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Quarter 2 > Physiology Exam 1 > Flashcards

Physiology Exam 1 Flashcards

1
Q

Gaba-ergic synapse

A

Inhibitory
Chloride channels
neurotransmitter: GABA
ion gates (making it Ionotropic, ligand gated still)
Hyperpolarizes the postsynaptic cell, inhibits neuron firing!

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2
Q

Excitatory Adrenergic Synapse

A

Metabotropic example (Slower response)
G protein coupled receptor- requiring second messenger
Neurotransmitter: Norepinephrine (aka noradreniline)
Receptor: transmembrane associated with G protein
1. Binding of NE to receptor releases the G protein
2. G protien binds to Adenylate Cyclase
3. activated cAMP
4. cAMP does many things. In this case, triggers Ligand gated Sodium (Na+) channels to open
5. Result: depolarization!

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3
Q

Classic Cholinergic Synapse

A

Ionotropic, Ligand gated (quick response!)
Neurotransmitter: AcH
1. Ach diffuses across cleft and binds to receptors on postsynaptic cell
2. triggers opening of ligand gated Na+ channels producing local graded potentials
3. If graded potential gets to -55 mV, action potential is triggered!

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4
Q

Removal of AcH at cleft

A

Has it’s own enzyme for this: AcHE (achetylcholinesterase)
AcHE breaks AcH into two parts: Acetate & Choline
Acetate: cheap. made as a byproduct of Glycolysis. diffuses away
Choline: $$$ Expensive. pumped back into presynaptic knob

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5
Q

SNARE concept

A

Proteins on the vesicle:

  1. Synaptobrevin
  2. Synaptagmin (what Ca2+ binds to)

Proteins on the terminal membrane of pre-synaptic cell

  1. SNAP25
  2. Syntaxin
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6
Q

What happens with SNARE?

A

The proteins on the vesicle and the proteins on the terminal membrane work together to bring the vesicle to the membrane to release the Ach contents

Depolarization of knob triggers Calcium to enter and bind to SYNAPTAGMIN which tells the cell it’s ready for AcH to be brought to the forefront and released from the vesicle

The vesicle and terminal membrane proteins are intertwined together to always have a vesicle ready and “on deck” to be brought to the forefront and released

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7
Q

Receptors in postynaptic cell

A

the greater the # of receptors, the greater the response!

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8
Q

Myasthenia Gravis

A

a condition in which AcH (acetylcholine) receptors on the post-synaptic cell are degraded and therefore this neurotransmitter cannot be detected
result: muscle weakness

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9
Q

4 main ways to end a signal

A

Diffusion- slow, not the most common way. diffusion of the neurotransmitter away from the cleft
Enzyme Degradation- there are enzymes at the cleft that bind to the neurotransmitter and degrade them
Re-uptake (2 ways within) neurotransmitter is taken back up into the presynaptic knob
A. Recycled: stored in knob for later use
B. Destroyed: enzymes in the KNOB destroy the neurotransmitter

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10
Q

Cocaine and Dopamine

A

Cocaine acts on the body by preventing the re-uptake of Dopamine back into the pre-synaptic knob so it always hangs out in the cleft and keeps firing the happy signal
(eventually, the receptors tire out and you crash)

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11
Q

Epi & Norepi

A

Sympathetic Nervous System

“fight or flight”

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12
Q

AcH

A

Neurotransmitter at the Neuromuscular Junction

Always excitatory!

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13
Q

Glycine

A

always inhibitory

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14
Q

GABA

A

inhibitory neurotransmitter operating by CHLORIDE channels

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15
Q

Nitrous Oxide

A

gas that works to inhibit the CNS via diffusion

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16
Q

Receptor types

A

Ionotropic- fast, ligand gated, most of what we talk about

Metabotropic- slower, G protein coupled receptors, ex: DAG, cAMP, IP3

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17
Q

Saltatory Conduction

A

jumping from nodes of ranvier- where the myelination is lacking

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18
Q

How do we code for stimulus intensity?

Stimulus: graded potential

A

the RATE of firing. How quickly are the Action Potentials firing one after another?

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19
Q

A neuron can terminate at 3 things

A

another neuron (synapse
muscle
gland

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20
Q

Sodium has two channels

A

Activation

Inactivation

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21
Q

Potassium

A

only has one voltage gated channel
opens & closes slowly
Flux of K happens for a longer period of time than Na+ flux. Reason for overshoot!

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22
Q

Graded potential examples

A

Synaptic potential in post synaptic neuron

Glutamate binding to Ionotropic

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23
Q

Temporal summation

A

rapid firing one after another until they build to reach threshold and fire AP
ONE LOCATION

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24
Q

Spatial summation

A

signal coming from MANY diff LOCATIONS

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25
Q

Potassium

A

Big concentration flow OUTWARD
Small electrical flow INWARD
Overall: weak outward flux but
HIGH permeability

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26
Q

Sodium

A

Big concentration flow inward
Big electrical flow inward
Overall: Strong inward flux but
LOW permeability

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27
Q

Graded potential characteristics:

A

Chemically gated channels
Transient
How far they get depends on the strength of the stimulus
Gets weaker the further it travels
Change in potential is proportional to the stimulus

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28
Q

Hyperkalemic

Hypernatremic

A

depolarization!

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29
Q

Membrane potential

A

most of it is d/t the diffusion of Na and K down their respective conc. gradients through background channels

the pump only contributes ~20%

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30
Q

Hypokalemia

Hyponatremia

A

Hyperpolarizatoin

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31
Q

Nernst eq’n

A

tells us the electrical force required to balance out the concentration gradient force for a particular ion

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32
Q

K+ Potassium wants to move out bc of its conc. gradient and it gets pulled back in (by negative anions)

A

Na+ wants to move into cell bc of its conc. gradient and it gets pulled back out (by Cl- ions)

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33
Q

Nernst eq’n

A

Eion= (60/z) * log(outside conc/inside conc)

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34
Q

Ohm’s Law

A

Em= (GkEk) + (GnaEna) / Gk+Gna

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35
Q

Plasma Osmolarity

A

2Na + Gluc/18 + BUN/ 2.8

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36
Q

Total Body Water

A

TBW= 0.7LBM + 0.1Adipose

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37
Q

Magnitude of electrical potential

A

depends on the # of charges separated across a membrane

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38
Q

Dehyration

A

osmolarity increases!

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39
Q

Too much water

A

osmolarity decreases

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40
Q

Diarrhea, water deprivation, Aldosterone insufficiency

A

Osmolarity increases!

volume contraction-decrease in ECF

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41
Q

High NaCl intake/infusion of Isotonic NaCl

Pure water intake

A

Osmolarity decreases!

volume expansion- increase in ECF

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42
Q

Box problems

A

Step 1: Are the RBC changing shape? Is the cell changing shape? (If it’s hypo or hyper in ECF, it will! Figure out which direction)

Step 2: What direction is plasma protein conc. going? The Hct will follow, and size of arrow depends on answer to #1)

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43
Q

Intracellular composition

A

K+ ions
negative proteins (-)
organic phosphates (-)
more protein anions are here

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44
Q

Difference between plasma and interstitial fluid

A

plasma has proteins

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45
Q

Extracellular fluid

A

plasma and interstitial fluid contents:
Na+
Cl-
HCO3-

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46
Q

Net movement of water will stop when

A

Hydrostatic pressure = osmotic pressure

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47
Q

Osmolarity is:

A

total conc of particles per amount of solution

48
Q

3 types of Active Transport

A

Uniporter (1 thing, straight pump)
Symporter/cotransport (2 things going int eh same direction)
Antiporter/Countertransport (2 things going in opposite direction

49
Q

Countertransport/ Antiporter example

A

Na+/K+ ATPase pump

3Na out 2 K+ in

50
Q

Inhibitors of the Na+/K+ ATPase pump

A

Cardiac glycosides

Ouabain (cardiac stimulant)

51
Q

Symporter/cotransport example

A

Potassium K & Hydrogen H pump
2 things are carried in same direction
can be reason for acid reflux
Meds: Omeprazol (Prilosec) inhibits the proton pump

52
Q

Symport/cotransport example

A

Glucose transport

Sodium comes into cell (with its own gradient) and brings glucose with it (against glucose’s gradient)

53
Q

Frick’s Law of Diffusion

A

On Top/Direct relationship: if these things increase, the rate of diffusion will also increase:
Concentration gradient
Surface area of membrane
Lipid Solubility

54
Q

Ways to slow down diffusion rate

A

On bottom of Frick’s Law of Diffusion:
size of molecule
distance it has to go

55
Q

Channel mediated transport

A

PASSIVE
main way ions move down their conc gradients
open in response to a stimulus
allow many ions to move at once

56
Q

Carrier Mediated Transport

A

can be PASSIVE or ACTIVE

Protein in membrane changes shape

57
Q

Passive Transport

A

Diffusion, Osmosis, Channel mediated, Facilitated Diffusion

58
Q

Active Transport

A

Primary (energy made on site)

Secondary (energy made elsewhere. i.e. Sodium & Glucose)

59
Q

Primary Hypoadrenocorticism

A

Problem right at the Adrenal Gland
Autoimmune
Addison’s Disease
Elevated ACTH keeps telling adrenal to produce but it can’t bc it’s broken

60
Q

ACTH Deficiency

A

No Tropic Hormone production
This is the “mother telling you to produce something” an upstream problem bc there is nothing telling the Adrenal gland to do it’s thing
Problem @ the Anterior Pituitary

61
Q

How to distinguish b/w ACTH Deficiency and Primary Hypoadrenocorticism

A

ACTH Stimulation test

If cortisol levels rise, we know that Adrenal gland is working and its an ACTH Deficiency problem

62
Q

Hypothalamus releases

A

releasing hormones to the Ant.Pituitary

63
Q

Ant. Pituitary releases

A

Tropic hormones to the target organs (adrenal gland, gonad, thyroid)

64
Q

The target organ releases

A

things like cortisol, thyroid hormone, etc, AND have an imp job:
negative feedback to the Ant Pituitary and Hypothalamus to tell it to stop releasing it’s hormone bc the job is done

65
Q

Which systems work to coordinate the function of our bodies

A

Nervous & Endocrine

66
Q

Examples of when set points change

A

Pregnancy

Fever

67
Q

Exogenous pryogens

A

bacteria, virus cause a rise in fever set point

68
Q

Endogenous pyrogens

A

immune cells cause a rise in fever set point

69
Q

Muscle fiber has two parts with very diff compositions:

A

Motor end plate

Sarcolemma

70
Q

Motor end plate characteristics

A

Directly across from synaptic terminal
Similar to membranes in soma & dendrites on neuron
Chemically gated ion channels
End Plate Potentials (graded)

71
Q

Sarcolemma characteristics

A

Plasma membrane of muscle fiber
Similar to axon membranes of neurons
Action Potentials
Voltage gated

72
Q

Factors affecting End Plate Potential

A
  • voltage gated Ca2+ function
  • amount of Ach released
  • rate of Ach breakdown
  • Ach receptor agonist/antagonist
73
Q

Curare (D-tubocurarine) is an example of

A 
Non-depolarizing blocker
Competitively binds to ACh receptor
Blocks the ion channel from opening
Insufficient or NO EPP is produced
Flaccid paralysis
74
Q

Depolarizing blocker

A

Contraction followed by paralysis
Prolonged activation of ACh makes the receptors exhausted
Continuous depolarization 2-3 min
Voltage gated Na+ in sarcolemma become inactivated
CLINICAL: used as short acting depolarization muscle relaxant for Tracheal Intubation

75
Q

Neostigmine

Pyridostigmine

A

ACHe inhibitors
ACh accumulates in cleft
Tx of Myasthenia Gravis

76
Q

Anectine (Succinylcholine)

A

a short acting depolarizing muscle relaxant for tracheal intubation

77
Q

Black Widow

A

can lead to depolarizing paralysis by inducing Ca2+ flow

forms pores in the lipid membrane and allows Ca2+ to enter easier

78
Q

Lambert Eaton Syndrome

A

autoimmune attack on voltage gated Ca channels
Fewer vesicles of ACh released as a result
Weaker EPP!!!

79
Q

How to treat Lambert Eaton Syndrome

A

3,4DAP blocks the efflux of K ions which prolongs the depolarization and gives the fewer Ca2+ channels longer to work

80
Q

Sarcoplasmic Reticulum

A

the site of Ca2+ storage in muscle cells

81
Q

T tubules (where the action potential has travelled into) have slow activating voltage-gated Calcium channels

A

DHP
receptors in skeletal muscles
do not act as channels, act as SENSORS

82
Q

Sarcoplasmic Reticulum (the site of Calcium storage) contain Calcium release channels

A

RYR- Ryanide receptors

83
Q

Mechanical connection b/w DHP and RYR

A

DHP is like the wine bottle opener that opens RYR and lets Calcium out of the Sarcoplasmic Reticulum
Remember
DHP: on the T Tubule
RYR: on the Sarcoplasmic Reticulum

84
Q

Tropomyosin

A

Rod shaped

The chaperone that won’t let Myosin bind on Actin

85
Q

Troponin

A

Globular
The distracter that can get Tropomyosin off of Actin’s case
Tells Tropomyosin to get off when Calcium binds to Troponin

86
Q

Power stroke

A

Activated by: cross bridge formation
During: Phosphate released which releases energy!
After: ADP released

87
Q

In a skeletal muscle contraction, where is the Calcium coming from?

A

ONLY SARCOPLASMIC RETICULUM

88
Q

SERCE

A

Ca2+ ATP ase pump that pumps Calcium back into the Sarcoplasmic Reticulum

89
Q

Recruitment and Summation of muscle contraction are controlled by

A

Central Nervous System

90
Q

Velocity (rate) of contraction depends on:

A

Size of load

Type of Muscle Fiber

91
Q

Are there T-tubules in Smooth Muscle?

A

NO

92
Q

How many nuclei are in smooth muscles?

A

One single, central nucleus

93
Q

What is the Sarcoplasmic Reticulum like in Smooth muscle?

A

less developed, but in contact with the plasma membrane

94
Q

Caveolae

A

structures of smooth muscle. Membrane lipid rafts that provide means for extracellular communication (little divits in the membrane)

95
Q

Varicosity

A

little bulges of the post-synaptic neuron that extend into the smooth muscle cell. In the varicosity lies the vesicles containing the neurotransmitter and also mitochondrion

96
Q

Are there motor end plates in smooth muscle fibers?

A

NO

97
Q

Neurogenic sm. muscle

A

Multiunit

98
Q

Myogenic sm. muscle

A

Single unit

99
Q

Vascular smooth muscle

A

combo of Unitary and Multiunit smooth muscle

100
Q

Multiuinit

A

allow finer motor control- found in eyes, skin hair follicles, large blood vessels, small airways, vas deferens

101
Q

Single Unit

A

Gap junctions
One neuron supplying many muscle cells
GI tract, bladder, small blod vessels, uterus, & ureter

102
Q

Where are gap junctions found?

A

Single Unit smooth muscle

Cardiac muscle

103
Q

How are filament types different in smooth muscle?

A

Myosin is LONGER.
There is no Troponin (the distracter)
Tropomyosin is still present. The chaperone is everywhere.

104
Q

Dense bodies in smooth muscle

A

attachment site for actin filaments
same role as Z disks in skeletal muscle
Some dense bodies are attached to cell membrane

105
Q

Arrangement of thick and thin filaments in smooth muscle cell

A

Diamond shaped lattice

106
Q

Regulation of crossbridge cycling in smooth muscle

A

done by light weight proteins on myosin “myosin light chains”

107
Q

How is calcium entry in smooth muscle different?

A

It can enter from BOTH the Cell Membrane and from the Sarcoplasmic reticulum!

In skeletal muscle, calcium ONLY comes from the Sarcoplasmic Reticulum

108
Q

Grade of smooth muscle contraction is different from skeletal muscle how?

A

A single excitation in smooth muscle DOES NOT cause all cross bridges to switch on. The amount of Calcium is directly related to the amount of cross bridges recruited to make greater tension.

109
Q

More calcium release in smooth muscle=

A

greater tension contraction

110
Q

Calcium antagonist

A

block voltage gated Ca channels

If calcium cannot come into cell, no smooth muscle contraction will occur.

RESULT: Vasodilators
Examples: Nifedipine, Verapamil, Diltiazem

111
Q

Potassium Channel Openers

A

If potassium can flow out of cell, making the cell even more negative

Hyperpolarization

Keeps the cell further from its threshold, making it harder to contract, promoting smooth muscle relaxation

RESULT: Vasodilator
Example: Pinacidil

112
Q

cAMP

A

inhibits MLCK
keeps the Kinase from phosphorylating myosin even in the presence of Ca2+

Result: Vasodilator
Example: Albuterol, Beta-2 Adrenergic receptors that stimulate cAMP production from Adenylate Cyclase

113
Q

cGMP

A

activating MLCP (the guy that shuts down the party by dephosphorylating Myosin)

decreases Ca2+ as well

114
Q

Things that stimulate cGMP production

A

Nitroglycerin

115
Q

Things that inhibit cGMP degradation by phosphodiesterase

Phosphodiesterase inhibitors

A

End result: if cGMP is still working, it activates MLCP and decreases Ca2+ levels therefore leading to relaxation of smooth muscle

Example:Sildenafil- Erectile dysfunction

Quarter 2 (16 decks)

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