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Year 1 - Semester 1 > Week 5 - Neurology > Flashcards

Week 5 - Neurology Flashcards

1
Q

What are the two types of cells in the nervous system?

A

Neurons - cell body called soma, neurites are projections from the cell body - neurites divided into dendrites and axons.
Dendrites receive input from other neurons
Axons - action potential propagates through these
Law of dynamic polarisation - preferred direction of current flow

Glial cells - astrocytes - fill spaces between neurons and regulate the chemical content of the extracellular space
- oligodendrocytes/Schwann cells - provide myelination or axons - oligodendrocytes in CNS and Schwann in peripheral NS

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2
Q

Afferent vs efferent axons

A

Afferent - carry sensory info from the peripheries of the body and enter the spinal cord dorsally

Efferent - carries motor info from the CNS through ventral root ganglions to muscles

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3
Q

Which ions are at high concentration inside/outside of the cell?

A

Inside - potassium

Outside - sodium and chloride

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4
Q

How is the resting membrane potential maintained?

A

Sodium potassium pump

leaky potassium channels - only potassium moves out, along their concentration gradient - net negative charge in cell - equilibrium potential for K is roughly -80mV

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5
Q

What is the resting membrane potential?

A

Around -65mV

Equilibrium potential for - Na is positive
Equilibrium potential for - K is negative

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6
Q

What is the threshold potential?

A

-40mV

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7
Q

Describe voltage gated Na channels during action potential

A

Closed at rest
Threshold potential induces a conformational change in the protein
Pore allows Na in, depolarising rapidly
Stay open for around 1ms before deactivating

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8
Q

Describe voltage gated K channels during action potential

A

Require depolarisation to open
Slow to open ~1ms after depolarisation
Delayed rectifier
Channels close when membrane potential returns to rest

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9
Q

What is the refractory period

A

Time in which an excitable cell is unable to generate a subsequent action potential
Absolute - then all Na channels are open, no more to generate a subsequent one
Relative - after hyperpolarisation, less likely to produce one

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10
Q

Describe action potentials

A

Stimulus depolarises rising towards the threshold, if it passes, Na channels open leading to rapid depolarisation to around 30mV, when a physical block closes Na channels.
K channels take longer to open, but when they do, they repolarise the cell. This is the falling phase. then hyperpolarisation

Firing rate, not amplitude shows intensity of stimulus

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11
Q

How does a stimulus propagate?

A

Unmyelinated - passive propagation as adjacent sodium channels are activated by the depolarisation

Myelinated - nodes of Ranvier between myelin sheaths. These have high concentrations of sodium channels. APs initiated in an axon hillock. Propagation from node to node - saltatory conduction - much faster

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12
Q

What are mechanoreceptors

A

Unmyelinated fibres in the skin sensitive to stretch, bend, pressure

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13
Q

What are mechanosensitive ion channels

A

Gates opened by stretching of a membrane

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14
Q

What are the 4 types of sensory input neurons?

A

A alpha - 13-20 microns, 80-120m/s, myelinated, receptor- proprioceptors in skeletal muscle

A beta - 6-12 microns, 35-75 m/s, myelinated, mechanoreceptors

A delta - 1-5 microns, 5-30 m/s, myelinated, pain and temperature

C - 0.2-1.5 microns, 0.5 -2 m/s, unmyelinated, relative temperature, some pain, itching

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15
Q

What does the action potential firing frequency encode?

A

Stimulus strength and duration

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16
Q

What is encoded by the timing of the first and last AP?

A

Stimulus onset/offset

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17
Q

What makes a molecule a neurotransmitter?

A

Have precursor molecules and/or synthesis enzymes located in the presynaptic terminal

The chemical is present in the presynaptic terminal

It is available in sufficient quantity in the presynaptic neuron to affect the postsynaptic neuron

There are postsynaptic receptors for it to bind

Biochemical mechanisms for its inactivation are present

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18
Q

Classes of neurotransmitter

A

Amino acid - glutamate, GABA

Monoamines - dopamine, adrenaline, serotonin

Peptides - over 50

Others such as acetylcholine

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19
Q

Where are neurotransmitters generated?

A

In the presynaptic terminal

Enzymes required for synthesis are made in the cell body

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20
Q

What is exocytosis?

A

The release of neurotransmitter into the synaptic cleft

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21
Q

Sequence of events leading to neurotransmitter release: (called exocytosis)

A
  1. Action potential invades the presynaptic terminal
  2. Membrane depolarisation occurs
  3. Voltage-gated calcium channels open
  4. Increase in calcium promotes vesicle fusion
  5. Vesicles release neurotransmitters into the synaptic cleft
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22
Q

Exocytosis/endocytosis cycle

A
  1. Docking – vesicle binds to membrane before AP invades terminal
  2. Ca2+ sensing – Ca entry triggers fusion of the vesicle
  3. Endocytosis – new vesicle membrane “pinched off”
  4. Loading – new vesicle filled with neurotransmitter
  5. Cycle completes
23
Q

types of postsynaptic receptors

A

Ionotropic receptors are fast ligand-gated ion channels that open when the NT binds
Metabotropic receptors are slow because they activate a second messenger system (for example via GPCRs)

24
Q

what are the two types of synapse?

A

At an excitatory synapse, if sufficient NT binds to Na+ ionotropic receptors the membrane will depolarise to produce an excitatory post-synaptic potential (EPSP). IPSPs occur at inhibitory synapses because Cl- channels are opened instead, further polarising the membrane (making it more negative so it is harder to generate an action potential)

25
Q

what is the quantal hypothesis?

A

that each vesicle produces a quantal response in the postsynaptic receptors - so the release of 2 vesicles produces a response twice the size of that of 1 vesicle

26
Q

what are the two types of summation?

A

Spatial summation is when a neurone combines multiple EPSPs from different synapse connections

Temporal summation is when a neurone combines multiple consecutive EPSPs from the same synapse

Spatial summation and temporal summation both stop when the threshold is reached and an action potential is generated.

27
Q

how can drugs affect neurotransmission?

A

GABA- gated Cl channel can be affected by substances. Ethanol affects the level of inhibition, affects CNS and motor function. Barbiturates cause mild sedation to full anaesthesia

28
Q

What are the two types of autonomic NS?

A

Sympathetic

Parasympathetic

29
Q

Describe the sympathetic NS

A

Preganglionic neurones release ACh
Post ganglionic neurones release noradrenaline
Receptors therefore known as adrenoreceptors
Fight or flight - heart rate increase, relaxation of airways and inhibition of digestion

30
Q

Describe the parasympathetic NS

A

Day to day required
ACh
Airway constriction, digestive stimulation and slowing of heart rate

31
Q

what is the somatic motor system?

A

We choose to make a movement, this is generated by the motor cortex, propagates down the spinal cord, into upper motor neurons, then lower motor neurons and these then send out signals to the muscles. Lower motor neurons directly command muscle contraction. Each motor neurons innervates a single muscle. They are distributed within the ventral horn in a predictable way. Neurons innervating axial muscles are medial to those innervating distal muscles. Neurons innervating flexors are dorsal to those innervating extensor muscles.

32
Q

what is a motor unit?

A

The alpha motor neuron and all the muscle fibres it innervates

33
Q

what is the life cycle of acetylcholine?

A

ACh released. Binds to postsynaptic nicotinic receptors and causes sodium channel openings so the action potential can spread down the sarcolemma. ACh is then broken down via the enzyme acetylcholinesterase into choline and acetic acid. Choline transporters on the presynaptic terminal then take choline up back into the presynaptic terminal - used as a precursor for the generation of Ach. The choline will bind with acetyl CoA under the influence of the enzyme choline acetyltransferase. The acetic acid diffuses away.

34
Q

how is muscle contraction initiated?

A

by ACh release and binding to postsynaptic ACh receptors. 1 presynaptic AP is sufficient to trigger 1 postsynaptic AP in a muscle fibre.

35
Q

What is the sarcolemma?

A

Excitable cell membrane covering muscle fibres

36
Q

What is the sarcoplasmic reticulum?

A

Extensive intracellular sac that stores calcium

37
Q

What are myofibrils?

A

What contract in response to action potentials
Made up of actin and myosin strands
Repeating contractile units called sarcomeres

38
Q

What are the stages of muscle contraction?

A

Action potential generated in sarcolemma.

Release of calcium from sarcoplasmic reticulum

Binds to troponin which is normally bound to actin filaments

Actin is freed, exposing myosin binding sites

Myosin binds to actin and pivots, sliding actin along

Myosin detatches at the expense of ATP

39
Q

When does relaxation occur?

A

When calcium or ATP levels reduce

40
Q

Describe all steps of muscle contraction

A 
AP in alpha motor neuron
Exocytosis of ACh
Postsynaptic depolarisation
Ca release from sarcoplasmic reticulum
Sliding actin/myosin filaments
Muscle contraction
41
Q

What is a myotatic reflex?

A

Reciprocal innervation of flexor and extensor muscles

Sensory innervation comes from a contracting muscle to excite inhibitory neurons on the antagonist muscle.
If flexor contracts, paired extensor relaxes to allow movement

42
Q

What is the patellar reflex?

A

When hammer taps, firing frequency of sensory neurons increases, causes the motor neuron extensor firing frequency to increase, as well as interneuron firing frequency to suppress the motor neuron flexor activity

43
Q

What is the crossed extensor reflex?

A

On painful stimulus, sensory afferent axons activated and excitatory interneurons bring about efferent motor neuron excitation and therefore contraction.

Leg jerking away has excited flexors and inhibited extensors, opposite leg has inhibition flexors and excited extensors to allow weight to shift so as not to lose balance

44
Q

What is the vestibulo-ocular reflex?

A

Inhibition of extraocular muscles one one side and excitation on the other on detection of head rotation

Allows fixed position of eye even if the head is moving

45
Q

Describe hyponatremia

A

<135mmol/L
Common
Caused by diuretics, renal disease, congestive heart failure, cirrhosis

Muscle cramps, weakness, fatigue, reduced consciousness

BRAIN OEDEMA

46
Q

Describe hypernatremia

A

> 145mmol/L
Uncommon
Renal failure, fever, vomiting, diarrhoea

Tremor, seizures, hyperreflexia, thirst, lethargy, convulsions

BRAIN SHRINKAGE

47
Q

Describe hypokalemia

A

<3.5 mmol/L
Most common
Diuretics, renal failure, cirrhosis, malnutrition, malabsorption

Muscle weakness, fatigue, constipation, cardiac arrhythmias, muscle paralysis, respiratory paralysis

POTENTIALLY FATAL ARRHYTHMIAS

48
Q

Describe hyperkalemia

A

> 5.5 mmol/L
Uncommon
Drug interaction during treatment of kidney infections

Impairment of neuromuscular, cardiac and GI organ systems, ventricular fibrillation

INCREASED RISK OF CARDIAC ARREST

49
Q

What are channelopathies?

A

Diseases which affect ion channels and thus depolarisation/repolarisation of cells

Long QT syndrome - mutation in K channels leads to cardiac arrhythmias - rare inherited

50
Q

Describe demyelinating diseases

A

Multiple sclerosis - loss of myelin and damage to axons over many years by repeated episodes - possible stem cell repair

Charcot-Marie-Tooth - most common inherited disease - affects peripheral nerve conduction - affects legs then arms and hands

Guillan-Barre syndrome - inflammatory attack in myelin and peripheral nerves - very quick onset after something like stomach upset then goes away quickly - tingling, muscle weakness, possible paralysis and respiratory failure

51
Q

Describe peripheral neuropathies

A

Diabetic - chronic dysregulation of blood glucose - damage to sensory and motor axons in distal limbs - ulcerations, infections and gangrene

Autonomic - loss of sympathetic and parasympathetic nerves - poor circulation and healing - risk of gangrene

Neuritis - inflammation of cranial nerves from Lyme’s disease, meningitis, viral encephalitis

Optic neuritis - acute attack leading to loss of vision over several hours

Vestibular neuritis - acute, possibly via herpes simplex, loss of vestibular function on one or both sides leading to loss of balance

Bell’s palsy - weakness or paralysis of facial muscles, usually temporary and causes by viral inflammation (herpes simplex) of facial nerve

Trigeminal neuralgia - stabbing pain in face, usually on one side, triggered by loud sounds or touch/chewing

52
Q

Describe myasthenia gravis

A

Disorder of synaptic transmission
Autoimmune - loss of function of ACh receptors on skeletal muscle
Muscle weakness which worsens with activity and improves with rest
Difficulty talking, chewing, swallowing, simple locomotion
Ptosis and double vision

53
Q

Describe hyporeflexia

A 
Depressed or absent reflexes
Lower motor neuron lesions
Loss of motor neurons
Denervation of muscles (injury or disease)
Thyroid deficiency
54
Q

Describe hyperreflexia

A 
Exaggerated reflexes, spasticity and rigidity
Upper motor neuron lesions
Spinal trauma and trans-section
Brain haemorrhage
Drug misuse

Year 1 - Semester 1 (9 decks)

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