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Neurology Flashcards

1
Q

What is frontal lobe for?

A

Responsible for executive functions such as personality

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2
Q

What is the parietal lobe for?

A

Contains the somatic sensory cortex responsible for processing tactile information

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3
Q

What is temporal lobe for?

A

Contains important structures e.g- hippocampus (short term memory), the amygdala (behaviour) and Wernicke’s area (auditory perception & speech)

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4
Q

What is occipital lobe for?

A

Processing of visual information

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5
Q

Where is the brainstem and what is its overall function?

A

Dorsal region of CNS

Role in motor coordination, balance and posture

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6
Q

Functions of astrocyte

A

Cell repair: synthesise neurotrophic factors
Abundant
Structural: form the blood brain barrier
Homeostasis: removal and reuptake of neurotransmitter

‘star’ shape

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7
Q

Other cells of the NS

A

Schwann cells: myelinate one axon, PNS
Oligodendrocytes: myelinate many axons, CNS
Microglial: immune cells, similar to macrophages
Ependymal: line ventricles containing CSF, regulate CSF production, important for blood-brain barrier

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8
Q

What are the relative concentrations of these ions extracellularly?

A

Higher Na+

Higher Cl-

Lower K+

Higher Ca2+ (High conc. gradient)

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9
Q

Define flux

A

The number of molecules that cross a unit area per unit time

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10
Q

Define electrochemical equilibrium

A

When electrical force prevents further diffusion across a membrane

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11
Q

What is the Nernst and GHK equation used to calculate?

A

Nernst: equilibrium potential for a single ion
GHK: resting membrane potential

p = permeability

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12
Q

Explain how the ions are involved in the generation of an action potential?

A

Influx of Na+ via voltage gated sodium ion channels (VGSC) leads to further depolarisation

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13
Q

Explain how the ions are involved in the restoration of the resting membrane potential?

A

Voltage gated potassium ion channels (VGKC) opens at slower rate, leading to efflux of K+ from cell which repolarises the membrane

Permeability to Na+ decreases, as VGSCs close

Permeability to K+ increases

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14
Q

How is the Na+/K+ ATPase involved in restoring the ion gradients?

A

Resting configuration - Na+ & K+ enters vestibule & upon phosphorylation, ions are transported through the protein against conc. gradient –> phosphorylation doesn’t take place until active configuration –> Na+ removed from cell

Active configuration - Na+ removed from cell and K+ enters the vestibule against conc. gradient. The pump returns to resting configuration and K+ is transported back into cell

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15
Q

What are graded potentials?

A

NOT all or nothing

Changes in membrane potential in response to stimulation –> occur at synapses to prevent initiation of APs

Charge leaks from axon as impulse propagates –> NO AP generated

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16
Q

What is the function of Myelin in the travelling of the AP?

A

Prevents AP spreading because it has high resistance and low capacitance

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17
Q

What happens when the action potential reaches the Synapse?

A

AP opens voltage gated Ca2+ channels (VGCC) at pre-synaptic terminal

Ca2+ influx down conc. gradient → exocytosis of vesicles containing neurotransmitter

Neurotransmitter released into synaptic cleft

Neurotransmitter binds to receptors on post-synaptic membrane

Receptors modulate post-synaptic activity

Enzymes (cholinesterase) break down neurotransmitter to be uptaken again by pre-synaptic cleft

Or the neurotransmitter could be recycled by transporter proteins on the pre-synaptic cleft

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18
Q

How does an action potential travel across a neuromuscular junction?

A

Action potential propagated along axon (Na+ and K+) → Ca2+ entry at presynaptic terminal

Ca2+ entry → ACh release into synapse

ACh binds to nicotinic ACh receptors (nAChR) on skeletal muscle → change in end-plate potential (EPP)

Miniature EPP: Quantal ACh release = small depolarisation caused by release of single vesicle of ACh into synaptic cleft

AP travels through T-tubules that are continuous with sarcolemma & closely connected to sarcoplasmic reticulum

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19
Q

What is the function of the sarcoplasmic reticulum and what effect does it have?

A

Ca2+ storage → Ca2+ release following sarcolemma depolarisation

Ca2+ → myofibril contraction & muscle contraction

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20
Q

Describe excitation-contraction coupling

A
  1. Once nACh receptor is activated, sarcolemma is depolarised
  2. AP travels down sarcolemma into T-tubules
  3. Depolarisation at T-tubules eventually causes Ca to be released from SR
  4. SR surrounds myofibrils –> Ca release causes muscle contraction
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21
Q

What is Myasthenia Gravis and what does it cause?

A

Autoimmune disorder: antibodies directed against ACh receptor

Symptoms: fatigable weakness (becomes more pronounced with repetitive use)

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22
Q

What is Botulism, Myasthenia Gravis + LEMS?

A
  1. disrupts ACh release
  2. disrupts ACh receptor (autoimmune)
  3. disrupts VGCS = fatigue, weakness, weight loss, mild facial muscle weakness
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23
Q

Describe the steps of an action potential

A

Resting membrane potential - Permeability K+> Permeability Na+

Depolarisation - Stimulus depolarises membrane potential to move it in positive direction towards threshold

Upstroke - VGSC open quickly so Na+ enters cell down electrochemical gradient. VGPC open slowly so K+ leaves cell down electrochemical gradient.

Membrane potential moves towards Na+ equilibrium potential

Repolarisation - Decreased permeability of Na+ as VGSC close. Increased permeability of K+ as VGPC open so K+ leaves cell down its electrochemical gradient

Membrane potential moves towards K+ equilibrium potential

After-Hyperpolarisation - At rest VGPC are still open and so K+ leaves cell down electrochemical gradient

Membrane potential moves closer to K+ equilibrium so some VGPC then close and membrane potential returns to resting potential

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24
Q

What is the absolute refractory period?

A

Period where inactivation gate of VGSC is closed

Impossible to generate another AP

BOTH activation and inactivation gates are closed

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25
Q

What is the relative refractory period?

A

Period of time where you need a stronger than normal stimulus to trigger another action potential

Due to hyperpolarisation, more of a depolarisation is required to reach threshold and then cause another action potential

Only activation gate is closed

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26
Q

What does the propagation distance and velocity of the AP along the axon depend on?

A

Myelin thickness - Linear relationship between conduction velocity and myelin thickness

Diameter of axon - Larger diameter, faster travelling of action potential due to less resistance (conduction velocity proportional to square root of axon diameter)

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27
Q

3 factors that influence movement of ions across membrane

A
  • Conc. of ion on both sides of membrane
  • Charge on ion
  • Voltage across membrane
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28
Q

What are some causes of reduced conduction velocity?

A

REDUCED MYELINATION:

  • Multiple sclerosis
  • Guillian-Barre syndrome
  • Cold
  • Anoxia
  • Compression
  • Drugs
  • Parkinson’s

REDUCED AXONAL DIAMETER:
- Regrowth after injury

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29
Q

What are the 3 types of post synaptic cells?

A
  1. Axodendritic
  2. Axoaxonic
  3. Axosomatic
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30
Q

Define drug

A

A chemical substance that interacts with a specific target within a biological system to produce a physiological effect

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31
Q

How can you determine the most safe drug based on the dosage of the drug?

A

The safest drugs are those where there is a large difference between the dose required to induce the desired effect and the dose required to induce side effects/adverse effects

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32
Q

4 main classes of proteins that drugs usually target?

A

Receptors

Enzymes

Transport Proteins

Ion Channels

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33
Q

What class of protein does Atorvastatin act on?

A

Enzyme - HMG CoA reductase

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34
Q

What class of protein does Citalopram act on?

A

Transport Protein - Serotonin re-uptake protein

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35
Q

What class of protein does Salbutamol act on?

A

Receptor - Beta-2 Adrenergic receptor in lung

36
Q

What class of protein does Amlodipine act on?

A

Ion channel - Calcium channel

37
Q

Define side effect

A

An effect produced by the drug that is secondary to the intended effect

38
Q

As dose increases, selectivity…

A

decreases

39
Q

Which kind of effect increases as dosage of a drug increases?

A

Off-target effects

40
Q

EPILEPSY

  1. Causes
  2. Clinical features
  3. Symptoms
A
  1. traumatic brain injury, CNS infection, brain tumours, stroke, Alzheimer’s, prenatal injuries, family history
  2. abnormal taste, smell & touch sensations; deja vu; abdominal sensations
  3. Temporal lobe –> memory loss, speech production, smacking lips, picking at clothes
41
Q

How focal seizure differ from general event? Why seizures develop?

A

localised brain activity which then leads to symptoms that typically seize 1 side of body or 1 specific body part

Imbalance between inhibitory + excitatory input within certain regions of brain

42
Q

List 4 characteristics of synaptic transmission

A

Rapid timescale

Diversity

Plasticity

Learning and memory

43
Q

What are the 3 steps that occur when a dendrite of one neurone receives an electrical impulse from another neurone?

A

Information reception at dendrites

Integration (occurs at the soma)

Rapid transfer (action potential) - impulse passed along axon towards the synaptic terminals

44
Q

List 3 types of molecules that can be neurotransmitters and include examples of each

A

Amino acids - glutamate, gamma-aminobutyric acid (GABA), glycine
LAST 2 = Cl- influx, leads to hyperpolarisation

Amines - noradrenaline, dopamine, serotonin

Neuropeptides - enkephalins, opioid peptides

45
Q

What is the single-most important excitatory neurotransmitter in the brain?

A

Glutamate

46
Q

What is the single-most important inhibitory neurotransmitter in the brain?

A

GABA

47
Q

Where is glycine most active and is it excitatory or inhibitory?

A

Spinal cord and brainstem

Inhibitory

48
Q

Which neurotransmitter stimulates parasympathetic lacrimal gland secretion?

A

ACh - main NT in parasympathetic

  • -> Nicotinic ion channel receptors (NMJ)
  • -> Muscarinic G-protein coupled receptors
49
Q

What are the methods by which the neurotransmitter can be returned to the pre-synaptic terminal after depolarising the post-synaptic terminal?

A

Re-uptake of neurotransmitter via a protein transport channel

Enzymatic degradation within the synaptic cleft (e.g. acetylcholine broken down by acetylcholinesterase)

50
Q

What 2 things does neurotransmitter (NT) release require?

A

Calcium influx and RAPID transduction (electromechanical transduction - links the Ca2+ influx with NT release)

51
Q

What type of proteins on the vesicle and presynaptic membrane enable fusion and exocytosis?

A

SNARE proteins (vesicular proteins e.g. synapsin, synaptobrevin, snap25)

52
Q

What does the neurotoxin alpha larotoxin (from black widow spider) do?

A

Stimulate NT release until depletion of NT → muscular paralysis

53
Q

What do Zn2+ dependent endopeptidases do?

A

Inhibits transmitter release

54
Q

What does tetanus toxin cause and what bacteria produces it?

A

Causes spasms and paralysis as it inhibits GABA and glycine (both inhibitory in CNS)

Produced by Clostridium tetani

55
Q

What does botulinum toxin cause and how does it do this?

A

Flaccid paralysis (due to complete muscle relaxation)

Cleaves peptide bonds of vesicular proteins leading to inactivation hence docking, fusion and release of NT can’t occur

One of the most powerful toxins

56
Q

What responses do ion channel-linked receptors mediate? EXAMPLES

A

All FAST (msecs) excitatory and inhibitory transmission

CNS: glutamate, GABA, glycine
NMJ: nicotinic ACh receptors

57
Q

What type of responses do G-protein coupled receptors mediate? EXAMPLES

A

SLOWer (secs/mins) than ion channel-linked receptors

CNS: serotonin, noradrenaline, neuropeptides, dopamine
Parasympathetic: muscarinic ACh receptors

58
Q

Name the 2 main types of ion-channel linked glutamate receptors and what do they mediate?

A

AMPA - majority of FAST excitatory synapses. Rapid onset, offset and desensitisation. Only permeable to Na+

NMDA - SLOW component of excitatory transmission. Serve as coincidence detectors which underlie learning mechanisms. Permeable to both Na+ and Ca2+. Hippocampus has a very high density of these receptors

59
Q

Outline the process that occurs at an excitatory glutamate synapse

A

Glutamate synthesised from glucose via TCA cycle and transamination. Loaded into vesicles and released into synaptic cleft via exocytosis

Glutamate reversibly binds postsynaptic receptors (AMPA and NMDA)

Inactivation of glutamate (re-uptake into presynaptic terminal) + can also be re-uptaken into surrounding glial cells.

Rapid uptake of glutamate by excitatory amino acid transporters (EAATs)

60
Q

What happens when glutamate is in glial cells?

A

Glutamate is enzymatically modified by glutamine synthetase to glutamine, which can then be pumped back into the pre-synaptic terminal

61
Q

What can abnormal cell firing associated with excess glutamate lead to?

A

Seizures

Shown by spikes on an EEG

62
Q

Outline the process that occurs at an inhibitory GABA synapse

A

GABA synthesised in the pre-synaptic terminal by decarboxylation of glutamate by glutamic acid decarboxylase (GAD)

GABA reversibly binds to post-synaptic receptors (GABA a receptors) → opens chloride channels → influx of chloride ions into post-synaptic terminal leading to hyperpolarisation

Inactivated by rapid uptake into pre-synaptic terminal by GABA transporters (GATs)

OR GABA can be taken into glial cells where it is enzymatically modified by GABA-transaminase (GABA-T) to succinic semialdehyde

63
Q

Which drugs facilitate GABA transmission?

A

Barbiturates

Benzodiazepines

Steroids

Convulsants

Zn 2+

Ethanol

64
Q

What properties do drugs facilitating GABA transmission have?

A

Antiepileptic

Anxiolytic

Sedative

Muscle relaxant

65
Q

What are special nerves for?

A

Special senses: hearing, vision, taste, smell, balance

4Ss: smiling, speaking, masticating, swallowing

SVE: innervation of skeletal muscle jaw, face, larynx, pharynx

66
Q

Somatic vs visceral

Afferent vs efferent

A

skeletal muscle vs smooth muscle

Towards brain vs away from brain

67
Q

Compression at the optic chiasm is most likely to affect which blood vessel?

A

Anterior Communicating Cerebral Artery

68
Q

Where are the two spinal cord enlargements

A

CERVICAL: upper limbs innervation

LUMBAR: lower limbs innervation

69
Q

What non-skeletal peripheral functions does the ANS control?

A

Cardiac muscle

Internal organs

Smooth muscle

Skin

70
Q

What are the 2 afferent neurones of the sensory division?

A

Somatic sensory –> external stimuli, only skeletal muscles

Visceral sensory –> trunk organs, vessels, glands

71
Q

If there is a high blood pressure, how is this information relayed to the relevant visceral motors and which of the PNS and SNS are switched on?

A

Visceral sensory - baroreceptors detect increase in pressure

Signal sent to the PNS to be sent to CNS

Signal sent from CNS to PNS to visceral motors

Parasympathetic nervous system switched on to reduce blood flow

Sympathetic nervous system switched off to prevent further increase in blood flow

72
Q

Where is the autonomic sensory (afferent) information relayed to?

A

Hypothalamus

73
Q

Where do visceral motor nuclei originate?

A

Hypothalamus

74
Q

What is meant by a sympathetic (paravertebral) trunk?

A

Long chains running parallel to the spinal cord, with lots of sympathetic nerves coming out of the spinal cord will synapse within those sympathetic chains

Allows for mass activation, so lots of sympathetic neurons can be activated at the same time

Allows coordinated responses for flight or fight

75
Q

What is the exception to the two neuron arrangement in the ANS?

A

Adrenal gland

Single sympathetic nerve that innervates the adrenal gland

76
Q

What neurotransmitter does the Adrenal gland release?

A

Does not release neurotransmitter

Instead secretes hormone, Adrenaline (and some noradrenaline)

Into bloodstream

77
Q

What is the name of the complex neural network within the gut?

A

Enteric NS - largely responds to gut function and stimuli received withing gut without engaging brain

78
Q

How does sympathetic control occur in the lungs to initiate bronchodilation?

A

Adrenaline released from adrenal gland travels in the bloodstream and diffuses into the lung to cause bronchodilation that way

79
Q

Describe the micturition reflex

A

Bladder slowly fills and moderate pressure in the bladder, SNS is in charge at this point

Internal sphincter controlled by SNS is closed off to prevent urine leaving the bladder

Once pressure gets to certain point, sensory information is relayed to the brain

PNS switched on and SNS is switched off

PNS contracts detrusor muscle to squeeze bladder and force urine out

Internal Sphincter is relaxed as SNS is turned off so urine can leave the bladder

80
Q

What type of receptor is required at all autonomic ganglia?

A

Cholinergic (nicotinic acetylcholine) receptors

e.g, Ion channel receptors as they mediate all fast excitatory and inhibitory transmission

81
Q

At the nerve innervating the Adrenal gland in the SNS, what receptor is found?

A

Nicotinic Acetylcholine (nACh) ion channel receptors

82
Q

Where are the muscarinic G-coupled protein receptors found?

A

Post-ganglionic nerves of the PNS

83
Q

Where are the adrenergic G-coupled protein receptors found?

A

Post-ganglionic nerves of the SNS

84
Q

In the heart, what are the muscarinic and adrenergic receptors responsible for respectively?

A

Muscarinic - slowing down

Adrenergic - speeding up

85
Q

Describe the action of Noradrenaline at a synapse?

A

Tyrosine converted to DOPA by tyrosine hydroxylase

This DOPA then converted to dopamine by DOPA decarboxylase

Dopamine packaged into vesicles with dopamine Beta hydroxylase and Noradrenaline is the product

Action potential causes Ca2+ influx and exocytosis

Exocytosis and neurotransmitter release

Receptor activation (Adrenergic)

Removal of neurotransmitter from synapse via uptake into pre-synaptic terminal or glial cell; can be metabolised in the synapse prior to uptake

86
Q

What are the 2 enzymes that metabolise noradrenaline?

A

Monoamine oxidase A within pre-synaptic terminal

Catechol-O-methyltransferase (COMT) in glial cells

87
Q

Describe the action of Adrenaline in the nerve innervating the Adrenal gland

A

Tyrosine converted to DOPA by tyrosine hydroxylase and DOPA converted to dopamine by DOPA decarboxylase

Dopamine packaged into vesicles with dopamine Beta hydroxylase, Noradrenaline is the product

Noradrenaline converted to adrenaline in the cytoplasm by phenylethanol methyltransferase

Action potential causes Ca2+ influx & Exocytosis

Exocytosis & Neurotransmitter release

Adrenaline diffuses into capillaries and is transported to tissues in the blood

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