée en deux ou trois prises

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Leur éradication nécessite donc un niveau de concentration plus élevé. L’objectif est en fait de dépasser un certain seuil de concentration appelé « concentration prévenant l’émergence de mutants » (CPM). Atteindre cette concentration limite l’émergence de mutants résistants. La zone de concentration située entre la CMI des micro-organismes sen- sibles et cette CPM est appelée « fenêtre de sélec- tion de mutants ».

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%BOT MF DBT E BENJOJTUSBUJPO FO DPOUJOV TDIÏNB privilégié pour les antibiotiques à activité temps- dépendante, le prélèvement devra être fait au « plateau », lorsqu’on aura atteint l’équilibre phar- macocinétique ou l’état dit « stationnaire », soit après 5 à 7 demi-vies du médicament concerné.

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Hypothes.is is a clear winner for me on desktop and I'm using Instapaper for offline reading on Android.

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How to annotate literally everything | Mildly entertainingᵝ
ctionable like piece of advice or further reading. Not available for mobile yet, but perhaps on Android native select and share capabilities (e.g. into orgzly) makes more sense anyway. ¶Summary <span>Hypothes.is is a clear winner for me on desktop and I'm using Instapaper for offline reading on Android. ¶3 Annotating PDFs Small disclaimer: I don't own Mac/Windows/iPhone so have very little idea what's going on in their world. Sorry! You can take a look at a section I added with other p




Three distinct mechanisms underlie tachyarrhythmia induction: enhanced automaticity, reentry, and triggered activity

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MATION — While the term "arrhythmia" also includes bradyarrhythmias caused by a failure of impulse generation, this section will focus on the cellular and tissue mechanisms of tachyarrhythmias. <span>Three distinct mechanisms underlie tachyarrhythmia induction: enhanced automaticity, reentry, and triggered activity (figure 5) . Enhanced automaticity — Enhanced automaticity refers to abnormal phase 4 diastolic depolarization, and occurs when spontaneous depolarization develops during diastole (figu




Enhanced automaticity — Enhanced automaticity refers to abnormal phase 4 diastolic depolarization, and occurs when spontaneous depolarization develops during diastole (figure 5). While this is a normal phenomenon in nodal cells, and with subsidiary pacemakers at slower rates in all myocardial cells, enhanced or abnormal automaticity may lead to tachyarrhythmia. A typical example is automatic (ie, focal) atrial tachycardia. Common automaticity stimulants include excess catecholamine or situations causing hypoxia, acidosis, or ischemic related metabolites.

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ocus on the cellular and tissue mechanisms of tachyarrhythmias. Three distinct mechanisms underlie tachyarrhythmia induction: enhanced automaticity, reentry, and triggered activity (figure 5) . <span>Enhanced automaticity — Enhanced automaticity refers to abnormal phase 4 diastolic depolarization, and occurs when spontaneous depolarization develops during diastole (figure 5). While this is a normal phenomenon in nodal cells, and with subsidiary pacemakers at slower rates in all myocardial cells, enhanced or abnormal automaticity may lead to tachyarrhythmia. A typical example is automatic (ie, focal) atrial tachycardia. Common automaticity stimulants include excess catecholamine or situations causing hypoxia, acidosis, or ischemic related metabolites. (See "Focal atrial tachycardia" and "Enhanced cardiac automaticity".) Reentry — Reentry is the most commonly encountered arrhythmia mechanism and refers to any arrhythmia dependent on a




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Critical components for reentry include both of the following:

● The presence of fast and slow conduction with varying refractory/recovery periods

● A fixed or functional core about which the circuit moves

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nced cardiac automaticity".) Reentry — Reentry is the most commonly encountered arrhythmia mechanism and refers to any arrhythmia dependent on an electrical circuit within the heart (figure 5). <span>Critical components for reentry include both of the following: ●The presence of fast and slow conduction with varying refractory/recovery periods ●A fixed or functional core about which the circuit moves Initiation of reentry requires a unidirectional block within the reentrant path, such that one arm of the circuit conducts the approaching electrical wave front and the blocks it in the




Interventions to terminate reentrant arrhythmias differ from other mechanisms and are generally geared to modify the critical components of the reentrant circuit. Blocking Na+ or Ca2+ channels can slow or block conduction, while blocking K+ channels prolongs the action potential and therefore increases refractoriness

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slow conducting limb is the normal AV node. An example of fixed reentry arrhythmia is ventricular tachycardia with a fixed myocardial scar and variable conduction in the surrounding myocardium. <span>Interventions to terminate reentrant arrhythmias differ from other mechanisms and are generally geared to modify the critical components of the reentrant circuit. Blocking Na+ or Ca2+ channels can slow or block conduction, while blocking K+ channels prolongs the action potential and therefore increases refractoriness. Another approach is to improve functional properties such as ischemia in an area of functional block that can terminate the arrhythmia. Interventions that electrically interrupt the re




Triggered activity — Triggered activity refers to a depolarization that occurs after the initial depolarization wavefront and comes in two forms, either early or late. Secondary depolarizations that occur before the action potential has fully repolarized are early afterdepolarizations (EADs) (figure 5). Those that occur after the action potential has fully repolarized are delayed afterdepolarizations (DADs) (figure 5). Both EADs and DADs depend on the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism.

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nt loop (ie, cardioversion), or ablating tissue critical to the reentrant loop. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".) <span>Triggered activity — Triggered activity refers to a depolarization that occurs after the initial depolarization wavefront and comes in two forms, either early or late. Secondary depolarizations that occur before the action potential has fully repolarized are early afterdepolarizations (EADs) (figure 5). Those that occur after the action potential has fully repolarized are delayed afterdepolarizations (DADs) (figure 5). Both EADs and DADs depend on the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism. ●EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally




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EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS

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the previous action potential to trigger them, hence an afterdepolarization is said to be a triggered arrhythmia. However, it is important to understand that DADs and EADs differ in mechanism. ●<span>EADs — EADs are triggered during prolonged action potentials. A prolonged action potential allows a longer window for reopening of L-type Ca2+ channels during phase 2 (or occasionally phase 3) of the action potential. L-type Ca2+ current depolarizes the membrane before repolarization, triggering an afterdepolarization. Due to L-type Ca2+ channel time and voltage dependence, EADs occur at slow stimulation rates or after a ventricular pause when action potential duration (phase 2) is prolonged and they are suppressed with faster heart rates. EADs are thought to initiate the polymorphic ventricular arrhythmias torsades de pointes (TdP) found in inherited and acquired long QT syndrome (LQTS), for example drug-induced LQTS. A point of distinction to be made here is that triggered activity can initiate TdP, but TdP may be a re-entrant mechanism at the organ level with a functional (spiral reentry) rather t




DADs — DADs, which result from intracellular Ca2+ overload, are triggered after the action potential is fully repolarized. Under conditions of Ca2+ overload, Ca2+ taken back up by the sarcoplasmic reticulum is then transiently re-released into the cytoplasm. This in turn causes a transient rise in cytoplasmic Ca2+ activating Ca2+-dependent depolarizing membrane current mostly through the Na+-Ca2+ exchanger. The exchange of three Na+ for two Ca2+ produces a net inward and transient depolarization or a DAD.

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be a re-entrant mechanism at the organ level with a functional (spiral reentry) rather than fixed anatomical core. (See "Acquired long QT syndrome: Definitions, causes, and pathophysiology".) ●<span>DADs — DADs, which result from intracellular Ca2+ overload, are triggered after the action potential is fully repolarized. Under conditions of Ca2+ overload, Ca2+ taken back up by the sarcoplasmic reticulum is then transiently re-released into the cytoplasm. This in turn causes a transient rise in cytoplasmic Ca2+ activating Ca2+-dependent depolarizing membrane current mostly through the Na+-Ca2+ exchanger. The exchange of three Na+ for two Ca2+ produces a net inward and transient depolarization or a DAD. If the DAD reaches threshold voltage, it can initiate an action potential. Conditions which enhance cellular Ca2+ loading, such as rapid heart rates, enhance DAD susceptibility. DADs ma




Conditions which enhance cellular Ca 2+ loading, such as rapid heart rates, enhance DAD susceptibility

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a+-Ca2+ exchanger. The exchange of three Na+ for two Ca2+ produces a net inward and transient depolarization or a DAD. If the DAD reaches threshold voltage, it can initiate an action potential. <span>Conditions which enhance cellular Ca2+ loading, such as rapid heart rates, enhance DAD susceptibility. DADs may be important in myocardial ischemia, digoxin toxicity, and in some inherited arrhythmia syndromes such as catecholaminergic polymorphic ventricular tachycardia. (See "Cardiac




Certain arrhythmogenic substrates are common, such as those induced by ischemia or infarction. In this setting, a certain effect of a drug becomes predominant and predictable, as with class I activity in ischemia, and a drug classification appears accurate. However, the major drug effect may be quite different if a different proarrhythmic substrate exists. Consider, for example, the differences in digitalis action in hypokalemia and hyperkalemia.

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rmed by arrhythmogenic factors interacts with antiarrhythmic drugs. Depending upon the substrate encountered, the resulting substrate may be antiarrhythmic, antifibrillatory, or proarrhythmic. ●<span>Certain arrhythmogenic substrates are common, such as those induced by ischemia or infarction. In this setting, a certain effect of a drug becomes predominant and predictable, as with class I activity in ischemia, and a drug classification appears accurate. However, the major drug effect may be quite different if a different proarrhythmic substrate exists. Consider, for example, the differences in digitalis action in hypokalemia and hyperkalemia. Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. Class I — The class




Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate.

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However, the major drug effect may be quite different if a different proarrhythmic substrate exists. Consider, for example, the differences in digitalis action in hypokalemia and hyperkalemia. <span>Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably




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Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel.

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ypokalemia and hyperkalemia. Class 0 — Drugs in the newly proposed Class 0 modulate the pacemaker channel HCN4, affecting the pacemaker current If [11]. The blocker ivabradine slows heart rate. <span>Class I — The class I drugs act by modulating or blocking the sodium channels, thereby inhibiting phase 0 depolarization. They are all at least in part positively charged and presumably interact with specific amino acid residues in the internal pore of the sodium channel. Three different subgroups (table 2 and table 3) have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dis




● The class Ic agents have the slowest binding and dissociation from the binding site.

● The class Ib agents have the most rapid binding and dissociation from the binding site.

● The class Ia agents are intermediate in terms of the speed of binding and dissociation from the binding site.

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2 and table 3) have been identified because their mechanism or duration of action is somewhat different due to variable rates of drug binding to and dissociation from the channel receptor [14]: <span>●The class Ic agents have the slowest binding and dissociation from the binding site. ●The class Ib agents have the most rapid binding and dissociation from the binding site. ●The class Ia agents are intermediate in terms of the speed of binding and dissociation from the binding site. During faster heart rates, less time exists for the drug to dissociate from the receptor, resulting in an increased number of blocked channels and enhanced blockade. These pharmacologic




During faster heart rates, less time exists for the drug to dissociate from the receptor, resulting in an increased number of blocked channels and enhanced blockade. These pharmacologic effects may cause a progressive decrease in impulse conduction velocity and a widening of the QRS complex. This property is known as "use-dependence" and is seen most frequently with the class Ic agents, less frequently with the class Ia drugs, and rarely with the class Ib agents

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lass Ib agents have the most rapid binding and dissociation from the binding site. ●The class Ia agents are intermediate in terms of the speed of binding and dissociation from the binding site. <span>During faster heart rates, less time exists for the drug to dissociate from the receptor, resulting in an increased number of blocked channels and enhanced blockade. These pharmacologic effects may cause a progressive decrease in impulse conduction velocity and a widening of the QRS complex. This property is known as "use-dependence" and is seen most frequently with the class Ic agents, less frequently with the class Ia drugs, and rarely with the class Ib agents [15]. ●Class Ia drugs (quinidine, procainamide, and disopyramide) depress phase 0 (sodium-dependent) depolarization, thereby slowing conduction. They also have moderate potassium channe




Class Ia drugs (quinidine, procainamide, and disopyramide) depress phase 0 (sodium-dependent) depolarization, thereby slowing conduction. They also have moderate potassium channel blocking activity (which tends to slow the rate of repolarization and prolong action potential duration [APD])

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QRS complex. This property is known as "use-dependence" and is seen most frequently with the class Ic agents, less frequently with the class Ia drugs, and rarely with the class Ib agents [15]. ●<span>Class Ia drugs (quinidine, procainamide, and disopyramide) depress phase 0 (sodium-dependent) depolarization, thereby slowing conduction. They also have moderate potassium channel blocking activity (which tends to slow the rate of repolarization and prolong action potential duration [APD]), and quinidine in particular also blocks potassium current ITo, which is useful for suppressing certain ventricular arrhythmias such as those found in the Brugada syndrome. Class Ia age




Class Ia agents also have anticholinergic activity and tend to depress myocardial contractility. At slower heart rates, when use-dependent blockade of the sodium current is not significant, potassium channel blockade may become predominant (reverse use-dependence), leading to prolongation of the APD and QT interval and increased automaticity

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tial duration [APD]), and quinidine in particular also blocks potassium current ITo, which is useful for suppressing certain ventricular arrhythmias such as those found in the Brugada syndrome. <span>Class Ia agents also have anticholinergic activity and tend to depress myocardial contractility. At slower heart rates, when use-dependent blockade of the sodium current is not significant, potassium channel blockade may become predominant (reverse use-dependence), leading to prolongation of the APD and QT interval and increased automaticity. One difference between the drugs is that quinidine and procainamide generally decrease vascular resistance, whereas disopyramide increases vascular resistance. In addition, N-acetyl-pr




One difference between the drugs is that quinidine and procainamide generally decrease vascular resistance, whereas disopyramide increases vascular resistance.

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the sodium current is not significant, potassium channel blockade may become predominant (reverse use-dependence), leading to prolongation of the APD and QT interval and increased automaticity. <span>One difference between the drugs is that quinidine and procainamide generally decrease vascular resistance, whereas disopyramide increases vascular resistance. In addition, N-acetyl-procainamide (NAPA), a metabolite of procainamide, has little sodium current blocking activity, while retaining potassium current blocking activity. Thus, NAPA beh




The class Ib drugs (lidocaine and mexiletine) have less prominent sodium channel blocking activity at rest, but effectively block the sodium channel in depolarized tissues.

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metabolite of procainamide, has little sodium current blocking activity, while retaining potassium current blocking activity. Thus, NAPA behaves like a class III drug. (See 'Class III' below.) ●<span>The class Ib drugs (lidocaine and mexiletine) have less prominent sodium channel blocking activity at rest, but effectively block the sodium channel in depolarized tissues. They tend to bind in the inactivated state (which is induced by depolarization) and dissociate from the sodium channel more rapidly than other class I drugs. As a result, they are more




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Class Ic drugs (flecainide and propafenone) primarily block open sodium channels and slow conduction. They dissociate slowly from the sodium channels during diastole, resulting in increased effect at a more rapid rate (use-dependence). This characteristic is the basis for their antiarrhythmic efficacy, especially against supraventricular arrhythmias. Use-dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia

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induced by depolarization) and dissociate from the sodium channel more rapidly than other class I drugs. As a result, they are more effective with tachyarrhythmias than with slow arrhythmias. ●<span>Class Ic drugs (flecainide and propafenone) primarily block open sodium channels and slow conduction. They dissociate slowly from the sodium channels during diastole, resulting in increased effect at a more rapid rate (use-dependence). This characteristic is the basis for their antiarrhythmic efficacy, especially against supraventricular arrhythmias. Use-dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia. Flecainide and propafenone also have potassium channel blocking activity and can increase the APD in ventricular myocytes. Propafenone has significant beta blocking activity. Another r




Flecainide and propafenone also have potassium channel blocking activity and can increase the APD in ventricular myocytes. Propafenone has significant beta blocking activity.

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aventricular arrhythmias. Use-dependence may also contribute to the proarrhythmic activity of these drugs, especially in the diseased myocardium, resulting in incessant ventricular tachycardia. <span>Flecainide and propafenone also have potassium channel blocking activity and can increase the APD in ventricular myocytes. Propafenone has significant beta blocking activity. Another recognized target for antiarrhythmic action is the late sodium current, which is enhanced in both acquired and inherited arrhythmias. When enhanced, it lengthens the APD and can




Class II — Class II drugs act by inhibiting sympathetic activity, primarily by causing beta blockade. They may also have a mild inhibitory effect on the sodium channels.

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ing drug is ranolazine, a drug approved for the treatment of chronic angina, but which may have antiarrhythmic activity [16]. This target has been proposed as a new sub-classification, Id [11]. <span>Class II — Class II drugs act by inhibiting sympathetic activity, primarily by causing beta blockade. They may also have a mild inhibitory effect on the sodium channels. Sympathetic stimulation has the following potential proarrhythmic actions [17]: ●An increase in automaticity due to enhancement of phase 4 spontaneous depolarization (see "Enhanced card




Sympathetic stimulation has the following potential proarrhythmic actions [ 17]:

● An increase in automaticity due to enhancement of phase 4 spontaneous depolarization (see "Enhanced cardiac automaticity").

● An increase in membrane excitability due to shortening in refractoriness (phases 2 and 3 of the action potential).

● An increase in the rate of impulse conduction through the myocardial membrane, resulting from acceleration of phase 0 upstroke velocity or the rate of membrane depolarization.

● An increase in delayed afterpotentials, especially when the cell is calcium loaded, such as in digoxin toxicity.

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lassification, Id [11]. Class II — Class II drugs act by inhibiting sympathetic activity, primarily by causing beta blockade. They may also have a mild inhibitory effect on the sodium channels. <span>Sympathetic stimulation has the following potential proarrhythmic actions [17]: ●An increase in automaticity due to enhancement of phase 4 spontaneous depolarization (see "Enhanced cardiac automaticity"). ●An increase in membrane excitability due to shortening in refractoriness (phases 2 and 3 of the action potential). ●An increase in the rate of impulse conduction through the myocardial membrane, resulting from acceleration of phase 0 upstroke velocity or the rate of membrane depolarization. ●An increase in delayed afterpotentials, especially when the cell is calcium loaded, such as in digoxin toxicity. By blocking catecholamine and sympathetically mediated actions, beta blockers slow the rate of discharge of the sinus and ectopic pacemakers, and increase the effective refractory perio




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By blocking catecholamine and sympathetically mediated actions, beta blockers slow the rate of discharge of the sinus and ectopic pacemakers, and increase the effective refractory period of the AV node. They also slow both antegrade and retrograde conduction in anomalous pathways [18].

Carvedilol is a beta-blocker with unique additional properties. In addition to beta- and alpha-adrenergic blockade, carvedilol can also block potassium (KCNH2, formerly HERG), calcium, and sodium currents and modestly prolong APD. However, when administered chronically, carvedilol increases the number of these channels, which is probably a favorable effect in diseased hearts [19].

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celeration of phase 0 upstroke velocity or the rate of membrane depolarization. ●An increase in delayed afterpotentials, especially when the cell is calcium loaded, such as in digoxin toxicity. <span>By blocking catecholamine and sympathetically mediated actions, beta blockers slow the rate of discharge of the sinus and ectopic pacemakers, and increase the effective refractory period of the AV node. They also slow both antegrade and retrograde conduction in anomalous pathways [18]. Carvedilol is a beta-blocker with unique additional properties. In addition to beta- and alpha-adrenergic blockade, carvedilol can also block potassium (KCNH2, formerly HERG), calcium, and sodium currents and modestly prolong APD. However, when administered chronically, carvedilol increases the number of these channels, which is probably a favorable effect in diseased hearts [19]. The most recent classification (table 2 and table 3) expands the definition of class II to include "autonomic inhibitors and activators," with subclass IIa as beta adrenergic blockers s