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Advanced Patho UC > Exam #1 > Flashcards

Exam #1 Flashcards

1
Q

Factors that affect rate of diffusion - remember diffusion is movement of particles from high to low concentration

A
  1. concentration difference
  2. electrical potential - aka charge difference
    - remember that movement occurs to equalize the charge across the membrane
  3. pressure difference - higher pressure results in increased energy available to cause net movement from high to low pressure
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2
Q

Osmosis

A

PASSIVE transport of fluid across a membrane from an area of lower solute concentration into an area of higher solute concentration (less fluid comparatively)

*AKA water moves down it’s concentration gradient

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3
Q

Osmotic pressure

A

difference in solute concentration across the membrane creates osmotic pressure difference (osmosis occurs)

  • isotonic = no water flow
  • hypotonic = low solute - fluid will rush into cell
  • hypertonic = high solute - fluid out of cell (given to help with dehydration)
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4
Q

Facilitated diffusion

A

molecules move along electrochemical concentration gradient (down concentration gradient) attached to “carrier” protein molecule that facilitates its passage
-no energy is required bc it does NOT move against it’s electrochemical gradient

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5
Q

Primary ACTIVE Transport

-what is an example?

A

molecules ARE moved/pumped against (UPHILL) a concentration gradient

  • example is Na+,K+, ATPase pump
  • MUST HAVE ATP to do this
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6
Q

What is the Na+,K+, ATPase pump and how does it work?

  • plays an important role in?
  • requires how much energy?
  • ATPase does what?
A
  • It is a carrier protein located on the plasma membrane of ALL cells
  • Na/K ATPase = enzyme that converts ATP to ADP to release energy
  • Plays important role in regulating osmotic balance by maintaining Na and K balance, preventing cells from swelling and bursting
  • Requires 1-2/3 of cells energy
  • Also important in establishing negative electrical voltage inside the cells which is the basis for nerve function
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7
Q

With the Na/K pump - what is pumped out and what is pumped in?

A

3 Na+ are pumped out, and 2 K+ are pumped in

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8
Q

Ca2+ ATPase function and what is it? where is it located?

A

uses primary active transport

  • present on the cell membrane and the sarcoplasmic reticulum
  • MAINTAINS LOW CYTOSOLIC Ca2+ concentration
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9
Q

H+ ATPase
where is it found?
what does it do?

A

uses primary active transport

  • found in parietal cells of gastric glands (HCl secretion) and intercalated cells of renal tubules (controls blood pH)
  • concentrates H+ ions up to 1 million-fold
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10
Q

Secondary active transport

how is transport driven? how is it created?

A
  • secondary active transport is driven by energy stored in the concentration gradient of another molecule (Na+)
  • created originally by primary active transport (INDIRECT USE OF ENERGY)
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11
Q

Secondary active transport co-transport - This is indirect use of energy

A

co-transport (co-porters): substance is transported in the same direction as the “driver” ion

  • example Na+ and bicarb into cell- remember this is what stops being driven into the cell during metabolic acidosis. Assuming this makes bicarb more available to balance the low pH
  • other examples = Na+ & AA into the cell; Na+ and glucose into the cell
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12
Q

Secondary active transport counter-transport

A

anti-porters = substance is transported in the OPPOSITE direction as the “driver” ion (Na+)

examples: Na driven inside and H driven out; Na driven in and Ca driven out, Na+/HCO3- in and Cl-/H+ to outside of cell

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13
Q

How do cardiac glycosides increase cardiac contractility?

A

By inhibiting the Na/K pump, this causes Na+ to stay inside the cell and reduces the sodium gradient - this means that Na and Ca2+ can not be exchanged thereby keeping more calcium inside the cell and increasing cardiac contractility

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14
Q

Remember that facilitated diffusion does not use…

A

ENERGY

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15
Q

Ungated ion channels - allow ions through depending on what?

A

size, shape, distribution of charge, etc.

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16
Q

Gated ion channel - 2 types and explain

A

voltage dependent gated ion channels - voltage depends on Na+ channels

chemically gated channels - only open/close whether specific substance has attached. Ex. nicotinic ACh receptor channels

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17
Q

The diffusion potential level across a membrane that exactly opposes the net diffusion of a particular ion through the membrane

A

Nernst potential (or equilibrium potential of that ion)

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18
Q

the chemical and electrical driving forces acting on an ion are equal and opposite, and no further net diffusion occurs

A

Electrochemical equilibrium

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19
Q

The resting membrane potential is established by…

A

by the diffusion potentials that result from concentration differences of permeable ions

-each permeable ion will attempt to drive the membrane towards its equilibrium potential, and ions with the highest permeabilities, or conductance, will make the greatest contributions (aka K+)

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20
Q

The electrical potential that counters net diffusion of K+ is called the…

A

K+ equilibrium potential

21
Q

The potassium Nernst potential (aka the equilibrium potential) would be what? if the membrane were only permeable to K+?

A

Ek = -94mV

22
Q

The sodium Nernst potential if the membrane were only permeable to Na+ would be

A

Ena = +61mV

23
Q

Vm =

what is it normally?

A

resting membrane potential

normally -70 to -90 mV

24
Q

What calculate Vm when more than one ion is involved and what is the take home message?

A

Goldman-Hodgkin-Katz equation
-Take home message is the resting membrane potential is closest to the equilibrium potential for the ion with the highest permeability

25
Q

Action potential rely on what type of ion channels?

A

voltage-gated ion channels -ion channels that are activated by changes in the electrical membrane potential near the channel. The membrane potential alters the conformation of the channel proteins, regulating their opening and closing

26
Q

Membrane potential at which occurrence of the AP is inevitable

A

threshold potential

27
Q

portion of the AP where the membrane potential is positive (cell interior is positive)

A

OVERSHOOT

28
Q

also called the hyerpolarizing after-potential, the portion of the AP following repolarization where the membrane potential is actually more negative than at rest

A

UNDERSHOOT

29
Q

Flow of positive charge into the cell

-example: Na+ flows into the cell during the ______ of the AP

A

inward current; during the upstroke of the action potential

30
Q

Flow of positive charge out of the cell is called? example? creates what kind of stroke?

A

outward current

  • these currents hyperpolarize the membrane potential
  • ex. flow of K+ out of the cell during the repolarization phase of the AP, creating a downward stroke
31
Q

When action potential occurs what happens to let sodium inside. Change in membrane potential causes these channels to open…

A

voltage gated channels open to let Na+ in, then AP reached and they close – then K+ moves out and causes hyperpolarization b/c stay open slightly longer

32
Q

At rest the inactivation gate is _______ and the activation gate is ________

A

inactivation gate is open; activation gate is closed

33
Q

during the upstroke of the AP, both gates are ______

A

both gates are open and Na+ flows into the cell down its electrochemical potential gradient

34
Q

During the repolarization period, the inactivation gate is ______ and the activation gate is ________

A

inactivation gate is closed; activation gate is open

35
Q

Myelination - what is it, and what does it do?

A

myelin is a lipid substance that decreases ion flow through the membrane - allows the nerve signal to be transmitted quickly and efficiently

36
Q

What interrupts the the myelin sheath every 1-3mm? And what is it’s function

A

node of Ranvier

  • this is the only place on the nerve cell where action potentials can occur (Na channels are concentrated here!)
  • allows for increased velocity of nerve transmission
  • allows for energy conservation for the axon
37
Q

Remember the difference b/w gap junction and chemical synapse?

A

gap junctions are electrical synapses that allow current to flow from one excitable cell directly through space b/w cells - a gap junction connects the cytoplasm of two cells (connection is direct b/w the presynaptic neuron and the postsynaptic neuron)

a neuromuscular junction is a chemical synapse - there is a gap b/w the pre and postsynaptic cell - uses neurotransmitters to transmit information across the cleft

38
Q

What occurs at a chemical synapse

A

1- AP reaches axon terminal and depolarizes membrane
2- voltage-gated ca channels open and calcium comes into cell
3- ca influx triggers synaptic vesicles to release neurotransmitters
4- neurotransmitters bind to postsynaptic cell and elicit AP (Na+ rushes in)

39
Q

change in membrane potential can be _____ or _____

A

excitatory - meaning that depolarization occurs

inhibitory - meaning that hyperpolarization occurs of the postsynaptic cell

40
Q

specialized synapse b/w a motoneuron and a muscle fiber

A

occurs at a structure on the m. fiber called the motor end plate. this is also the same as the neuromuscular junction (usually only one per fiber)

action potential can apparently travel in both directions

41
Q

motor end plate = ______ = ________

A

neuromuscular junction, chemical synapse

42
Q

what neurotransmitters are released from motoneurons and to what do they bind on muscle cells

A

ACh and they bind nicotinic receptors which open Na/K channels and result in an AP in the muscle tissue

43
Q

how is ACh degraded and what happens to it?

A

it is degraded by Acetylcholine esterase and (AChE) into acetate and choline –> choline is taken back up by the presynaptic terminal of the motoneuron on a Na choline co-transporter (Na and choline go into the cell at the same time) –> rem. counter transport would be opposite

44
Q

Opening of nicotinic ACh receptor channels produces an __________ which will normally initiate an AP in the local spread of current is sufficient to open voltage sodium channels

How is this process terminated?

A

end plate potential

-this process is terminated by AChE b/c this makes ACh less available at the motor end plate or chemical synapse or neuromuscular junction

45
Q

Drug effects on the end plate potential - inhibitors

A

curariform drugs (d-turbocurarine) - block nicotinic ACh channels by competing for ACh binding sites; reduces amplitude of end plate potential therefore, no AP

botulinum toxin

  • decrease the release of ACh from nerve terminals
  • insufficient stimulus to initiate AP
46
Q

Curariform drugs (D-turbocurarine)

A

blocks nicotinic ACh channels by competing for ACh binding sites

this reduces amplitude of end plate potential - therefore, no AP

-generally used in anesthesia - m. relax - can cause paralysis and death in maximal doses

47
Q

botulinum toxin

A

decreases release of ACh from the nerve terminal (motoneuron terminal)

insufficient stimulus to initiate an AP - no skeletal m. contraction

can cause respiratory failure and death

48
Q

Stimulants - Drug effect on end plate potential

A

ACh-like drugs (methacholine, carbachol, nicotine)

  • bind and activate nicotinic ACh receptors
  • not destroyed by AChE b/c it’s not ACh - so there is a prolonged effect

Anti-AChE (neostigmine, physostigmine, diisopropyl fluorophosphate or “nerve gas”)

  • inactivate AChE
  • prolong effect of ACh
  • these drugs can be used in myasthenia gravis to prolong effect of ACh since there is a decrease in nicotinic receptors

Advanced Patho UC (14 decks)

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