physiology-menti

Question 1

Answer 1

inwards

Question 2

Answer 2

False

Question 3

Answer 3

ganglion cell stimulation will be highest in dark

Question 4

Answer 4

B

Question 5

Answer 5

None of the above
-the direct innervation occurs in the lateral genicular nucleus

Question 6

Answer 6

cyclic GMP activated Na influx

E

Question 7

Answer 7

Enhances contrast (B)

Question 8

Answer 8

E

Question 9

Answer 9

D

Question 10

Answer 10

middle ear

Question 11

Answer 11

B

Question 12

Answer 12

D

Question 13

Answer 13

C

Question 14

Answer 14

Option 4

Question 15

Answer 15

False- scala media has endolymph

Question 16

Answer 16

2. False- its glutenate

D

Question 17

Where do motor neurones that innervate skeletal muscle arise from?

Answer 17

ventral/ anterior horn of the spinal cord

Question 18

what does the terminal portion of a motor neurone give rise to?

Answer 18

the terminal portion of a motor neurone gives rise to fine projections that run along the muscle cell

Question 19

what is a motor end plate?

Answer 19

a synapse formed between the motor neurone and muscle

Question 20

how many muscle cells can a single motor neurone control?

Answer 20

a single motor neurone can control multiple muscle cells but each muscle cell will only respond to a single motor neurone

Question 21

Explain the physiology behind muscle contraction (at a action potential/ synaptic level)

Answer 21

1. Action potential travels down the nerve
2. AP triggers voltage gated Calcium channels to open, allowing an influx of Calcium
3. ACh vesicles are released into synaptic cleft
4. ACh diffuses across the synaptic cleft
5. ACh receptors open and render membrane permeable to Na/K ions
6. The depolarisation starts an action potential at the motor end plate
   7.Transmission is stopped by acetylcholinesterase, which removed ACh in the synaptic gutter, turns it into acetate and cholinr and gets taken up by the presynaptic vesicles

Question 22

which direction do Sodium and Potassium in regards to the cell and Sodium Potassium channel?

Answer 22

3 Sodium go out of the cell
2 Potassium come into the cell

Na- nah im leaving
K- okay ill come in

Question 23

how and why does conduction differ in myelinated and unmyelinated axons?

Answer 23

it is faster in myelinated as the action potential can ‘jump’ from one node of Ranvier to the next

Question 24

why is the nerve cell membrane described as leaky and what effect does it have on passive signals?

Answer 24

nerve cell membrane has can allow passive movement of potassium out of the cell and sodium into the cell (meaning it is not a perfect insulator)

-This means passive signals do not spread far from site of origin

(imagine a leaky garden hose as an analogy for an axon)

Question 25

what can be done to increase the passive current spread (and this action potential velocity) of a neurone?

Answer 25

-decrease ri by increasing axon diameter -increase rm by adding insulating material (myelin)

Question 26

what are acetylcholine, amino acids and amines released from?

Answer 26

synaptic vesicles

Question 27

what are peptides released from?

Answer 27

secretory vesicles

Question 28

what can activate ionotropic ligand- gated ion channels (LGICs)?

Answer 28

Glutamate, GABA, glycine, acetylcholine and 5-HT

Question 29

neurotransmitter may act directly or indirectly on ion channels what receptors are involved in direct gating?

Answer 29

ionotropic receptors

Question 30

neurotransmitter may act directly or indirectly on ion channels what receptors are involved in indirect gating

Answer 30

Metabotropic receptors

Question 31

fast EPSP is due to the activation of what type of receptors?

Answer 31

Ionotropic receptors (direct gating= gating of channels is rapid)

Question 32

what type of gating is involved in ionotropic and metabotropic receptors?

Answer 32

ionotropic= ligand gated ion channels metabotropic= G protein coupled receptors

Question 33

is glutamate inhibitory or excitatory?

Answer 33

glutamate is excitatory but has an inhibitory effect on metabotropic receptors

Question 34

is gaba inhibitory or excitatory?

Answer 34

gaba is inhibitory

Question 35

is potassium or sodium more permeable to the cell in neurones

Answer 35

Potassium is (so it 'leaks' more)

Question 36

does sodium de or repolarise the post synaptic membrane?

Answer 36

Sodium depolarises it

Question 37

what is the initial resting potential of post synaptic membrane?

Answer 37

-70 mV

Question 38

what is the threshold action potential of the post synaptic membrane?

Answer 38

-10 mV

Question 39

Give examples of excitatory neurotransmitters

Answer 39

Glutamate, acetylcholine and aspartate

Question 40

explain how EPSP works (excitatory post synaptic potential)

Answer 40

1. There is a release of excitatory neurotransmitter e.g. glutamate, acetylcholine, aspartate 2. Glutamate attaches to the post synaptic membrane, allowing the post synaptic non selective (sodium and potassium) permeable channel to open 3. 3 x Na+ influx dominates the 2 x k+ efflux, causing the post synaptic membrane potential to become depolarised by 10mv (this is the excitatory psp) 4. EPSP summate, allowing the threshold (-10mV) to be reached, creating an action potential

Question 41

what are examples of inhibitory neurotransmitters?

Answer 41

GABA (gaBa= Block) Glycene Glutamate (if bound to metabotropic receptor)

Question 42

explain how IPSP works (inhibitory post synaptic potential)

Answer 42

1. Pre synaptic membranes release inhibitory neurotransmitter e.g. GABA 2. GABA binds to metabotropic receptor (indirect) on post synaptic membrane 3. This causes opening of ligand gated chloride (Cl-) channel 4. This causes an influx of Cl-, causing a hyperpolarisation (more negative) 5. This hyperpolarisation causes the membrane potential to go from -70mV (it's resting membrane potential) to -85mV, decreasing the excitability of the post synaptic neurone, making the neurone further from firing action potential

Question 43

what are some clinical signs of decreased neuronal excitability/ conduction?

Answer 43

-weakness -ataxia (balance, coordination + speech) -hyporeflexia -paralysis -sensory deficit

Question 44

what ion disturbances can lead to decreased neuronal excitability/ conduction?

Answer 44

-hypokalaemia -chronic hyperkalaemia -hypercalcaemia

Question 45

Clinical signs of increased neuronal excitability/ conduction?

Answer 45

-hyper reflexia -spasms -fasciculations -tetany -tremors -paraesthesias -convulsions

Question 46

examples of ion disturbances that may cause increased neuronal excitability/ conduction?

Answer 46

acute hyperkalaemia hypocalcaemia