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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
Potassium
Big concentration flow OUTWARD Small electrical flow INWARD Overall: weak outward flux but HIGH permeability
26
Sodium
Big concentration flow inward Big electrical flow inward Overall: Strong inward flux but LOW permeability
27
Graded potential characteristics:
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
28
Hyperkalemic | Hypernatremic
depolarization!
29
Membrane potential
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%
30
Hypokalemia | Hyponatremia
Hyperpolarizatoin
31
Nernst eq'n
tells us the electrical force required to balance out the concentration gradient force for a particular ion
32
K+ Potassium wants to move out bc of its conc. gradient and it gets pulled back in (by negative anions)
Na+ wants to move into cell bc of its conc. gradient and it gets pulled back out (by Cl- ions)
33
Nernst eq'n
Eion= (60/z) * log(outside conc/inside conc)
34
Ohm's Law
Em= (Gk*Ek) + (Gna*Ena) / Gk+Gna
35
Plasma Osmolarity
2Na + Gluc/18 + BUN/ 2.8
36
Total Body Water
TBW= 0.7LBM + 0.1Adipose
37
Magnitude of electrical potential
depends on the # of charges separated across a membrane
38
Dehyration
osmolarity increases!
39
Too much water
osmolarity decreases
40
Diarrhea, water deprivation, Aldosterone insufficiency
Osmolarity increases! volume contraction-decrease in ECF
41
High NaCl intake/infusion of Isotonic NaCl | Pure water intake
Osmolarity decreases! volume expansion- increase in ECF
42
Box problems
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)
43
Intracellular composition
K+ ions negative proteins (-) organic phosphates (-) more protein anions are here
44
Difference between plasma and interstitial fluid
plasma has proteins
45
Extracellular fluid
plasma and interstitial fluid contents: Na+ Cl- HCO3-
46
Net movement of water will stop when
Hydrostatic pressure = osmotic pressure
47
Osmolarity is:
total conc of particles per amount of solution
48
3 types of Active Transport
Uniporter (1 thing, straight pump) Symporter/cotransport (2 things going int eh same direction) Antiporter/Countertransport (2 things going in opposite direction
49
Countertransport/ Antiporter example
Na+/K+ ATPase pump | 3Na out 2 K+ in
50
Inhibitors of the Na+/K+ ATPase pump
Cardiac glycosides | Ouabain (cardiac stimulant)
51
Symporter/cotransport example
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
Symport/cotransport example
Glucose transport | Sodium comes into cell (with its own gradient) and brings glucose with it (against glucose's gradient)
53
Frick's Law of Diffusion
On Top/Direct relationship: if these things increase, the rate of diffusion will also increase: Concentration gradient Surface area of membrane Lipid Solubility
54
Ways to slow down diffusion rate
On bottom of Frick's Law of Diffusion: size of molecule distance it has to go
55
Channel mediated transport
PASSIVE main way ions move down their conc gradients open in response to a stimulus allow many ions to move at once
56
Carrier Mediated Transport
can be PASSIVE or ACTIVE | Protein in membrane changes shape
57
Passive Transport
Diffusion, Osmosis, Channel mediated, Facilitated Diffusion
58
Active Transport
Primary (energy made on site) | Secondary (energy made elsewhere. i.e. Sodium & Glucose)
59
Primary Hypoadrenocorticism
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
ACTH Deficiency
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
How to distinguish b/w ACTH Deficiency and Primary Hypoadrenocorticism
ACTH Stimulation test | If cortisol levels rise, we know that Adrenal gland is working and its an ACTH Deficiency problem
62
Hypothalamus releases
releasing hormones to the Ant.Pituitary
63
Ant. Pituitary releases
Tropic hormones to the target organs (adrenal gland, gonad, thyroid)
64
The target organ releases
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
Which systems work to coordinate the function of our bodies
Nervous & Endocrine
66
Examples of when set points change
Pregnancy | Fever
67
Exogenous pryogens
bacteria, virus cause a rise in fever set point
68
Endogenous pyrogens
immune cells cause a rise in fever set point
69
Muscle fiber has two parts with very diff compositions:
Motor end plate | Sarcolemma
70
Motor end plate characteristics
Directly across from synaptic terminal Similar to membranes in soma & dendrites on neuron Chemically gated ion channels End Plate Potentials (graded)
71
Sarcolemma characteristics
Plasma membrane of muscle fiber Similar to axon membranes of neurons Action Potentials Voltage gated
72
Factors affecting End Plate Potential
- voltage gated Ca2+ function - amount of Ach released - rate of Ach breakdown - Ach receptor agonist/antagonist
73
Curare (D-tubocurarine) is an example of
``` Non-depolarizing blocker Competitively binds to ACh receptor Blocks the ion channel from opening Insufficient or NO EPP is produced Flaccid paralysis ```
74
Depolarizing blocker
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
Neostigmine | Pyridostigmine
ACHe inhibitors ACh accumulates in cleft Tx of Myasthenia Gravis
76
Anectine (Succinylcholine)
a short acting depolarizing muscle relaxant for tracheal intubation
77
Black Widow
can lead to depolarizing paralysis by inducing Ca2+ flow | forms pores in the lipid membrane and allows Ca2+ to enter easier
78
Lambert Eaton Syndrome
autoimmune attack on voltage gated Ca channels Fewer vesicles of ACh released as a result Weaker EPP!!!
79
How to treat Lambert Eaton Syndrome
3,4DAP blocks the efflux of K ions which prolongs the depolarization and gives the fewer Ca2+ channels longer to work
80
Sarcoplasmic Reticulum
the site of Ca2+ storage in muscle cells
81
T tubules (where the action potential has travelled into) have slow activating voltage-gated Calcium channels
DHP receptors in skeletal muscles do not act as channels, act as SENSORS
82
Sarcoplasmic Reticulum (the site of Calcium storage) contain Calcium release channels
RYR- Ryanide receptors
83
Mechanical connection b/w DHP and RYR
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
Tropomyosin
Rod shaped | The chaperone that won't let Myosin bind on Actin
85
Troponin
Globular The distracter that can get Tropomyosin off of Actin's case Tells Tropomyosin to get off when Calcium binds to Troponin
86
Power stroke
Activated by: cross bridge formation During: Phosphate released which releases energy! After: ADP released
87
In a skeletal muscle contraction, where is the Calcium coming from?
ONLY SARCOPLASMIC RETICULUM
88
SERCE
Ca2+ ATP ase pump that pumps Calcium back into the Sarcoplasmic Reticulum
89
Recruitment and Summation of muscle contraction are controlled by
Central Nervous System
90
Velocity (rate) of contraction depends on:
Size of load | Type of Muscle Fiber
91
Are there T-tubules in Smooth Muscle?
NO
92
How many nuclei are in smooth muscles?
One single, central nucleus
93
What is the Sarcoplasmic Reticulum like in Smooth muscle?
less developed, but in contact with the plasma membrane
94
Caveolae
structures of smooth muscle. Membrane lipid rafts that provide means for extracellular communication (little divits in the membrane)
95
Varicosity
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
Are there motor end plates in smooth muscle fibers?
NO
97
Neurogenic sm. muscle
Multiunit
98
Myogenic sm. muscle
Single unit
99
Vascular smooth muscle
combo of Unitary and Multiunit smooth muscle
100
Multiuinit
allow finer motor control- found in eyes, skin hair follicles, large blood vessels, small airways, vas deferens
101
Single Unit
Gap junctions One neuron supplying many muscle cells GI tract, bladder, small blod vessels, uterus, & ureter
102
Where are gap junctions found?
Single Unit smooth muscle | Cardiac muscle
103
How are filament types different in smooth muscle?
Myosin is LONGER. There is no Troponin (the distracter) Tropomyosin is still present. The chaperone is everywhere.
104
Dense bodies in smooth muscle
attachment site for actin filaments same role as Z disks in skeletal muscle Some dense bodies are attached to cell membrane
105
Arrangement of thick and thin filaments in smooth muscle cell
Diamond shaped lattice
106
Regulation of crossbridge cycling in smooth muscle
done by light weight proteins on myosin "myosin light chains"
107
How is calcium entry in smooth muscle different?
It can enter from BOTH the Cell Membrane and from the Sarcoplasmic reticulum! In skeletal muscle, calcium ONLY comes from the Sarcoplasmic Reticulum
108
Grade of smooth muscle contraction is different from skeletal muscle how?
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
More calcium release in smooth muscle=
greater tension contraction
110
Calcium antagonist
block voltage gated Ca channels If calcium cannot come into cell, no smooth muscle contraction will occur. RESULT: Vasodilators Examples: Nifedipine, Verapamil, Diltiazem
111
Potassium Channel Openers
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
cAMP
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
cGMP
activating MLCP (the guy that shuts down the party by dephosphorylating Myosin) decreases Ca2+ as well
114
Things that stimulate cGMP production
Nitroglycerin
115
Things that inhibit cGMP degradation by phosphodiesterase Phosphodiesterase inhibitors
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

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