Neuro

Question 1

Name the physical features of the frontal lobe

Answer 1

Precentral gyrus (primary motor cortex)
Superior frontal gyrus
Middle frontal gyrus
Inferior frontal gyrus

Question 2

Name the physical features of the parietal lobe

Answer 2

Postcentral gyrus
Supramarginal gyrus
Angular gyrus

Question 3

Name the physical features of the temporal lobe

Answer 3

Superior temporal gyrus
Middle temporal gyrus
Inferior temporal gyrus
temporal pole

Question 4

Name the physical features of the occipital lobe

Answer 4

Occipital pole

Preoccipital notch

Question 5

Name the main features visible on the medial aspect of the brain

Answer 5

Corpus callosum
Cingulate gyrus
lateral, third ventricles
Pons and medulla
Thalamus

Question 6

What is the function of the cingulate gyrus?

Answer 6

Gateway to the frontal cortex, higher functioning, and the flight and fight areas of the brain

Question 7

Describe the precentral gyrus and its associations

Answer 7

It is the primary motor cortex, and it is arranged in a homuncular fashion. This means that the part for the face is located basally, then eyes, hands, torso, legs etc. It is associated with the motor planning area of the frontal cortex, which includes broca’s area, eye fields and exter’s area.

Question 8

Describe the rest of the frontal lobe and its overall function

Answer 8

The frontal lobe contains the superior, middle and inferior frontal gyri. Its function is in intelligence, behaviour, personality, mood and cognitive function.

Question 9

Describe the SMAGLA and the overall function of the parietal lobe

Answer 9

SMAGLA is associated with reading and writing, respectively, and have connections to the eye fields and exter’s area. The parietal lobe is associated with spatial awareness, 3d recognition and abstract awareness on the LHS, and music, non verbal communication and nuance on the RHS.

Question 10

Describe Wernicke’s area and the primary auditory cortex

Answer 10

Wernicke’s area surrounds the primary auditory cortex on the superior temporal gyrus. The auditory cortex receives input from CNVIII to separate deep vs high sound pitches. Wernicke’s area interprets the sound, and has a connection to broca’s area called the arcuate fasciculus. It also has a connection to the SMG.

Question 11

Describe the overall structure of the temporal lobe and its function

Answer 11

The temporal lobe has superior, middle and inferior gyri. It is involved in mood, memory, aggression and intelligence.

Question 12

Describe the different aphasias that can form and how to tell two apart

Answer 12

Connectional aphasia: Understand what is being said and can verbalize, but the response is not appropriate
Sensory aphasia: Lesion in Wernicke’s area. CCannot understand what is being said but can produce words.
Motor aphasia: Can understand what is being said but cannot verbalise
Can tell the difference by asking for a written response to a verbal question

Question 13

Describe the occipital lobe’s structure

Answer 13

It has the primary visual cortex at the occipital pole, which then dives deep. It also has a secondary cortex surrounding it and dipping into the temporal lobe, which is used to interpret the raw info given by the primary

Question 14

What is the difference ebtween allocortex and neocortex?

Answer 14

Most of the brain’s cortex is neocortex, which is made of 6 distinct cell layers
Allocortex has 3 layers of mixed cell type, and only covers a very small portion of the inferior brain. It is associated with fight or flight, the hippocampus and the olfactory centre

Question 15

What are the 6 layers of the cerebral cortex and what is its general pattern?

Answer 15

I:  Molecular
II:  External granular
III:  External pyramidal
IV:  Internal granular
V:  Internal pyramidal
VI:  Multiform
The upper 3 layers are involved in information from brain  to the brain
The lower 3 layers are involved in relaying information between the brain and spinal cord

Question 16

Describe the molecular layer of the cerebral cortex

Answer 16

Nonspecific cells. Important for development as it’s where radial fibres stick into the neocortex and allow its integration into the brain

Question 17

Describe the external granular layer of the brain

Answer 17

Made of small granular neurons, which receive sensory input from other brain areas (eg. ears)

Question 18

Describe the external pyramidal layer of the brain

Answer 18

Cells taking info to other cortex areas. They only carry information a short distance and so are small cells (10-40um)

Question 19

Describe the internal granular layer of the cortex

Answer 19

Granular cells that receive sensory input from the periphery

Question 20

Describe the internal pyramidal level of the cortex

Answer 20

Betz cells. Large motor neurons of the pyramidal tract (UMNs). 60-120um.

Question 21

Describe the multiform layer of the cortex

Answer 21

Integrate different sensory inputs of the brain

Question 22

What can afferent and efferent fibres also be called when in the brain?

Answer 22

• Efferents can also be called corticofugal.

- Afferents can also be called Corticopetal

Question 23

What are the major forms of arrangement of these six layers, and where are they likely to be found?

Answer 23

It can be homotypical- around equal amounts of each cell type. Found where many types of info are received and sent. Eg. Prefrontal cortex, parietal cortex, temporal cortex
Heterotypical is divided into two categories
Agranular hetero typical is when there are more pyramidal cell types as their primary function is projection to other areas or to the spinal cord. Areas III and V are increased, while II and IV decrease. Eg. Primary motor cortex

Granular heterotypical is where there are more granule cells as the primary function is reception of info. II increases, IV increases massively, and III and V decrease. Eg. Primary somatosensory, visual or auditory cortices.

Question 24

Describe the circle of willis

Answer 24

Posterior cerebral arteries join the middle cerebral arteries via the posterior communicating arteries. The middle cerebral arteries (arising from internal carotids) join to the anterior cerebral arteries via anterior communicating arteries

Question 25

Describe the circulation of the posterior brain

Answer 25

2 vertebral arteries join to form the basilar, which then give anterior cerebellar, superior cerebellar, pontine and posterior cerebral arteries

Question 26

Describe the structure and associated function of the internal capsule

Answer 26

The anterior internal capsule takes info to the frontal lobe from the thalamus (eg. memory) The curve in the internal capsule is called the genu. It separates the lens and the caudate nucleus The outer posterior IC takes motor information from the primary motor cortex to the spinal cord The inner posterior IC takes sensory info from the spinal cord to the primary sensory cortex. These two areas are arranged in a homuncular fashion, with the genu representing the face, and the rest of the body located more posteriorly

Question 27

What does each thalamic nucleus do?

Answer 27

The ventroposterior nucleus is responsible for receiving sensory information and sending it out to the primary sensory cortex. The medial part represents the face and the lateral represents the body. The VAVL nuclei receives info from the basal ganglia and sends it to the motor planning area The Anterior nuclear group allows memories to be retrieved from and sent to the frontal cortex via papez's circuit. The medial and lateral groups integrate sensory input from the association cortices, with the lateral being particularly involved in secondary visual information. The lateral geniculate body receives visual information from the eyes and sends it to the primary visual cortex The medial geniculate body receives auditory information from the ears and sends it to the primary auditory cortex. The Intralaminar nuclear group is responsible for consciousness.

Question 28

What are the overall functions of the thalamus?

Answer 28

Monitors and gatekeeps info for higher cortex Consciousness Integrating regionalized brain function Motor planning and refining

Question 29

Describe the reticular sheet

Answer 29

A membrane beneath the thalamus which controls UMN sensitivity

Question 30

Describe papez's circuit

Answer 30

Info is sent in a circle from the anterior thalamic nuclei, to the cingulate gyrus, to the parrahippocampal gyrus, to the hippocampus, to the fornix, to the mamillary body, and back to the anterior thalamic nuclei. The cingulate gyrus also communicates with the frontal cortex.

Question 31

Describe the basic shape and ending of the spinal cord

Answer 31

There are two enlargements- the cervical and lumbar. The cord terminates at the bottom of L1, and forms the cauda equina. The filum terminale of this is attached to the base of the coccyx. The arachnoid mater terminates at S2 level, and the dura mater ends at S3.

Question 32

What are rexed's laminae?

Answer 32

``` 10 subdivisions of the gray matter of the spinal cord 1. Posteromarginal nucleus 2. Sustantia gelatinosa 3-4. Nucleus proprius 5-6 7. Intermediate zone 8-9. Medial and lateral motor columns 10 ```

Question 33

Describe the functions of the different parts of the gray matter of the spinal cord in terms of non discriminative sensation

Answer 33

The posteromarginal nucleus and substantia gelatinosa perform the same function in pain and temperature sensation, although the SG has opioid receptors, so pain referred here can be lessened with analgesics. A further neuron carries the information either to area 8/9, which has LMNs necessary for creating a polysynaptic reflex, or decussates at the anterior white commissure, to be transferred to the brain via the lateral spinothalamic tract.

Question 34

Describe the functions of the different parts of the gray matter of the spinal cord in terms of discriminative sensation

Answer 34

The nerve fiber enters either directly to the gracile/cuneate fasciculi (25%) or else enter areas 3/4 or the dorsal nucleus of clark. These then conglomerate to form another neuron stretching from the gray matter into the dorsal funiculus, which prevents increasing spinal cord size superiorly. Alternately, the fiber could go into area 8/9 to provide a myotactic reflex (although this is slow due to unmyelinated fibers)

Question 35

Describe the functions of areas 5-7 of the gray matter

Answer 35

5-6: Abdominal and internal organs' sympathetic supply | 7: Intermediate zone for sympathetic input.

Question 36

Describe where sensory vs motor neurons are located in the thalamus, cortex and spinal cord

Answer 36

Sensory fibers are located posteriorly, motor are anterior

Question 37

Describe the function of the gray matter in terms of motor input

Answer 37

UMNs descend via the motor columns, allowing motor info to travel down to the spinal cord. These move into areas 8/9, where they synapse with LMNs and exit via the ventral root

Question 38

Describe the organization of the midbrain

Answer 38

Most anterior is the crux cerebri, which transmit motor info from the primary motor cortex to the spinal cord, helping to start off the corticospinal pathway. It is arranged in a homuncular fashion, with face medial and body lateral for each of the legs. Posterior to this is the substantia nigra, which produces dopamine Deep to this is the tegmentum, which also extends through the brainstem. It is here called the midbrain tegmentum, and receives sensory info from the spinal cord, sending it to the brain. Most posteriorly are the superior (sight reflex) and inferior (sound reflex) colliculi, made of 4 nerve fibers. Collectively they are called the tectum or corpora quadrigemina

Question 39

Describe the arrangement of the pons part of the brainstem

Answer 39

Most anterior is the pons, which is overlaid by the basilar artery It contains the pontine nuclei, which form a conduit from the cortex to the cranial nerve nuclei via the brainstem. This then transmits motor info to the face. This overlays the pontine tegmentum, then the fourth ventricle, and most posteriorly is the cerebellar peducle, which transmits info to and from the cerebellum

Question 40

Describe the arrangement of the medulla part of the brainstem

Answer 40

Most anteriorly is the medullary pyraminds, which are where motor info decussates This overlays the medullary tegmentum, where the gracile and cuneate nuclei are found, and also contains the inferior olives, which coordinate exchange of info between the spinal cord and cerebellum

Question 41

Describe the corticospinal pathway

Answer 41

It begins in the primary motor cortex before descending through the crus cerebri in the midbrain, into the pons, and then 85% cross over in the medullary pyramids. It then forms the lateral corticospinal tract, which descends into area 8/9 of the gray matter before exiting the ventral root. 15% descends straight down, and crosses over the anterior white commissure. It is thought that these are axial muscle fibers

Question 42

Describe the corticobulbar tract

Answer 42

It begins in the primary motor cortex before descending through the crus cerebri in the midbrain. Once it enters the pons it synapses with the nucleus of the cranial nerve it supplies, which then runs out of the pons to the face

Question 43

Describe the dorsal column- medial lemniscus pathway

Answer 43

It enters the spinal cord through the dorsal root ganglion, before entering the gracile/cuneate fasciculi. Then it runs up the dorsal funiculus before synapsing at the gracile/cuneate nuclei. They decussate as internal arcuate fibers, and run up the medial meniscus pathway. They enter the thalamus at the VP nucleus, and then run through the internal capsule to the homuncular part of the primary somatosensory cortex

Question 44

Describe the lateral spinothalamic tract

Answer 44

Enters the dorsal root ganglion, into regions 1/2 of the gray matter. It then synapses, and decussates at the anterior white commissure. It ascends in the lateral spinothalamic tract, where it then joins the medial lemniscus pathway and enters the VP nucleus of the thalamus. From there it runs in the internal capsule to the homuncular part of the primary somatosensory cortex.

Question 45

What is the mnemonic used to remember the functions of each of the cranial nerves?

Answer 45

Some Say Marry Money But My Brother Says Big Brains Matter More

Question 46

What are the 12 cranial nerves?

Answer 46

1: Olfactory 2: Optic 3: Optothalamic 4: Trochlear 5: Trigeminal 6: Abducens 7: Facial 8: Vestibulocochlear 9: Glossopharyngeal 10: Vagus 11: Accessory 12: Hypoglossal

Question 47

Where do each of the nerves exit the brain?

Answer 47

``` Cribiform Plate: I Optic Canal: II Superior Orbital Fissure: III, IV, V1, VI Foramen Rotundum: V2 Foramen Ovale: V3 Internal Accoustic Meatus: VII, VIII Jugular Foramen: IX, X, XI Hypoglossal Canal: XII ```

Question 48

What is the function of the Olfactory nerve and what can happen if it goes wrong?

Answer 48

- Smell - Fright and flight response as only input into the limbic system e.g. smell burning --> Run fast - Issue can cause loss of smell sensation

Question 49

What is the function of the optic nerve and what can happen if it goes wrong?

Answer 49

- Transmits visual information - There is a chiasma where the medial fibers of each nerve decussate. If there is a lesion before the chiasma, there will be full blindness in one eye If there is a lesion post chiasma, there will be partial blindness

Question 50

What is the function of the oculomotor nerve and what can happen if it goes wrong?

Answer 50

``` Innervates ciliary muscle, sphincter of pupil and all external eye muscles except superior oblique muscle and lateral rectus muscle Muscles: Superior rectus, medial rectus, inferior rectus, inferior oblique - Damage --> Loss of light reflex, dilated pupil (Decreased tone of the constrictor pupillae muscle), downward, abducted eye on the affected side due to the unopposed action of the superior oblique and lateral rectus muscle ```

Question 51

What is the function of the trochlear nerve and what happens if it goes wrong?

Answer 51

"Innervates superior oblique muscle (pulley) - pulls eye up and outwards" Trochlear nerve palsy - downward, inwards gaze

Question 52

What is the function of the trigeminal nerve and what happens if it goes wrong?

Answer 52

Takes info about sensation back to the brain. It innervates skin as well as internal mucoase. - V1 = Carries info from Opthalmic division - V2 = Carries info from maxillary division - V3 = carries info fromMandibular division. ALSO HAS MOTOR FUNC. innervates chewing muscles. Innervates some salivary glands - Trigeminal neuralgia = sudden attacks of pain which are triggered by touching the face, chewing, speaking or brushing teeth.

Question 53

What is the function of the abducens nerve and what happens if it goes wrong?

Answer 53

``` "Innervates lateral rectus muscle (involved in lateral gaze - used in visual tracking or fixation on an object)" - Abducens nerve palsy --> The affected eye turns in towards the nose and is unable to abduct properly (double vision) ```

Question 54

What is the function of the facial nerve and what happens if it goes wrong?

Answer 54

``` - Motor = Muscles of facial expression - Parasympathetic = submandibular, sublingual, lacrimal glands - Sensory = anterior 2/3 of tongue, soft palate - Facial nerve palsy - facial paralysis due to a lesion in the facial nerve (symptoms also include dry mouth and altered taste. Called bell's palsy and is due to compression of the nerve through the facial canal. ```

Question 55

What is the vestibulocochlear nerve and what happens if it goes wrong?

Answer 55

``` Transmits sound (Cochlear) and balance (Vestibular) information from inner ear to the brain Damage to nerve - hearing loss, vertigo, false sense of motion, loss of equilibrium, nystagmus, motion sickness, tinnitus ```

Question 56

What is the function of the glossopharyngeal nerve and what happens if it goes wrong?

Answer 56

``` - Sensory = posterior 1/3 of tongue, tonsil, pharynx, middle ear - Motor - stylopharyngeus, upper pharyngeal muscles, parotid gland - Damage to glossopharyngeal nerve = loss of taste (esp bitter & sour flavours), trouble swallowing, absent gag reflex ```

Question 57

What is the function of the vagus nerve and what happens if it goes wrong?

Answer 57

``` - Parasympathetic input to GI system and Heart - Motor = heart, lungs, palate, pharynx, larynx, trachea, bronchi, GI tract - Sensory = heart, lungs, trachea, bronchi, larynx, pharynx, GI tract, external ear - If diabetes has damaged the vagus nerve, it can cause gastroparesis: muscles of the stomach and intestine arent able to efficiently move food through the GI system. Symptoms : nausea, vomiting, heartburn, constipation, abdominal bloat, stomach spasms and decreased appetite ```

Question 58

What is the function of the accessory nerve and what happens if it goes wrong?

Answer 58

``` Innervates: - Stemocleidomastoid (Tilt & rotate head) - Trapezium (elevate shoulders) Accessory nerve disorder - inability to shrug shoulders and rotate head ```

Question 59

What is the function of the hypoglossal nerve and what happens if it goes wrong?

Answer 59

``` Tongue muscles & strap muscles by ansa cervicalis. Also controls hyoid bone alongside some spinal nerves Paralysed tongue, or deviated away from injured side. See problems swallowing, chewing, speaking ```

Question 60

Where are the cranial nerve nuclei? (generally)

Answer 60

I & II: Allocortex/Limbus The rest sit within the midbrain and hindbrain There can be multiple nerves associated with one nucleus, or one nucleus associated with one nerve

Question 61

What are the different categories of sensory vs motor nerves?

Answer 61

``` Sensory can be: - General somatic (skin) - General visceral (organs) - Special somatic (sight, sound, balance) - Special visceral (taste/smell) Motor can be: - General somatic (skeletal) - General visceral (smooth) - Special visceral (pharyngeal arches) ```

Question 62

What are the different patterns of sensory loss?

Answer 62

- Localized numbness - Generalized one sided numbness - Loss of sensation below a spinal level - Glove and stocking loss - Dermatome loss - Trunk or plexus loss

Question 63

How do different spinal cord lesions present?

Answer 63

- Can give weakness below a certain sensory level even if no discriminative sensation is lost. This is because a partial lesion can preserve the posterior columns, so pinprick sensation must be tested to determine whether the ventrolateral areas have been compromised - Can give bilateral signs or paralysis - Central lesions can also spare the posterior columns and power as they compress the anterior white commissure. Hemicord lesions cause motor weakness and loss of discriminative sensation on the same side as the lesion, and loss of non discriminatve sensation on the opposite side to the lesion

Question 64

How do PNS lesions present?

Answer 64

Mononeuropathy can be an AI disease, vasculitis or nerve compression. Sensory loss and weakness in the supplied area Polyneuropathy presents as motor, sensory or a combination of both. Different issues can affect myelinated or unmyelinated fibers, or even myelin itself. Eg. Diabetes attacks axons so it starts in the longest (feet) before moving into the hands Plexus lesions (eg. slipped disc) is a single nerve issue in a dermatome Guillain Barré syndrome is an example of a demyelinating disease

Question 65

How do UMN vs LMN symptoms present?

Answer 65

UMN issues show weakness, increased tone and reflexes. Half body or spinal level may be affected LMN issues show weakness, decreased tone and reflexes. They are due to nerve root or peripheral distal issues

Question 66

What is the best way to do a sensory exam?

Answer 66

Keep questions unslanted, ie. does this feel the same as this? Do it at the end of an interview to confirm a hypothesis, rather than to generate one

Question 67

What are some common sensory exams and how do you do them?

Answer 67

Light touch: Dab a cotton wisp onto the skin, looking for lack of perception, no difference in perception, or different quality of perception (ie felt as pain) Pinprick: Lightly touch the sharp end to the skin, but not hard enough to puncture. Can also use to differentiate sharp vs. dull Joint position: Stabilize the joint with hand and then move it while the patient's eyes are closed, asking them to tell you in which direction it's being moved Vibration: Press a tuning fork to the pulp of middle finger or big toe, and then bony prominences if necessary. See if vibration is felt and how long for (approx. 8 sec is normal) Graphaesthesia: Can patient recognize a digit traced on their palm?

Question 68

How do you move when testing sensation?

Answer 68

Move randomly when testing for any numbness | Move from numb area outwards when testing for border of numbness.

Question 69

What are the three goals of anaesthesia and how are these achieved?

Answer 69

- Hypnosis- normally and IV or volatile agent - Immobility- normally a muscle relaxant - Autonomic Areflexia- normally opioids Modern anaesthesia uses balanced anaesthesia, with different drugs for different purposes

Question 70

What is the mechanism of uptake and release of volatile agents?

Answer 70

PI > PA > Pa > Pbr (start of anaesthesia) | PI < PA < Pa < Pbr (end of anaesthesia)

Question 71

How do volatile anaesthetics work?

Answer 71

They likely modulate gaba in the brain and glycine in the spinal cord to reduce synapse transmission

Question 72

What is the MAC and what factors affect it?

Answer 72

Minimal alveolar concentration producing immobility on standard surgical stimulus in 50% of patients. It is usually expressed as a percentage. The lower the percentage the more potent the drug. Factors increasing MAC include young age, hyperthermia, hyperthyroid, drugs, and heavy alcohol Factors decreasing MAC include old age, hypothermia, hypothyroid, drugs, pregnancy and low O2/High CO2

Question 73

How is volatile anaesthetic dosing monitored?

Answer 73

The FI is compared to the FE, adjusting for minute ventilation, FA and transfer into the blood to estimate blood concentration.

Question 74

What are the effects of volatile anaesthetics?

Answer 74

Hypnosis, immobility and amnesia Decreased CMRO2, and increased CBF and ICP- so there are protective and harmful factors for neuro Peripheral vasolilation, lower BP. Unchanged HR and SV Resp depression, impaired reflexes to hypoxia and hypercapnia. Bronchodilation

Question 75

What are some of the features of NO?

Answer 75

``` Odourless, non flammable inhaled anaesthetic Low potency Low blood-gas solubility, rapid onset Analgesic Nausea and vomiting ```

Question 76

What are some of the features of isoflurane?

Answer 76

Potent inhaled anaesthetic, good CVS stability

Question 77

What are some of the features of sevoflurane?

Answer 77

Non pungent and least resp. depression- good for gaseous induction anaesthesia Low solubility, rapid onset Theoretical renal toxicity

Question 78

What are some of the features of desflurane?

Answer 78

- Pungent inhaled anaesthetic | - Low blood gas solubility, rapid onset and offset

Question 79

What are some categories of IV anaesthetic and how do they work?

Answer 79

Barbituates (thiopentone) Phenols (propofol) Imidazoles (Etomidate) Ketamine Benzodiazepines (Midazolam) All but ketamines act on GABA receptors to enhance GABA, increase Cl- current and cause hyperpolarization Ketamines act on NDMA receptors in PCP receptrs to antagonize glutamate, suppress excitation and cause analgesia

Question 80

How do IV agents act in the body?

Answer 80

They are highly lipid soluble and cross the blood-brain barrier Drug is taken up by well perfused organs, and then decrease blood concentration and they see a concentration drop as the drug leaves the well perfused organs and is metabolized in the liver or is redistributed to tissues.

Question 81

Describe some of the properties of thiopentone

Answer 81

Very rapid onset and offset, with slow clearance so accumulation will occur Metabolized in the liver Causes decreased PVR and BP, as well as rep depression and reflex loss Mostly used in emergency cesarians and ED

Question 82

Describe some of the properties of propofol

Answer 82

Moderately rapid onset and offset, with fast clearance allowing for maintenance infusions Metabolised in liver Significant decrease in PVR and BP, resp. depression and loss of airway reflexes It is the standard IV anaesthetics as it reduces CBF and ICP, has less of a hangover and can be used for maintenance

Question 83

Describe some of the properties of etomidate

Answer 83

It shows CV stability, less resp depression and rapid clearance. However, it shows adrenocortical inhibition, which prevents HPA axis functioning and reduces stress hormones, which are important for recovery

Question 84

Describe some of the properties of ketabine

Answer 84

Analgesic Stimulates CVS and preserves resp reflexes and drive Increased CMRO2, CBF and ICP so not good for neurosurgery Good for shock but slow and dysphoric emergence

Question 85

Describe total intravenous anaesthesia, and its pros and cons

Answer 85

Avoids inhalation, and complications of this (malignant hyperthermia, PONV, increased ICP) However, it's expensive and unable to be effectively monitored.

Question 86

Describe the structure of local anaesthetics

Answer 86

They have a hydrophobic aromatic group at one end, a hydrophilic amide group at the other end, and are linked together by either amides or esters.

Question 87

How does the link of local anaesthetics affect their properties?

Answer 87

- Esters are more rapidly metabolized, and so have shorter action, and are more allergenic. Amides have the opposite. Additionally, lengthening the alkyl chain length increases the lipid's solubility, making it more potent.

Question 88

What are some examples of ester vs amide local anaesthetics?

Answer 88

Esters include cocaine, procaine, benzocaine, tetracaine | Amides are prilocaine, lignocaine, bupivacaine, and ropivacaine

Question 89

What is the main property of local anaesthetics that determines their speed of action?

Answer 89

Their pKa. The closer their pKa to physiological, the more free base there will be in the body, allowing it to enter the cell and block nerve transmission from the inside

Question 90

What is the fastest acting local anaesthetic?

Answer 90

Mepivacaine, followed by lignocaine

Question 91

What does protein binding have to do with duration of action for LAs?

Answer 91

The higher the degree of protein binding, the longer the duration of action.

Question 92

How are LAs metabolised?

Answer 92

Esters by plasma cholinesterases | Amides by liver metabolism

Question 93

Describe the properties of lignocaine

Answer 93

Low solubility and potency Low pKa so fast onset Low protein binding so short duration Ideal for short surgical procedures

Question 94

Describe the properties of bupivacaine

Answer 94

More potent, longer lasting and slower onset compared to lignocaine. May cause cardiac arrest before the neurotoxicity warning sign. Ideal for nerve blocks for analgesia

Question 95

Describe the general properties of cocaine, prilocaine, and ropivacaine

Answer 95

Cocaine- ester, topical to nose, vasoconstrictor Prilocaine- amide, safest, used in IV regional anaesthesia with a tourniquet to prevent arrest Ropivacaine- amide, slow onset, long acting but less CVS toxicity

Question 96

How do you assess LA toxicity?

Answer 96

Allergic reactions are rare, however, CNS and CVS toxicity can develop, of which CVS is much more life threatening Thankfully they are dose dependent, and CNS tends to occur earlier than CVS- simply watch for neuro and don't give any more!

Question 97

How do you administer LAs topically, and why?

Answer 97

They can be topical to the skin in a mixture of LAs in oil. This allows most to be free base and cross the skin. It is used in insertion of IV cannulae in children Topical to mucus membranes: Cocain has the added advantage of vasoconstriction. Used for instrumentation of the nose/mouth/pharynx as in awake intubation

Question 98

How do you administer LAs to the soft tissue?

Answer 98

For minor interventions like a mole removal, you use a fast, short duration agent For post op pain relief you use a slow, long duration agent

Question 99

What is a peripheral nerve block?

Answer 99

The LA ins infiltrated around a specific nerve or plexus. Sensory fibers are more susceptible, but motor nerves can also be affected. USed for surgery without a GA, or postop pain relief

Question 100

What is a neuraxial blockade?

Answer 100

LA is injectd into the intrathecal space below L2. It produces a profound distal motor and sensory block, allowing major distal surgery while awake

Question 101

What is an epidural anaesthetic?

Answer 101

A small catheter is inserted into the epidural space and LA is infused around the spinal nerves nearby. It can be done at any level, and produces a distal sensory and motor blockade. It allows maintenance infusion, and is excellent for postop and labour analgesia

Question 102

What do NMBAs do?

Answer 102

They paralyse patients undergoing surgery or requiring intubation. They do not sedate, cause amnesia, or have analgesic effects.

Question 103

Why are NMBAs necessary for intubation?

Answer 103

They paralyze the vocal cords, decreasing damage and postop hoarseness. It also allows control of ventilation intraoperatively, allowing oxygen consumption to be decreased and barotrauma to be prevented. Ventilating also lowers ICP.

Question 104

What are the 3 areas of the NMJ and their general functions?

Answer 104

Presynaptic- ACh synthesis and storage. Release of ACh and reuptake of Ch Synaptic cleft: Side of AChE, ACh crosses Postsynaptic- AChRs anchored in folds

Question 105

Describe the events at synapse including quantal theory

Answer 105

ACh is stored in vesicles. Ca2+ flows into the cell after an AP, causing the ACh vesicles to fuse with the presynaptic membrane and release ACh into the cleft. The number released is proportional to Ca2+. usually about 200 units with 5000 ACh each. About half are immediately hydrolysed, though more is released than necessary for a single transmission. Approx. 500000 AChRs are bound, allowing Na+ to flow in and causing endplate depolarization.

Question 106

Describe AChRs

Answer 106

Ligand gated ion channels with 5 subunits each- 2a, b, y, e. Both a units must be bound simultaneously, causing a conformation change, opening the channel and allowing ions to flow in.

Question 107

Describe AChE

Answer 107

An enzyme present primarily in the synaptic cleft, and to some extent in the extrajunctional area. It is secreted by the muscle and attached to the basal lamina by collagen.

Question 108

Describe depolarising muscle relaxants

Answer 108

Known as Sux (suxamethonium). It is similar in structure to ACh, and is comprised of 2 ACh molecules bound together. It mimics the effect of ACh by causing depolarization, although it causes fasciculation (a brief flicker of movement) and then relaxation lasting 3-5 mins. It is not hydrolyzed by AChE, but by pseudocholinesterase. Its neuromuscular blocking activity is terminated by diffusion into the plasma. Its time of action depends on the time taken to excrete it.

Question 109

What are some of the side effects of Sux?

Answer 109

``` It cannot be reversed pharmacologically Anaphylaxis Fasciculations and postoperative myalgia Cardiac dysrhythmias Hyperkalaemia Increased ICP, IGP and IOP Malignant hyperpyrexia Masseter spasm ```

Question 110

What are the positives of Sux?

Answer 110

It provides the quickest, most reliable relaxation for airway control, giving excellent intubating conditions with minimal time for aspiration. It is mainly emergent

Question 111

Describe how non-depolarising NMBAs work

Answer 111

They are positively charged quaternary N compounds They compete with ACh and bind to one or both a subunits, preventing ACh binding and opening of the ion channel. As only one molecule of the drug is required to do this, it is biased towards favouring the antagonist Blockade starts when receptors are more than 70% occupied, and is complete when more than 90% are occupied

Question 112

What are the two ways of grouping Non depolarising NMBAs?

Answer 112

Chemical structure: Aminosteroies have ammonium on a steroid- Rocuronium, Vecuronium and Pancuronium. Benzylisoquinolones have 2 ammonium joined by methyl. Atracurium, Cisatracurium and Mivacurium Duration of action: Short acting (Mivacurium) Intermediate acting: Atracurium, Vecuronium, Rocuronium Long acting: Pancuronium

Question 113

Describe atracurium

Answer 113

A NMBA with an intermediate duration and a 3-5 minute onset. It has 2 elimination pathways- Hoffman is nonenzymatic, and dependent on temperature and pH. Its inactive products are excreted. It is also partly removed by renal excretion and ester hydrolysis. It can cause histamine, hypotension and tachycardia. Its advantages are in elderly or kidney dysfunction patients as it is not dependent on renal excretion

Question 114

Describe mivacurium

Answer 114

3x more potent than atracurium, slow onset of 3-5 mins short duration of action, hydrolysed by pseudocholinesterases. Less histamine. Used mainly in ambulatory surgery

Question 115

Describe rocuronium

Answer 115

Rapid onset and intermediate duration. Used for rapid sequence induction instead of Sux, but longer duration. Can have anaphylaxis. 90% hepatic elimination

Question 116

Describe vecuronium

Answer 116

Intermediate duration. Show onset, but no CV side effects. Active metabolites, renally excreted- means it accumulates in renal failure. Used ful in CVS disease patients, with least anyphylaxis and histamine

Question 117

Describe pancuronium

Answer 117

Long duration of action, high potency and slow onset. Longest duration. Increases BP, HR and CO, so ideal for long cardiac surgery. Minimal histamines. Difficult to reverse

Question 118

Describe the perfect NMBA

Answer 118

``` Rapid onset Titratable effect Easily reversible No histamine or anaphylaxis No haemodynamic effects Inactive metabolites No accumulation Low cost ```

Question 119

How can you reverse NMBAs?

Answer 119

You cannot reverse depolarising NMBAs. Strategies for reversing the others include titrating perfectly for their duration of action, but this is hard as both patients and surgeons can be unpredictable. Additionally, you could accelerate their reversal, which is safer and more reliable. It can be acheived by increasing the concentration of ACh at the receptor, or decreasing the NMBA. Increasing ACh is done by using AChE inhibiting drugs, although these act on all receptors throughout the body. This means they have side effects such as bradycardia, bradyarrhythmias, bronchospasm, salivation and increased bowel motility. To counteract these, antimuscarinic agents are given in combination

Question 120

What is sugammadex?

Answer 120

A perfect antidote for rocuronium and vecuronium, by selectively binding rocuronium and rendering it incapable of binding to the AChR. It favours movement of rocuronium from the NMJ to the plasma, allowing muscle function to return within 2 minutes.

Question 121

How do you monitor a neuromuscular blockade?

Answer 121

Stimulate the peripheral nerve, assessing the response of the muscle. A stimulator is connected to the ulnar nerve, and 4 stimuli 0.5 seconds apart are given at a frequency of 2hz. The movement of adductor pollicis is assessed, with the TOF count and the TOF ratio. TOF is the number of twitches seen, TOF ratio is the ratio of the 4th to 1st twitch as a percentage. Intact neurotransmission shows four twitches of identical height. Recovery from a neuromuscular block causes twitches to come back slowly.

Question 122

What is TOF fade?

Answer 122

A deficiency of neuromuscular transmission requiring intervention. It is only seen in non-depolarising NMBAs. Different muscle groups respond differently. The diaphragm is less susceptible than peripheral nerves, so adductor pollicis is used as a proxy. It shows

Question 123

What is double burst stimulation?

Answer 123

The fade of the second twitch is compared to the first. Two to three short bursts of stimuli are administered twice, comparing the twitches. Full recovery is two equal twitches.

Question 124

What are the five basal ganglia?

Answer 124

The caudate nucleus, putamen (collectively called the striatum), globus pallidus, hypothalamus, and substantia nigra.

Question 125

What is the function of the basal ganglia?

Answer 125

They smooth out and plan motor movement.

Question 126

What are the three capsules of the basal ganglia?

Answer 126

The internal capsule, external capsule (separating the claustrum from the putamen) and the extreme capsule (separating the alimentary cortex from the basal ganglia)

Question 127

What are the claustrum and alimentary cortex?

Answer 127

Claustrum is the centre for visual attention | The alimentary cortex represents the GI system.

Question 128

Describe the direct and indirect pathways of the basal ganglia

Answer 128

Direct pathway is GLUT from planning area to striatum, GABA to GPi, GABA to VaVL and GLUT to planning Indirect pathway is GLUT from planning to striatum, GABA to GPe, TABA to subthal, GLUT to GPi, GABA to VaVL and GLUT to planning

Question 129

What is the nigrostriatal pathway?

Answer 129

Dopamine pathway between the substantia nigra pars reticulata, and then the SN pars compacta to the striatum. It produces dopamine which is then transferred back to the striatum, holding the cells at a tonically active state

Question 130

How does the pathology of huntingtons disease occur?

Answer 130

The pathway from the striatum to the GPe is inhibited. The fibres from GPe to SUT aren't inhibited, and are free to inhibit the GLUT pathway to GPi. GPi then in turn inhibits the VaVL less, allowing uninhibited firing of the VAVL nucleus to the planning area.

Question 131

What are the symptoms of and treatment of huntington's disease?

Answer 131

Symptoms include behavioural and cognitive changes, hyperkinesia and involuntary movements. It is due to trinucleotide repeats within the base sequences. Males hand down longer copies of repeats, with women handing down the same length. Therefore, genetic anticipation can happen, where longer and longer chains cause the offspring to get it earlier and more violently than their parents.

Question 132

What are the symptoms of parkinson's disease, and how does this relate to its

Answer 132

It's due to a failure of the nigrostriatal pathway, which produces dopamine. The lack of dopamine means that the striatum is unable to fire, leading to hypokinesia, emotionally flat moot, tremor at rest (esp. pill rolling) and rigidity. It can be treated with oral levodopa (although this can cause toxicity), a pallidotomy, or thalamotomy, on one side of the brain, or deep brain stimulation (an adjustable pacemaker implant)

Question 133

What are the different nuclei within the cerebellum and what do they do?

Answer 133

Fastigial nucleus: Sends info on proprioception to the reticular formation and lateral vestibular nucleus, to be transferred to the lower montorneuron pool. The interpositus nucleus sends information on automated movement to the red nucleus, which then sends the information via the rubrospinal tract to LMNs The dentate nucleus sends info on fine movement to the red nucleus and Vent. Lat nucleus, which then sends it ot UMNs and LMNs.

Question 134

How is the cerebellum divided and what do each of the parts do?

Answer 134

It has lateral part, intermediate part, and vermis. There is also and anterior lobe, posterior lobe, and focculonodular lobe. The neocerebellum receives input from pontocerebellar and olivocerebellar fibres, for fine motor control, rebound reflex and correction of movement (ie when somebody bumps into you while walking). The palaeocerebellum is in the intermediate part, and receives proprioception info from the spinocerebellar fibres and olivocerebellar fibres The archicerebellum is in the flocculonodular lobe and is the first part to develop. It receives vestibular info from the bod

Question 135

What happens when there are issues with different parts of the cerebellum?

Answer 135

Issue with neocerebellum means issues with fine movement, like an intention tremor Issue with the palaeocerebellum means there is an issue with postural instability Issue with archicerebellum means there are problems with general balance, eye movements become quick, cannot focus.

Question 136

What are the peduncles of the cerebellum and what goes through them?

Answer 136

The inferior peduncle receives info from the olivocerebellar fibres, and vestibulocerebellar fibres from the inf olive and vestibular nucleus The middle cerebellar peduncle receives fibres from the pontine nuclei The superior cerebellar peduncle receives info from the cerebellum's nuclei and redirects it to the thalamus, vestibular nucleus, inf. olive, spinal cord etc,

Question 137

Define drug tolerance and sensitization

Answer 137

Tolerance to a drug is the reduction in response to a drug after repeated administrations. It may be innate or acquired. Sensitization is the opposite process

Question 138

What is physical drug dependence and withdrawal syndrome?

Answer 138

Physical dependence is the state that develops as a result of tolerance, produced by the resetting of homeostatic mechanisms in response to repeated drug abuse. Withdrawal syndrome is the evidence of physical dependence- usually characterised by CNS hyperarousal. It is characteristic to the drug category and tends to cause the opposite effects of the drug itself. For example, opioids cause restlessness, cravings, nausea, aches, anxiety, tachycardia when withdrawn.

Question 139

How is the mesolimbic system involved in addiction?

Answer 139

The stimulis hits the ventral trigeminal area, which gives a pleasurable sensation. It then continues through the nucleus accumbens, where it ends in the prefrontal cortex. Dopamine is the important neurotransmitter in this pathway.

Question 140

What is substance dependence syndrome?

Answer 140

Continued use of a substance despite problems related to it Tolerance Withdrawal symptoms Dependence is three of these (addiction), one or two indicates abuse.

Question 141

What are the three sources of substance dependence?

Answer 141

The agent, host or environment.

Question 142

How does the agent create substance abuse?

Answer 142

Reinforcement is the property that makes the user want to take the drug again- associated with central neurotransmitters and the rapidity of onset of the drug and its method of use.

Question 143

How does the host create substance abuse?

Answer 143

People show variability in their pharmacokinetic response to drugs, pharmacodynamic response, and their behavioural response to drugs. Some people have polymorphic inheritance for propensity to addiction. Innate tolerance also occurs. Some physiological changes prevent addiction (ie. those with increase alcohol dehydrogenase will never be alcoholics) Psychiatric disorders can also increase the risk of drug addiction

Question 144

How does the environment create addiction?

Answer 144

Societal norms and their view of addiction. Additionally, peer pressure, low employment and low educational levels are important.

Question 145

Describe alcohol as an addictive drug

Answer 145

It's a CNS depressant (but a stimulant at low doses). It impairs recent memory, motor coordination, and causes sedation in high doses. As tolerance develops, sedation is reduced but the lethal dose is unchanged- more dangerous. Withdrawal symptoms include craving, tremor, irratability, nausea, tachycardia, etc. Delerium tremens is caused by long term alcohol abuse and subsequent withdrawal. It shows agitation, confusion, hallucination, sweating etc.

Question 146

How is alcohol metabolized?

Answer 146

It is metabolized in the liver by alcohol dehydrogynase. The decay is relatively quick for the first few drinks, but changes to zero order once the process becomes saturated, allowing a dangerous buildup.

Question 147

What can long term use of alcohol cause?

Answer 147

Liver cirrhosis, myopathy, endocrine issues, FAS, mental retardation.

Question 148

How are opioids as drugs of addiction?

Answer 148

It is used mainly as an analgesic, although its prescription rate has skyrocketed and its affordability plummeted. This has lead people to source cheaper versions from other sources. There are short acting rapid onsets (morphine, fentanyl) and long acting slow onsets (methadone)

Question 149

Describe heroin as a drug of addiction

Answer 149

It is the most important opioid of abuse, and is illegal in USA and NZ. It is associated with abnormal pituitary function, irregular menses, reduced sexual performance, high mortality.

Question 150

What are the withdrawal symptoms of opioids?

Answer 150

Craving, restlessness, irritability, pain sensitivity, nausea, cramps dysphoria, anxiety Signs include dilated pupils. sweating, piloerection, tachycardia etc.

Question 151

Describe cocaine as a drug of addiction

Answer 151

It blocks transporters that recover dopamine from the synapse, leading to increased dopaminergic stimulation. This results in arousal, enhanced performance, increase in HR and BP Repeated doses lead to stereotyped behaviour, irratibility, violence, and addiction in some users. Toxicity can result in arrhythmias, psychosis, seizure etc.

Question 152

Describe meth as a drug of addiction

Answer 152

It releases high levels of dopamine, enhancing mood and body movement. It is neurotoxic, and damages dopamine and serotonin containing cells. Toxicity includes CNS issues increased wakefulness, increased physical activity, decreased appetite etc.

Question 153

Describe cannabinoids as a drug of addiction

Answer 153

Burning cannabis leaves contain over 61 cannabinoids, and is the commonest illegal drug in the US. The drug activates cannabinoid receptors in the brain, which results in a high, a reduction in cognitive function, reaction time, learning and memory long term. Anxiety attacks and hallucination may also occur.

Question 154

Describe propofol as a drug of addiction

Answer 154

- Anaesthetic induction agent with a very narrow therapeutic index

Question 155

Define epilepsy

Answer 155

A condition in which patients have recurrent, unprovoked epileptic seizures. This comprises an abnormal and excessive electrical discharge from neurones in the cerebral cortex, and is often associated with a loss of consciousness.

Question 156

What can cause epilepsy?

Answer 156

Can be structural, genetic or metabolic dysfunction

Question 157

What are the different categories of seizures?

Answer 157

Partial seizures involve neurones in one part of the brain only. A generalized seizure involves all the neurones of the brain

Question 158

What is the physiology of a seizure?

Answer 158

An imbalance between excitatory and inhibitatory neurotransmitters. It is caused by the synchronous activation of large numbers of hyperexcitable neurones. This can be propogated by normal and abnormal pathways It can involve GLUT. NMDA receptors open the channel for Na+, K+ and Ca2_ cations, and is activated by NMDA Non-NMDA receptors are activated by AMPA and kainic acid, not NMDA. It is permeable to Na+ and K+, but reasonably impermeable to Ca2+. It's rapidly activated and inactivated It can also involve GABA. Seizures can be caused by blocking of GABA, activation of GLUT receptors, blocking glycine or K+ channels, and unblocking NMDA receptors.

Question 159

How do you treat epileptic seizures?

Answer 159

Can block Na+ channels (phenytoin). It stabilizes Na+ currents and prevents repetetive firing from sustained depolarization It also enhanses GABA and reduces GLUT

Question 160

What are some mutations that can cause epilepsy?

Answer 160

Na+ channel mutation can cause severe myoclonic epilepsy of infancy (causes intellectual impairment) as well as benign epilepsy Ca2+ channel mutations in the thalamus cause hyperpolarized thalamic neurons, producing cortical depolarization. It is especially common for absence seizures.

Question 161

What are the different ways of causing an epileptic seizure?

Answer 161

Anatomic rearrangement of local circuits Frequency dependent changes in synaptic efficacy Changes in local receptors

Question 162

How does anatomic rearrangement of local circuits cause epilepsy?

Answer 162

Excitatory axons have collateral branches activating neurones in local regions of the CNS. They can contribute to feedback inhibition or excitation, of which inhibition is typically more powerful., If there is neuronal death, new circuits grow in to replace them, forming new uninhibited circuits

Question 163

How does a change in local receptors cause epileptic seizures?

Answer 163

NDMA receptors may change, and it can be either perpetuated by seizures or by mutation from birth. This is the principle of kindling, where a repeated exposure to subthreshold stimulation produces spontaneous seizures.

Question 164

Describe different generalised seizures

Answer 164

A generalized seizure involves both hemispheres of the brain, and may have major or minor motor manifestations. Types can be- tonic- sustained contraction of muscle Clonic- regular repeated jerks Tonic clonic- sustained followed by jerks Myoclonic- brief jerks of axial and limb muscles Epileptic- brief contractions of limbs and axial, with an initial myoclonic component. Absence- go completely blank Frontal lobe- sudden, abrupt limb posturing

Question 165

Describe partial seizures

Answer 165

They preserve consciousness, and only involve a certain part of the brain Can be visual, somatosensory, auditory, psychic, abdominal, olfactory, versive, or focal motor Complex partial seixures have a loss of consciousness and are unresponsive.

Question 166

Why do we need sleep?

Answer 166

Most likely to do with synaptic shrinkage. This allows the brain to tidy up and lose unnecessary memories, to permit the formation of new circuits the next day

Question 167

What are the different sleep stages?

Answer 167

``` 1- on the verge of sleep 2- light sleep 3- deep sleep 4- unwakeable REM- dreaming ```

Question 168

What sort of things are necessary to ask in a sleep history?

Answer 168

Sleep onset, interruptions, quality, extra sleep features (ie snoring, sleep walking)

Question 169

What are the 3 main groups of sleep symptoms?

Answer 169

Insomnia Excessive daytime sleepiness Parasomnia

Question 170

What is insomnia?

Answer 170

Inability to get enough sleep. Can be primary or secondary (due to to substances, neurological condition), circadian, jet lag, or shift work disorder. It can be due to thinking style- more likely to be insomniac if you are a perfectionist, overthinker or a controlling type.

Question 171

What is excessive daytime sleepiness?

Answer 171

- Difficulty in maintaining the desired level of wakefulness - Falling asleep at inappropriate times - Excessive amount of sleep - Can be idiomatic, due to substances, circadian rhythm disorder, deprivation or narcolepsy

Question 172

What is parasomnia?

Answer 172

Sleepwalking/talking/eating/sex/screaming | Limb movements, restless limb

Question 173

How do you manage sleep disorders? General

Answer 173

First step is getting the diagnosis correct. Then examine possible psychological, behavioural and biological factors

Question 174

What are countermeasures for sleep deprivation?

Answer 174

Sleeping, or taking short naps. Modafinil Caffeine

Question 175

How do you enhance sleep?

Answer 175

Mindfulness, avoiding stimulating substances, activities and devices Minimize alcohol Only go to bed when tired, and get up at the same time Physical bed Only use bed for sleep and sex

Question 176

What are the benefits of sleep?

Answer 176

- Better health | - Better relationships

Question 177

What are common causes of hearing loss in children?

Answer 177

Genetics Cytomegalovirus Otitis media Infections Trauma

Question 178

What are common causes of hearing loss in adults?

Answer 178

``` Age related Noise exposure Genetics Trauma Tumours Ototoxic drugs (aminoglycoside antibiotics and cytotoxic drugs) ```

Question 179

What are the consequences of hearing loss?

Answer 179

- Increased falls and dizziness - Reduced cognition - CNS issues - Dementia risk increases - Poor speech and language - Social isolation - Decreased literacy, learning, education and employment - tinnitus - Depression

Question 180

How does sound travel from the environment to the inner ear?

Answer 180

These structures are located in the temporal bone Sound is transmitted through the middle ear to the inner ear, where the vibrations are transduced into neural activity by the sensory cells. In the cochlea, the organ of corti separates the complex sounds into individual frequency components.

Question 181

What are the components and functions of the outer ear?

Answer 181

The outer ear is made up of the pinna and external auditory meatus, and terminates at the tympanic membrane. It protects the middle ear, is important or sound localization, secretes wax from cerumen glands and cleanses the ear itself.

Question 182

Describe the middle ear and its components

Answer 182

The middle ear is filled with air, and sits within the temporal bone. It begins at the tympanic membrane, and communicates inf/ant with the nasopharynx via the eustacian tube. It contains the ossicular chain, made of the malleus, incus and stapes. The stapes articulates with the oval window of the internal ear. It has a mucosal lining

Question 183

What is the function of the eustacian tube?

Answer 183

It aerates the middle ear, enabling it to maintain equal air pressure across the tympanic membrane. However, infection can enter the middle ear using this route, causing middle ear disease, and contributing to otitis media with effusion.

Question 184

What is the function of the ossicular chain?

Answer 184

The bones conduct airborne sound to the oval window. A change in their structure or misattachment causes a conductive hearing loss.

Question 185

What is the overarching function of the middle ear?

Answer 185

It acts as an impedance transformer, overcoming the mismatch in density between air and inner ear fluid. This allows our auditory system to be much more sensitive.

Question 186

How does the middle ear transfer sound?

Answer 186

The increased surface area of the tympanic membrane transfers more energy onto the smaller stapes foot plate. The malleus arm is also longer than the incus, allowing generation of greater leverage and force on the stapes.

Question 187

What is the overall difference between conductive and sensorineural hearing loss?

Answer 187

Conductive is due to outer or middle ear damage, while sensorineural is due to sensory or neural elements of the inner ear

Question 188

What structures make up the inner ear?

Answer 188

There are three semicircular canals and vestibule of the vestibular system, as well as the spiral cochlea, which contains the organ of corti (sensory organ).

Question 189

Describe the cochlea

Answer 189

It is a fluid filled tube spiralling around a bony core called the modiolus, which contains the auditory nerve and vascular supply. The fluid is called perilymph, which has a composition similar to ECF (lots of Na+, small K+)

Question 190

Describe the cochlear duct

Answer 190

It is a cavity lying within the perilymphatic cavity. The floor of this is called the basilar membrane, projecting from the modiolus, that has the organ of corti sitting on it. It divides the perilymph space into the scala vestibuli above and scala tympani below. The space between is the scala media. It contains endolymph, which has a high K+ and low Na+ concentration. This is produced by the stria vascularis on the lateral duct.

Question 191

Describe the organ of Corti

Answer 191

It is attached to the basilar membrane of the cochlear duct, and is comprised of approx 20k hair cells, named for the stereocilia projecting apically into the endolymph

Question 192

Describe the classification of hair cells

Answer 192

Inner hair cells comprise 25% of cells and have a single row. These are responsible for the afferent fibres, type I myelenated fibres, which take sensory information to the cortex Outer hair cells comprise 75% of cells and sit in 3-5 rows. They only take 10% of afferent fibres to the brain, and these are small and unmyelinated. They receive efferent fibres and function as motor cells, enhancing the wave motion of the balisar membrane, to increase the sensitivity and frequency selectivity of the ear. This is energy expensive, but necessary to overcome the friction of the fluids vs corti. Sound causes them to mechanically oscillate in a frequency specific matter, due to their motor proteins (prestin) in their membranes

Question 193

What is the function of the round window in the inner ear?

Answer 193

It relieves the pressure created by the stapes pressing in the oval window. This helps a whiplike sound wave form along the basilar membrane

Question 194

Describe how the sound wave triggers depolarization of hair cells

Answer 194

The basilar membrane varies in mass and stiffness- it's small and stiff at the base, which changes as it goes. As the wave of displacement travels along, it rises in amplitude and slows. For a particular frequency, the wave reaches peak amplitude at the region corresponding to it, and then dissipates. Therefore, the basal cochlea responds to high frequency, and apical to progressiely lower. The movement of the wave over the stereocilia causes shearing forces to open the transduction channels running from shaft down to tip of the cilia. This causes the rushing in of potassium ions, which triggers an action potential

Question 195

Describe the transduction channels

Answer 195

They run from the shaft of one stereocilium to the tip of an adjacent one. The anchor on the shaft is made of myosin, with a MET channel on the adjacent tip allowing the ions in. The bridge itself is made of E. Cadherin 23. These channels are very vulnerable to excessive sound as they maintain tension. They are unlikely to grow back if broken.

Question 196

Describe the potassium recycling within the cochlea

Answer 196

K+ diffuses out of the hair cells and into the scala tympani. This is very fast due to high difference in concentrations, so there's no need for high energy channels, reducing the need for a great blood supply. This then flows back into the stria vascularis to be reproduced, via fibroblasts with gap junctions.

Question 197

How does the cochlea separate frequency?

Answer 197

Place coding: The base of the organ of corti is narrow and stiff. Individual hair cells respond to particular frequencies depending on their location, and this is reflected in the auditory nerve. It has differences in tonotopicity, with each fibre only responding to a certain range of frequencies and intensities. The best frequency is determined by the location of the hair cell it innervates. Basal hair cells have high frequencies, while apical cells have low frequencies. Volley Principle: Discharge rates are sychronized with frequency of stimulus. These are locked on to a single cycle of stimulus, so they only detect the ones they are synched to. This is known as phase locking, and only occurs in the auditory nerve for frequencies lower than 1-2000hz

Question 198

How does the cochlea determine intensity?

Answer 198

Intensity is determined by both the number of fibres activated, and their rate of firing. Discharge rates increase with intensity.

Question 199

Describe how sensorineural deafness occurs within the cochlea

Answer 199

It can be due to congenital abnormalities, infection, drugs, fluid homeostatic disturbances, trauma, noise exposure, age or idiopathy. It is due to damage to sensory or neural structures of the cochlea. It is the msot common form of deafness, and can cause loss of hearing sensitivity at frequencies damaged, loss of discrimination, poor loudness balance and tolerance, and poor speech recognition. It is due to the loss of fine frequency tuning and intensity detection methods, and these cells do not regenerate.

Question 200

What is the pathway from cochlea to cortex?

Answer 200

Cochlea Cochlear nuclei (sensory integration with vest. system) Sup. Olivary complex (binaural integration, localization and focus on speech) Inf. colliculus (sens integration, sound localization and visual enhancement of sound) Medial geniculate body (radiates to heschel's gyrus in temp. lobe) Auditory cortex

Question 201

How does hearing loss affect the cochlea's tonotopicity?

Answer 201

It becomes disturbed, with high frequency areas being taken over by low frequency ones

Question 202

Why is binaural hearing important?

Answer 202

It is used for lound localisation and complex auditory perception. It is done using differences in intensity between the ears (for high frequency) and differences in timing of reception between the ears (for low frequencies). This is because low frequency sounds tend to wrap around the head and so produce little intensity difference. Most sound responses are greater when heard binaurally. Above the cranial nucleus level, binaural responses dominate

Question 203

How do cells receiving inputs from both ears localize sound?

Answer 203

Cells in the SOC, IC, MGB and cortex receive inputs from both, and are either excited by both ears (EE) or excited by one and inhibited by the other (EI) These cells are divided into low freq units sensitive to time differencs (MSO) or to level differences (LSO)

Question 204

Describe the parts of the cochlear nucleus

Answer 204

The dorsal part projects to the midbrain, while the ventral goes directly to the superior olive

Question 205

What is tinnitus?

Answer 205

Reduced inhibition of the dorsal cranial nucleus, causing a phantom sound

Question 206

What are the main types of hearing loss?

Answer 206

Conductive- outer/middle ear damage Sensorineural- inner ear damage Mixed- both Central- issues with nerves or cortex

Question 207

What do we need to find in a hearing exam?

Answer 207

Onset of loss- rapid vs. gradual, constant vs. fluctuating Precipitating factors Assoc. symptoms- tinnitus, vertigo etc.

Question 208

How do we use tests to determine between conductive and sensorineural hearing loss?

Answer 208

Weber test involves placing a tuning fork on the frontal bone and seeing whether it is heard. This will be referred to the better ear if sensorineural loss, or else not heard at all. In conductive loss, it will be referred to the deafer ear, or still heard. Rinne test involves striking a tuning fork and holding it on the mastoid process, and then in front of the ear. It will be heard in the bone but not air in conductive hearing loss, and not heard in either for sensorineural

Question 209

What are some potential causes of conductive deafness?

Answer 209

``` Inflammation Osteosclerosis or arthritis Ossicle issues Tumour Trauma Stenosis Exostoses Microtia ```

Question 210

Describe microtia

Answer 210

The pinna is not developed but inner ear is normal

Question 211

Describe glue ear

Answer 211

The eardrum has fluid built up behind it, so sound cannot travel through

Question 212

Describe mastoiditis

Answer 212

Pus behind the ear builds up, putting pressure on and blocking nerve conduction

Question 213

What are some potential causes of sensorineural deafness?

Answer 213

Can be congenital - hereditary, delayed hereditary | Can be acquired- noise induced, trauma, infection, ototoxicity.

Question 214

How do the different hearing losses perceive sounds?

Answer 214

Conductive sounds muffled, maybe tinnitus Sensorineural has frequency and speech discrimination issues with sound distortion, loudness imbalance, tinnitus and missing frequencies

Question 215

Describe central auditory disorders

Answer 215

This is issues in auditory processing. It can be amlyaudia (lazy ear), hyperacusis (hypersensitivity) or tinnitus. Mainly caused by peripheral injury or developmental/neurological disorders

Question 216

Describe some behavioural assessment of hearing

Answer 216

Audiometry- give a pure tone at air and bone conduction, then speech. Normal is hearing below 20Db. Bone conduction bypasses the middle ear and so can confirm conductive hearing oss Speech audiometry- assess comprehension and detection of speech. It can be affected by background noise etc. and needs to be age appropriate Tympanometry- assesses ear drum mobility and pressure This is important as a negative eardrum pressure can suck infections into the middle ear via the eustachian tube. It also assesses the integrity of middle ear muscles

Question 217

What are some physiological assessments of hearing?

Answer 217

- Neural activity of the cochlea and brain centres can be studied in disabled, very young, or people with no behavioural measure - ABR tests obtain hearing thresholds Screening for every newborn NZer a few days after birth

Question 218

What are some treatments for congenital hearing loss?

Answer 218

Hearing aids Implants Sign language Implantable hearing aids or teeth conductors- good for conductive loss

Question 219

Describe cochlear implants

Answer 219

A silicone stent with 22 electrodes. This is inserted into the cochlea of people with no sensory cells. it stimulates the first 2/3 of the cochlea, but needs a good nerve supply It is ideal for very young children or adults with good language- this is because plasticity for language starts to close at 5 years.

Question 220

What are some recent developments in hearing technology?

Answer 220

Can have fully implanted cochlear implants Drugs given via implants to stimulate nerve growth Bilateral implants Preservation of residual hearing Cochlear nucleus implants

Question 221

How does the brain get imaged on CT?

Answer 221

The bone is visible as bright white, with grey matter grey, white matter dark grey, CSF and fat dar, muscle medium grey and blood showing low-high intensity It can have vascular contrast, but this doesn't cross the BBB. It is iodinated in CTs. The contrast enters tumours and strokes due to the presence of leaky vessels. However, it can exacerbate poor kidney function They are fast, available, provide 3D imaging and have an immediate cost. They're great for looking at strokes, and whether it's still bleeding. They can also do tumours, abscesses and trauma

Question 222

How does the brain get imaged on X ray?

Answer 222

It can be used to check vertebral body and process alignment, as well as the prevertebral soft tissue. Can show spurs on vertebrae, which is a sign of osteoarthritis, as well as examining aneurysms and their repair It's cheap, easy and fast However, it uses radiation, and only shows limited TD info. It is overused in head trauma as it can only show skull fracture, which is not always involved in brain trauma

Question 223

How does the brain get imaged on MRI?

Answer 223

There are two most common types: T1 shows CSF as hypointense and fat as hyperintense T2 shows CSF as hyperintense and fat as hypointense The DWI signal for early strokes appears bright on MRI due to the restriction of water moving out of the cell- this is more useful for stroke imaging than CTs DTI tractography can trace axon bundles, making it good for signal planning. Functional MRIs can give locations of tumour and relation to the cortex responsible for a function It is good as it gives no radiation, is great for the brain, is versatile, can have contrast manipulated, shows immediate early ischaemia, tumours, angiography with gadolinium contrast, and shows a multiplanar view that is good for prenatal imaging However, it takes a long time and has poor access, is expensive, motion sensitive, needs lots of experience, and has some safety issues. The gadoliunium contrast can also be taken into bones

Question 224

What are tips for imaging the brain and describing the results?

Answer 224

Describe the patient, side of lesion, why it's important, appearance, location, and other features. Look at history, image and then cues around it.

Question 225

Is MRI and CT better for imaging stroke, tumour, reconstrction, angiography or spine?

Answer 225

``` Stroke- both Tumour- both Bony reconstruction- CT Angiography- MRI (slight) Spine- MRI ```

Question 226

How is US used to image the brain?

Answer 226

Paediatric through fontanelles- good for ventrices and haemorrhage

Question 227

What are the major effects of opioid analgesics? What is its limit?

Answer 227

Analgesia and impaired consciousness | However, the analgesia doesn't apply to neuropathic pain (only nociceptive and inflammatory pain)

Question 228

How can opioids be administered?

Answer 228

Can be oral, parenternal (intramuscular/venous/intermittent/PCA) Transmucosal Transdermal

Question 229

What are opiates vs opioids?

Answer 229

Opiates are derived from opium poppies, derived naturally (eg. morphine, heroin, codeine) Opioids are synthetic narcotics mimicing its function- eg. pethidine, fentanyl, methadone etc

Question 230

How do opiates act on opioid receptors?

Answer 230

They can activate Gi proteins to inhibit adenylate cyclase, and decrease the Ca2+ channels permeability and block release of neurotransmitter They can also increase K+ conductance in the postsynaptic membrane, causing hyperpolarization and decreased response

Question 231

What are the different opioid receptors and where are they primarily located?

Answer 231

mu receptors are located in the CNS, along with kappa receptors. Delta receptors tend to be more around the pleasure pathways

Question 232

Describe how receptors are synthesized in peripheral inflammation

Answer 232

In the periphery, receptors are synthesized due to inflammation by the dorsal root ganglion. This is transferred all over the neuron, so opioids can attach to all of these to cause decreased pain. Additionally, inflammatory cells attracted can also produce endogenous opioids.

Question 233

Describe what activation of Mu-1, Mu-2 and kappa receptors can do

Answer 233

Mu-1 produces analgesia only Mu-2 produces analgesia, as well as other side effects, euphoria and physical dependence Kappa produces analgesia and dysphoria

Question 234

Describe the various agonists and antagonists in opioid analgesics

Answer 234

Agonists activate all subclasses, but with varying affinities Antagonists cause a lack of activity in all receptor classes Agonist-antagonists agonize one type and antagonize another Partial agonists cause activity at one or more but not all receptor types

Question 235

Describe the adverse effects of opioids

Answer 235

- Respiratory depression, drowsiness, dizziness, constipation, ileus, itching, nausea/vomiting, bradycardia and hypotension

Question 236

What are semi synthetic vs fully synthetic opioids?

Answer 236

Semisynthetics include bup-re-norphine, oxycodone and di-acetyl morphine Full synthetics include fentanyl, pethidine, methadone and tramadol

Question 237

What are some of the body's endogenous opioids?

Answer 237

Endorphins Endomorphins Enkephalins Dynorphins

Question 238

What happens when there is a withdrawal from opioids?

Answer 238

BP changes, HR and RR may increase, GI has cramps, N&V, diarrhoea Neuromuscular issues, pilorection, sweating

Question 239

How do you manage opioid withdrawal?

Answer 239

- Give methadone or bup-re-norphine, with clonidine, or another adjunctive to manage sside effects (ie diarrhoea). This involves one opioid being replaced with another, which is then slowly withdrawn OR rapid detox treatment is done within 2 hours. Under GA the patient is not subject to withdrawal. Give high doses of naltrexone, followed by maintenance to reduce relapse

Question 240

Describe morphine and its side effects

Answer 240

Powerful analgesia, sedation, cough suppression. Causes miosis, alatered mood, N&V, addiction, resp depression, constipation, itching and hypotension (due to histamines), biliary colic and bradycardia. Can be administered orally, IV, epidural or intramuscularly Metabolized in the liverto an inactive form as well as some morphine 6-glucuronide, which has at least half the potency Excreted in urine

Question 241

Describe pethidine and its side effects

Answer 241

It's s synthetic opiate designed as an anticholinergic. It gives less marked miosis, dry mouth, tachycardia, and can be given in tablet form. It is metabolized and conjugated in the liver, although it gives the product norpethidine, which may accumulate in renal failure to cause seizures and hallucinations. It interacts with MAOI to cause coma, convulsions etc.

Question 242

Describe fentanyl and its side effects

Answer 242

Synthetic opioid with a fast onset. Strong agonist of mu receptors, 100x more potent than morphine Given by IV, IM, transdermally. transmucosal lozenges, nasal spray or sublingual tablets

Question 243

Describe iontophoresis

Answer 243

A method of transdermal PCA as the drug and an intert agent are placed on the skin, connected by a power supply. When the electric field is on, the drug is ionized and allowd to move through the skin

Question 244

Describe methadone and its side effects

Answer 244

Fully synthetic, well absorbed from all routes of administration. Rapid analgesia onset. No cognitive impairment, no euphoria, safe in renal and liver failure Used for chronic or neuropathic pain, opioid withdrawal and detox

Question 245

Describe tramadol and its side effects

Answer 245

It's a synthetic codeine analog, weak mu opioid receptor agonist Inhibits serotonin uptake so may cause serotonin syndrome if administered to an SSRI patient Caution for epilepsy patients

Question 246

Describe codiene and its side effects

Answer 246

Treats mild to moderate pain Marketed as single ingredient and combination drugs Can cause drowsiness and constipation, physical dependence, etc. Some patients are slow vs rapid metabolizers

Question 247

What are the opioid antagonists?

Answer 247

Naloxone, naltrexone

Question 248

Describe nitrous oxide and its side effects

Answer 248

Powerful analgesic normally given 50% with Oxygen. Used in maternity, field and wound dressing Can cause euphoria, nausea and vomiting, bone marrow depression

Question 249

What are some co analgesics?

Answer 249

Adjuvent drugs are those whose primary indication is for a purpose other than pain relief, but they demonstrate some analgesic enhancement Eg. some tricyclic antidepressants, anticonvulsants, anxiolytics, corticosteroids and others

Question 250

List the symptoms of cerebellar disease

Answer 250

``` Truncal and gait ataxia Limb ataxia Dysarthria Abnormal eye movement Vertigo Nausea and vomiting Normal or reduced tone Normal power, tendon reflexes, plantar response and sensation Dysphagia ```

Question 251

Describe truncal and gait ataxia

Answer 251

Unsteady while sitting, walks unsteadily with broad base Side to side steps Cannot walk heel toe

Question 252

Describe limb ataxia

Answer 252

Clumsiness and difficulty writing. Reboud after displacement of limb Intention tremor, overshooting of finger nose finger etc Impaired rapid alternating movements (dysdiadochokinesia) Issues judging pressure of grip

Question 253

Describe dysarthria

Answer 253

Loss of articulation producing slurred and staccato speech. This is different from brocas stroke as it's about the physical formation of the words

Question 254

What are the abnormal eye movements that can come with cerebellar disease

Answer 254

Nystagmus- rhythmic oscillatory movements of one or both eyes when held at extremes of movement Diplopia Oscillopsia- environment moves Broken pursuit of eve motion when tracking a moving target Square wave jerks- eye flicks up and around when trying to hold straight

Question 255

Describe some of the causes of cerebellar disease

Answer 255

Multiple sclerosis Ischaemic stroke Also congenital or inherited defects, tumours, infections and metabolic disorders

Question 256

What are the features of an upper motor neuron lesion?

Answer 256

No wating or fasciculation, increased tone with spastic catch, reduced power, increased tendon reflex. Extensor tendon reflex (babinsky reflex), and reduced rapid alternating movements

Question 257

What are the features of a lower motor neuron lesion?

Answer 257

Increased muscle wasting and possible fasciculations (random jerks). Normal or decreased tone, decreased or absent reflexes, flexor plantar response and normal rapid alternating movements

Question 258

What are the features of a pyramidal lesion?

Answer 258

No wasting or fasciculations, increased tone, normal power, normal tendon reflexes, flexor plantar response, reduced rapid alternating movement.

Question 259

What is the pathway for a muscle stretch reflex?

Answer 259

Muscle stretched so golgi tendon organ stretches 1a nerve afferent fires Sent to dorsal horn of assoc spinal cord level Monosynaptic connections with alpha motor neurons to the same or synergystic muscle Also synapses with an inhibitor alpha motor neuron for antagonist muscles

Question 260

What are the different classes of reflexes?

Answer 260

0 is absent + and ++ are normal and brisk normal +++ are exaggerated ++++ are clonus (give repeated contractions)

Question 261

What are reflexes?

Answer 261

Involuntary, stereotypical and non fatiguing movements Response is dependent on strength of stimulus There is variation between people Can be increased by activiating assoc muscles Can be increased when anxious and decreased when sleeping

Question 262

What would be seen with a spinal cord lesion at C5?

Answer 262

LMN issues at C5 & 6 | UMN and sensory issues below

Question 263

What are some of the symptoms of movement disorders?

Answer 263

Paralysis- can be mono/hemi/para/tetraplegia Paresis (weakness) Abnormalities of muscle tone (spasticity, rigidity) Ataxia- can be decomposition (jerkiness) or dysmetria (over or undershooting) Involuntary movements- eg. tremor and dyskinesia These can be focal or diffuse, and acute or chronic

Question 264

What are some example of focal and diffuse or acute and chronic movement disorders?

Answer 264

Focal acute: trauma or vascular issue Focal chronic: tumour Diffuse acute: toxin or infection Diffuse chronic: Neurodegenerative

Question 265

Where are (lower) motoneurons, and what are their types?

Answer 265

They can be in the spinal cord (anterior horn) or in the brainstem for CN III-VII and IX-XII These may be alpha motoneurons- innervate extrafusal muscle for force generation- or gamma motoneurons- innergate intrafusal muscle fibres to control stretch receptor excitability

Question 266

What pathways are alphamotoneurons involved in?

Answer 266

Descending tracts- pyramidal, rubrospinal (red nucleus), vestibule-spinal (coordination), tecto-spinal (head and eye coordination) and reticulospinal (muscle tone) Also brainstem or spinal interneurons that synapse with them- like Ia inhibitory interneurons 1a afferents from muscle spindles

Question 267

What makes up a motor unit?

Answer 267

Dendrites, cell body, axon, axon collateral, NMJ, muscle fibres

Question 268

What is myotonic muscular dystrophy?

Answer 268

Progressive watsting and weakness of muscles due to CTG repeats causing defective myotonin. It's dominant inherited, and causes myotonia (muscle stiffness) and failure to relax after contraction, even in the heart. In children this is duchenne's which is progressive wasting and weakness, due to defective dystrophin

Question 269

What is myasthenia gravis?

Answer 269

AI disease resulting in fewer ACh binding sites due to smaller junctional folds. This results in smaler amplitudes of end plate potentials, reducing transmission and causing weakness without wasting. It can be helped by blocking ACh esterase with tensilon, and treating the side effects (GI) with atropine

Question 270

What is botulism?

Answer 270

Food poisoning and muscle paralysis caused by clostridium botulinum. It is endocytosed, and proteolyses the membrane proteins involved in ACh release at all peripheral cholinergic synapses, preventing transmission. It causes weakness of striated and smooth muscles. In infants it can cause constipation, lethargy, difficulty feeding, paralysis and respiratory arrest

Question 271

What is the result of injury to axons?

Answer 271

Distal segment shows wallerian degenration, where the myelin deteriorates, transmission ability is lost and axon survival factor becomes lost. The proximal segment undergoes chromatolysis, where the histological stain colour changes due to migration of lysosomes into the dendrites In the periphery it can regenerate by 1-2mm per day, and is facilitated by schwann cells. It can re-innervate and give some return to function In the CNS this regeneration does not occur

Question 272

What is a stroke?

Answer 272

A group of disorders involving haemorrhage or occlusion of brain blood vessels It may be ischaemic (vessel blockage) or haemorrhaginc (rupture of vessels). It is mostly focal but can also be global (eg. caused by cardiac arrest)

Question 273

What are the risk factors of stroke?

Answer 273

Diabetes Hypertension Atherosclerosis Genetic polymorphisms

Question 274

Describe the anatomy of a stroke

Answer 274

The cells in the region with the greatest blood loss rapidly die by necrotic death. Surrounding this is the penumbra where nerve cells die by slower apoptotic mechanisms. Necrotic death is too rapid for intervention, so apoptotic death is the one targeted by therapy

Question 275

What causes delayed cell death?

Answer 275

Release of glutamate, causing transporter saturation Calcium influx Free radical production Activation of macrophages (called microglia) which release NO, superoxide, cytokines etc. Activation of intrinsic mechanisms

Question 276

What are the two main categories of glut receptor

Answer 276

Ionotripic (ligand gated) | Metabotropic (g protein linked)

Question 277

Describe ampa receptors

Answer 277

They are ligand gated ion channels with various subunits. Those with GluR2 subunits pass sodium but not calcium, while those with R3 but not R2 pass calcium only. Ischaemic injury downregulates the R2 subunit, causing increased Ca2_ influx

Question 278

Describe kainate reeptors

Answer 278

Ligand gated ion channels which cause influx of sodium

Question 279

Describe NMDA receptors

Answer 279

Ligand and voltage gated channels. It needs deoplarization with glutamate and glycine to open the channel. Mg2+ occupies and blocks the channel, so depolarisation causes an efflux of Mg2+ PCP binds inside the channel blocking ion flow.

Question 280

Describe metabotropic receptors

Answer 280

G protein coupled receptors Group 1 activate phospholipase C and depolarize neurons. Group II inhibit adenylate cyclase and inhibit neurotransmitter release

Question 281

Describe the pathway from stroke to cell death

Answer 281

Stroke causes increased glutamate, activating AMPA, NDMA and G gouple receptors This causes increased influx of Ca2+, causing apoptosis, and increased Na+, Cl- and H2O influx, causing necrosis

Question 282

How does calcium cause nerve cell death?

Answer 282

It activates calcium sensitive enzymes that carry out the cell suicide program it is suggested that these are mediated by caspase enzymes that cleaves substrates- esp. caspase 3

Question 283

How can strokes be treated?

Answer 283

TPA causes thrombolysis but must be given soon after stroke Glutamate antagonists don't work so far- it's complex Hypothermia Free radical scavengers Anti inflammatories

Question 284

How do glial cells interact with stroke?

Answer 284

Astrocytes link neural activity to blood, flow, allowing survival promotion. Astrocytes can be an important target for drug intervention. By keeping them alive it means that the neurovascular unit is maintained. Maintaining pericyte integrity promotes new vessel formation

Question 285

Describe the symptoms of parkinsons disease

Answer 285

It can be tremor at rest (often asymmetrical, Bradykinsesia or slowness of movement- emotionless face, impaired rapid alternating movement, abnormal gait, freezing, short steps Rigidity Postural abnormalities ie stoop

Question 286

How do you diagnose parkinsons disease?

Answer 286

Needs at least 2/4 of TRAP

Question 287

Describe the onset of parkinsons disease

Answer 287

It's gradual onset and often asymmentrical. Symmetrical onset indicates and abnormal parkinsons progression (ie medication driven) Premotor symptoms develop slowly, then it's normally 1-2 years before diagnosis. Treatment starts, a few years in the honeymoon phase. Motor symptoms develop over 10 or so years, with disability lasting after that

Question 288

What are the non motor symptoms of parkinsons?

Answer 288

Asomnia, constipation, pain, loss of smell, REM sleep behaviour disorder- ie acting out dreams

Question 289

What are the pathological changes associated with parkinsons disease?

Answer 289

It occurs when the substantia nigra's dopaminergic neurons deteriorate. It can cause synucleinopathy, and predisposes certain regions of the brain. The disease progression is topographically predictable. The longer parkinsons is in the body for, the more space it affects in the brain

Question 290

Describe levodopa treatment of parkinsons

Answer 290

Levodopa is given with an enzyme inhibitor of peripheral converting enzymes to ensure the maximum amount reaches the brain It has a short half life, so leads to large fluctuations. This means infusion should be used, with an agonist

Question 291

What are surgical treatments of parkinsons?

Answer 291

Pallidotomy or thalamotomy. Transplant using fetal tissue | DBS inhibiting overactive neurons without destroying them

Question 292

What does clonidine have to do with parkinsons?

Answer 292

It blocks dopamine receptors for the treatment of nausea, but can also cause parkinsonian symptoms by blocking CNS dopamine receptors

Question 293

What is the function of astrocytes?

Answer 293

They are important for brain function, including release and uptake of neurotransmitters, expression of receptors, regulation of synaptic transmission, electrical conduction, neurotrophin production, and possibly generation of new neurons They are also responsible for immune activation and scar tissue formation There are multiple types of astrocyte

Question 294

What are the different categories of astrocyte within the cortex?

Answer 294

Protoplasmic Interlaminar Fibrous Polarized

Question 295

Describe protoplasmic astrocytes

Answer 295

Most common, reside in layers 2-6 of neocortex Processes do not overlap One domain might cover 10 nerve cells, many synapses and 5 blood vessels. They are important in regulation of blood flow.

Question 296

Describe fibrous astrocytes

Answer 296

Found in the white and gray matter with intermingling processes. They serve a support role for neurons and help to form scar tissue

Question 297

What is gliotransmission?

Answer 297

The process of release of transmitters from astrocytes, acting on neurons. It may have a great use in terms of normal brain function- eg. memories may be encoded in astrocytes, astrocytes can induce sleep via caffeine receptors etc

Question 298

What are microglia?

Answer 298

They survey the microenvironment of the brain, and act in a role similar to macrophages They mediate the immune response, phagocytose debris, sculpt the brain during development and modulate neurotransmission

Question 299

What are pericytes?

Answer 299

They encase endothelial cells in capillaries and maintain the BBB.

Question 300

What are some targets in the brain for drugs?

Answer 300

Enzymes, structural proteins, uptake proteins, ion channels, receptors and transducer proteins

Question 301

How does chemical neurotransmission occur?

Answer 301

Chemical messengers can be released across the synaptic cleft, causing ion channel opening, and or generation of a second messenger. These can be excitatory or inhibitory. Termination is acheived by metabolism and/or reuptake by transporter proteins The effects of drugs will depend on which neurotransmitters it affects, and the anatomical localization of that particular system

Question 302

What are the different categories of neurotransmitters?

Answer 302

These can be monoamines (serotonin, noradrenaline, dopamine- from VTA and substantia nigra) Can be amino acids, like GABA, GLUT, gycine Can be ACh Neuropeptides

Question 303

What is the difference between neuromodulators and neurotrophic factors?

Answer 303

Neuromodulators have slower pre and post synaptic responses. They are released by nerve cells and astrocytes Neurotrophic factors are released by non neuronal cells and neurons, and work over long time scales. They act on TKRs to mediate growth morphology and functional properties

Question 304

What are neurotransmitters (general)?

Answer 304

They can be fast acting, and work via ion channels, or be slow acting via G coupled protein receptors

Question 305

What is polio?

Answer 305

An acute viral infection that is usually focal. It causes degeneration of motoneurons and muscles. Modified polio viruses can be used to treat brain cancer (glioblastomas)

Question 306

What are the disease facts assoc with ALS?

Answer 306

Most are sporadic, 10% have familial form Death is usually within 2-5 years unless benign form

Question 307

What are the symptoms of ALS?

Answer 307

Progressive muscle wasting, weakness and atrophy leading to paralysis Dysphagia (need percutaneous endoscopic gastronomy) and dysarthria Respiration impairment Increased stretch reflexes and spastic tone, with fibreillations and fasciculations No involvement of extraocular, anal and bladder muscles, or sensory/intellectual capabilities

Question 308

What causes ALS?

Answer 308

Progressive degeneration of motoneurons a and y in the spinal cord, brainstem motoneurons (but not III, IV or V) Upper motoneuron degeneration causing spasticity

Question 309

What are some theories of how ALS occurs?

Answer 309

Autoimmune- antibodies against Ca2+ channels Neurotrophic- reduced neurotrophic factors that promote motoneuron survival Oxidative stress hypothesis- mutation of superoxide dismutase, allowing free radicals to build up Fas induced sensitivity- increased sensitivity to Fas activation, increasing toxic NOS expression Excitotoxic- increased GLUT due to decreased glut transporter activity. Reduced expression of GluR2 in AMPA, predisposing them to higher calcium fluxes and oxidative damage TDP-Fus mutation- normally in the nucleus but some for shifts to the cytoplasm, aggregating and affective neuron function

Question 310

How do you treat ALS?

Answer 310

There is no effective drug available. There is a small benefit to Riluzone (blocks GLUT), baclophen (GABA agonist), and dexpramipexole (improves mitochondrial function with low DA receptor affinity

Question 311

What factors are integrated to acheive balance?

Answer 311

Visual, vestibular, proprioceptive, and superficial sensory information. Feedback about the head and eyes is independent of each other, as the eyes can be fixed while the head is moving It also has input into cognition, involves self motion perceptions, self consciousness, spatial navigation learning, memory and object recognition

Question 312

What kind of movement does the vestibular system provide?

Answer 312

Linear and angular acceleration

Question 313

What is vertigo and what causes it?

Answer 313

A derangement in vestibular finction- incolves sense of losing balance, disorientation and nausea. Accompanied by ANS symptoms. Ie. motion sickness when there is a mismatch between propriosensation inputs

Question 314

Describe the structure of the vestibular system?

Answer 314

The vestibular nuclei in the brainstem receive info via CVIII. Fibres project from here to the cerebellum, oculomotor nuclei and spinal cord. The inner ear contains the sensory organs for vestibular as well as auditory info. The vestibular system consists of three semicircular canals called the horizontal, anterior and posterior canals. They contain perilymph. These semicircles are paired with the one on the opposite side of the head (and with post, to create a line of direction) Each have an ampulla at one margin of the canal, containing the crista ampullaris and cupula a genatinous structure covering it. The otolithic organs )macula utriculus and macula sacculus) are located in the bestibule, with the utricle horizontal and the saccule vertical

Question 315

How is angular acceleration detected by the vestibular system?

Answer 315

When the endolymph within the ampullae moves due to its inertia, it displaces the cupula. If this displacement of the stereocilia is in the direction of kinocilium (one larger hair), the cell will be depolarized, whereas away from the kinocilium hyperpolarizes it. After inertia settles the cell returns to a steady state of firing.

Question 316

How is linear acceleration detected by the vestibular system?

Answer 316

The maculae sensory cells in the utriculus and sacculus contain calcium carbonate, which gives them mass and enough inertia to detect gravity. This allows it to provide static and up/down movement info for the head. When the movement of hairs is towards the kinocilium it is excited, and vice versa. When the head is held tilted, it simply reaches a steady state of firing.

Question 317

What happens if the vestibular system is off?

Answer 317

Can mess with vestibuloccular reflex- can't keep eyes adjusted to head movement. Eye movement can be a proxy for this Loss of posture and muscle tone maintenance No function in space- tend to see atryphy here

Question 318

Why doesn't the vestibular system get activated by sound?

Answer 318

The stapes sits over the saccule, and there is an empty space next to the cochlea- however there is a pressure gradient in the cochlea rather than the vestibular system

Question 319

What is supplied by the sup and inf vestibular nerves?

Answer 319

Sup: Utricle, and Saccule, int/ant semicircular canals Inf: Post saccule and post semicircular canal

Question 320

How are cilia oriented in the vestibular system?

Answer 320

In the semicircular canals are in opposite direction- movement in the head in one direction excites one side and inhibits the other. The comparieson between the two allows determination of direction In the macula, they hair cells are oriented in different directions so that tilt will depolarise and hypolarise different cells on the same side

Question 321

What is schizophrenia and what are its symptoms?

Answer 321

A disorder of abnormal thought, perception, behaviour, mood and attention Positive symptoms are delusions and auditory hallucinations Negative symptoms are withdrawal and flattened mood

Question 322

What is the dopamine theory of schizophrenia causes?

Answer 322

Dopamine- overactivity of dopamine systems from the frontal cortex, NA, olfactory and ventral striatum Amphetamines that increase DA release cause psychosis and exacerbate symtpms. All antipsychotic drugs block DA receptors

Question 323

What is the GLUT theory of schizophrenia causes?

Answer 323

Decreased glutamate leads to schiz Due to PCP giving the best model of psychosis, which is an antagonist of the NDMA glut receptor It is possible that it is a combination of increased DA and decreased GLUT that causes the symptoms

Question 324

What are the drugs used to treat schizophrenia?

Answer 324

Typicals include chorprozamine- tricyclic dopamine antagonist. However it is an antimuscarinic agent, and produces dry mouth with increased PNS stimulation Haloperidol also antagonises dopamine Atypicals are Clozapine, although it can cause decreased neutrophils

Question 325

What are the mechanisms of the schizophrenia drug?

Answer 325

All are dopamine antagonists, with typicals having equal D2 and D4 affinity, with clozapine having a 10x greater D4 affinity However, typicals show extrapyramidal side effects like dyskinesia and parkinsonian effects This could be due to the D2 affinity difference, or location of action

Question 326

What is depression?

Answer 326

An episodic, recurrent illness with periods of spontaneous remission.

Question 327

What are the two main types of depression?

Answer 327

Unipolar- affects mood, appetite, tiredness, negative self concept. Can be endogenous (unknown origin) or reactive (triggered by environmental event) Bipolar- manic depression. Mood fluctuates between depression and mainia, where there is heightened mood, iritability, poor decision making , delusion and hallucinations

Question 328

What is the simple monoamine theory and why is it problematic?

Answer 328

It suggessts that depression is due to a decrease in brain monoamines (eg. serotonin). However, while antidepressants do work by inactivating monoamine reuptake or breakdown, it only works after weeks of chronic use

Question 329

How do antidepressant drugs work?

Answer 329

First generation: Tricyclics block monoamine reuptake, though they decrease adrenoreceptors and cause antimuscarinic action Monoamine oxidase inhibitors irreversibly prevent breakdown of monoamines Second generation: Moclobemide selectively inhibits MAOs Fluoxetine is an SSRI

Question 330

How does lithium carbonate help manic depression?

Answer 330

It stabilizes both phases, and may dampen neurotransmission

Question 331

How does depression affect neurogenesis?

Answer 331

Stress impairs neurogenesis , and this decrease may have something to do with depression development. Treatment of depression helps to generate new brain tissue

Question 332

What do facial effects have to do with reundancy in stroke?

Answer 332

Upper face is innervated by both sides of the brain, whereas the lower face only receives fibres from the contralateral side. This means a lesion is more likely to appear in the lower face

Question 333

Describe what the possible consequences of an internal capsule lesion coule be

Answer 333

Ant limb: Lesion can cause head and neck muscle weakness (mainly lower face) Post limb contains corticospinal fibres so can cause UMN issue contralaterally Sublenticular nucleus has auditory fibres- opp side deafness Retrolenticular has visual info from lat geniculate body to visual cortex- can cause contralateral blindness Also cranial nerve fibres

Question 334

How do NSAIDS work?

Answer 334

They inhibit COX1 an COX2, though newer agents only inhibit COX2 They are mostly reversibly and incomplete, apart from aspirin, which selectively acetylates a serine residue of the enzyme and irreversibly inactivates it

Question 335

What do NSAIDS do?

Answer 335

They decrease inflammation and relieve mild pain by reducing PGs. They are also antipyretics and anticoagulants (decrease thromboxane)

Question 336

What are prostaglandins?

Answer 336

Lipid compoudnds with a wide spectrum of biological actions | - sensitize spinal neurons to pain, induce labour, regulate inflamm responses, platelet response, cell growth etc

Question 337

What is arachidonic acid?

Answer 337

Synthesized from linoleate- liberated by activation of phospholipase. Goes on to be converted to Prostaglandins, prostacycline and thromboxane by cox1 and cox2. Converted to leukotrines by leukocytes These are all eicosanoids

Question 338

Why should the different COX enzymes be activated or inhibited by NSAIDS?

Answer 338

Cox 1 is always functioning for many bodily functions, so it shouldn't be inhibited as it can affect other organs when given long term COX2 is involved in making inflammatory PGs, and so should be inhibited However, selective COX-2 inhibitors are assoc with GI issues, MI and stroke

Question 339

How are NSAIDS processed by the body?

Answer 339

They are lipophilic, absorbed rapidly and fully. They have low first pass metabolism and a high decree of protein binding, giving a small Vd Action onset is slow, metabolized into inactive products by the liver NSAIDS will displace other medications eg. digoxin, so will free them to act more in the body Enzyme inhibitors and inducers may enhance or decrease their activity

Question 340

What are the side effects of NSAIDS?

Answer 340

``` Bleeding GI issues Renal issues Liver toxicity Pregnancy/lactation problems Reye's syndrome ```

Question 341

How does aspirin work?

Answer 341

It is salicylic acid, bound to acetyl for better tolerance. This then binds to serum albumin, conjugated with glycine and glucuronic acid to be excreted in the urine. It competes with uric acid and so can exacerbate gout It irreversibly acetylates COX1, inhibiting platelet adhesion. While this does reduce MI and stroke risk, and spares PG12, a vasodilator, high doses can inhibit prostacyclins (also vasodilators) and cause the opposite effect

Question 342

What can NSAIDS do the GI and bleeding?

Answer 342

It can increase operative blood loss, and increase haematoma risk for epidurals It also inhibits a protective PG against gastric acid damage. This causes increased acid secretion and acidity, as well as reduced mucus synthesis and thickness It also causes diarrhoea, N&V etc.

Question 343

Describe how aspirin relates to asthma

Answer 343

It can induce asthma in a severe and life threatening way Presents as rhinitis and flushing, then asthma and polyps after a later stage This is because inhibition of COX causes decreased bronchodilator PGs, as well as lipoxygenases, which cause bronchospasm

Question 344

What is reye's syndrome?

Answer 344

Acute metabolic encephalopathy, with children more prone after a viral illness

Question 345

How do NSAIDS affect the kidneys and gestation>

Answer 345

NSAIDS can be assoc with renal failure in susceptible patients, including papillary necrosis, interstitial nephritis, and ATN NSAIDs can inhibit labour and close patent ductus arteriosus in premmies

Question 346

Describe apracetamol

Answer 346

An unknown method of analgesia and antipyretic Weak anti-inflam Few side effects, but can cause fatal hepatic damage due to N-acetyl benzo quinone once glutatione stores run out- N acetyl cystiene can augement glutatione reserves to bind the toxic metabolite

Question 347

Where is the CSF found?

Answer 347

In the ventricles and subarachnoid space

Question 348

Where and how is the CSF produced?

Answer 348

It is formed mainly by the choroid plexus in the lateral ventricles. Some is produced by brain IF by bulk flow The choroid plexus is found in the ventricles, and forms a network of fenestrated capillaries surrounding a single row of epithelial cells. The ventricular surface of the epithelium has a microvilli brush border. The first step in production is filtration across the choroidal capillary wall- dependent on hydrostatic capillary pressure Secondly, the epithelium actively secretes it, including vitamins, glucose and amino acids

Question 349

What is the route of CSF circulation?

Answer 349

It flows from the lateral to third ventricle through the foramina of monro. It then flows through the cerebral aqueduct to the fourthe ventricle. From the fourth ventricle, it leaves via a midline and two lateral foramina, entering the subarachnoid space. it collects in cisterns surrounding the brainstem, and also circulates in the subarachnoid space of the spinal chord and brain.

Question 350

How is CSF absorbed?

Answer 350

``` It is mostly done via the small arachnoid villi and larger arachnoid granulations. These are heriations of the arachnoid membrane into the lumina of the sup saggital sinus. Some is also absorbed where nerve roots exit the spinal canal, before the dura sleeves them off It is done by unidirectional bulk flow, relying on hydrostatic pressure. Unless CSF production is well above max absorption, this allows compensation of any increase or decrease in CSF production Some solutes (lipophilic) are reabsorbed by diffusion into the brain and capillaries ```

Question 351

What does the CSF normally consist of?

Answer 351

Few white blood cells, no RBCs, small amount of protein and some glucose depending on blood glucose and rate of its metabolism in the brain

Question 352

How do you test CSF composition?

Answer 352

With a lumbar puncture Patient has local anaesthesia and is lying in the left lateral recumbent position. Needle inserted into L3/4 and pressure is measured and sample removed

Question 353

What are some conditions that can cause variance in the CSF composition?

Answer 353

Meningitis- increased WBC and proteins, maybe decreased glucose Subarachnoid haemorrhage- increased RBCs, causing xanthochromia- yellow colour due to bilirubin from RBC breakdown Tumours- tumour cells present

Question 354

What are the functions of the CSF?

Answer 354

Homeostasis- maintains a constent environment for neurons and glia by facilitating entry of some metabolites, and removing toxic or unnecessary substances Mechanical protection- it cushions the brain from impact with the skull vault during movement and trauma Countering increases in ICP (increases reabsorption) Conducting hormones

Question 355

What is ICP normally?

Answer 355

Approx. 5-15mmHg

Question 356

What are the two methods of measuring intracranial pressure?

Answer 356

Lumbar puncture- although this is useless and potentially dangerous in transtentorial herniation due to lagging of spinal CSF pressure behind intracranial Intracranial pressure monitoring- can be inserted into lateral ventricle or epidural space

Question 357

What is the Monro-Kellie doctrine?

Answer 357

There are three intracranial components- the brain, CSF and blood. These components aren't able to be compressed, so an increase in one needs to be followed by a decrease in another to maintain ICP

Question 358

What are the compensatory mechanisms of the cranium in terms of maintaining ICP?

Answer 358

- Displacement of CSF from the intracrnial cavity into the spinal subarachnoid space Collapse of cerebral veins, reducing IC blood volume Increase in CSF absorption Some distensibility of the lumbosacral dura

Question 359

What can cause ICP compensatory mechanisms to fail?

Answer 359

Increase in brain volume by a space occupying lesion or oedema Increase in CSF volume due to obstruction of flow or reduced absorption (rarely, overproduction of CSF) Increase in blood volume by cerebral venous outflow obstruction, or loss of autoregulation

Question 360

What is brain oedema?

Answer 360

Increased brain water content. Can be due to - Vasogenic oedema (increased ECF due to increased endothelial cell permeability) - Cytotoxic oedema- swelling of cells due to energy depletion and ATP sodium pump failure, allowing hypertonic and hyperosmotic cells- or acute plasma hypoosmolality - Interstitial oedema- hyperosmolality of periventricular white matter due to transpendymal absorption of CSF

Question 361

What are the types of cerebral herniation?

Answer 361

- Displacement of one cerebral hemisphere across the midline (midline shift) which can compress the midline structures - Herniation of medial temporal lobe through the tentorial notch, compressing the upper midbrain, occulomotor nerves and post cerebral artery - Herniation of the inf cerebellum from the posterior fossa into the spinal canal, which compresses the underlying medulla Herniation of cingulate gyrus beneath the falx Upward herniation of the superior cerebellum through the tentorial notch

Question 362

What is cushings sign?

Answer 362

Arterial hypotension, bradycardia and slow resp rate. | This is due to decreasing blood to the medulla, distorting it and preventing its management of life supporting function

Question 363

How does arterial blood pressure affect ICP

Answer 363

- Arterial blood pressure- dependent on cerebral blood flow. Cerebral perfusion pressure = MAP - ICP Normally, Cerebral blood flow is constant due to autoregulation. Vasoactive factors mediate their constriction and dilation. A loss of cerebral autoregulation causes blood flow and blood volume to vary with any change in arterial blood pressure

Question 364

What besides arterial blood pressure affects ICP?

Answer 364

- Venous pressure- rapid compression of jugular veins cause immediate CSF pressure rise - Intrathoracic pressure- increased intrathoracic reduces venous return and increases ICP - Posture- ICP is higher lying down than erect - PaCo2- hypercapnia causes vasodilation, increasing blood flow and increasing CSF pressure - PaO2- hypoxia causes arteriole dilation, increasing cerebral blood volume, flow and ICP- although less pronounced than changes due to PaCo2 - Temperature- blood flow increases linearly with increasing core temperature

Question 365

What is a thunderclap headache and what does it indicate?

Answer 365

It is a sudden headache due to subarachnoid haemorrhage | It is associated with neck stiff ness due to pus and blood inflaming them, as well as loss of consciousness (potential)

Question 366

What is the function of the blood brain barrier?

Answer 366

Regulation of ionic balance Facilitation oftransport of essential substances into the brain Barrier against entry of potentially harmful molecules

Question 367

What are the features of the blood brain barrier?

Answer 367

Endothelial cells have no fenestrations, but they do have tight junctions. This limits the movement of even smaller molecules between cells, separating the plasma from the ECF of the brain They also have fewer pinocytotic vesicles, with a thicker basement membrane and more mitochondria (due to high active transport requirement) Astrocyte foot processes are very closely tied to the walls- allowing regulation of ions and brain volume

Question 368

What factors affect the transport of a molecule across the BBB?

Answer 368

- Molecule size - Lipid solubility (more soluble is easier) - Ionisation at physiological pH - Protein binding restricts entry - Presence of specific transport pathways (ie facilitated diffusion, active transport

Question 369

What are some disorders of the BBB?

Answer 369

- Tight junction disruption, allowing molecules to move between cells - Proteolysis of basement membranes - Disruption endothelial glial interactions - Altered specific transporter function - Formation of new, leaky blood vessels as in tumours - Sometimes, can primarily affect the BBB- eg. loss of GLUT1 glucose transporter in the brain Meningitis also breaks down the barrier, causing presence of WBCs and protein in the CSF

Question 370

What is the pattern of muscle weakness in hemiparesis pyramidal weakness?

Answer 370

In the upper limbs, the flexors can be weak, but still stronger than the extensors In the lower limbs, the extensorts may be week, but are still stronger than the flexors

Question 371

What can cause hemiparesis?

Answer 371

Subdural hematoma- midline shift, compressing motor cortex Left frontal meningioma- causes changes in cognition and personality, as well as pyramidal weakness Thrombus in middle cerebral artery leading to stroke Atrial fibrillation leading to multiple fragments of clots, causing many small strokes Subarachnoid haemorrhage

Question 372

What is used to test dysplasia?

Answer 372

Get the patient to name something, say something and do something

Question 373

What is a new possibility for treatment of stroke?

Answer 373

Solitaire stent retriever- thread a catheter into the blocked artery, surround the embolus with chicken wire esque stuff and pull it back out.

Question 374

What are the changes in memory associated with normal aging?

Answer 374

Variable loss of memory Reduced processing and decreased attention Divided-switching attention Reduced working memory Reduced episodic and some reduced semantic memory

Question 375

What is dementia?

Answer 375

A complex of symptoms, not a diagnosis A decline from previous level of function in terms of memory, and one or more other cognitive functions such as abstract thinking, judgement, language and praxis, or change in personality This change must be of sufficient magnitude to interfere with the patient's usual activities of life, such as work, social life or relationships

Question 376

Where is memory held within the body?

Answer 376

Mainly the brain, in the hippocampal formation. Some motor memory is held within the spinal cord

Question 377

What is delirium?

Answer 377

Acute deterioration of cognitive function associated with known or presumed organic cause

Question 378

What is SDAT?

Answer 378

Senile dementia of the alzheimer's type It involves findings of extensive, progressive neuron loss, and findings of tangles and plaques This shows shrinkage of gyri, with widened sulci and ventricles, and shrunken amygdala and hippocampus

Question 379

Describe neurofibrillary tangles

Answer 379

Found within neurons of SDAT brains, especially in the cortex and hippocampus. Their presence correlates well with cognitive impairment They are made up of paired helical filaments- polymers composed of z-protein Normally it functions to stabilize microtubules, to maintain cell structure and shape

Question 380

Describe extracellular plaques

Answer 380

They are a histological finding of small spherical deposits found in extracellular spaces of the cortex and hippocampus. They are formed of insoluble P-amyloid. Some are found in normal patients, but they are a universal finding of the SDAT brain Diffuse plaques may represent an early stage of the disease, while neuritic plaques have an amyloid core within a cluster of nerve endings.

Question 381

What is the theory of cholinergic depletion?

Answer 381

It is thought that, as SDAT brains show a reduction in ChAT synthesis of AChE, there is a large reduction in AChE that causes alzheimers This causes a defecit in presynaptic neurotransmission This loss is bilaterally symmetrical but variable. It may be due to loss o cholinergic innervation of the cortex, as cortical nicotinic receptors are significantly reduced So far, replacement therapy has produced limited results, and does not provide a complete explanation

Question 382

What is the amyloid theory of Alzheimers?

Answer 382

It is increased amyloid protein in the brain which leads to plaque formation, depletion, damage of the cortex and dementia It can be removed by immunotherapy, although there have been problems with immune reactions etc

Question 383

What are treatment bases of alzheimers?

Answer 383

Generally there is no cure- symptoms only Can use immunotherapy or increase neurotransmitter use. Reversing cholinergic defects has been attempted, and drugs such as donepezil show a 40% benefit

Question 384

What are the important components of taking a clinical evaluation for vestibular system function?

Answer 384

- History - Ear exam - Eye movement - Head thrust - Fukudu stepping - Fistulae - Dix hallpike movement - Lab tests

Question 385

What do we need to know about a vestibular history?

Answer 385

Whether it's a true vertigo or not (are you moving?) Episodic Euration Precipitating and associated factors

Question 386

What can be told about the vestibular system on examination, and what does this tell us?

Answer 386

If there is any nystagmus- the fast phase is the direction it is moving in. Remember COWS- cold (inhibitory) moves to the opposite side of the lesion, while warm (excitatory) moves to the same side as the movement.

Question 387

What can the head thrust test tell us?

Answer 387

it involves the head at 30 degrees downward so the lateral semicircular canal is horizontal. Turn the head quickly to each side to look for a catch up saccade- the lesion in one side of the brain will have eyes staying to that side and then flicking back

Question 388

What does the fukuda standing test tell us?

Answer 388

Have the person stand with eyes closed and arms straight out. Then march. The person will start turning to the direction the lesion is in.

Question 389

What is the calorics test?

Answer 389

Patient lies with the LSCC up and cosd water poured into the ear- the nystagmus goes towards the opposite- if warm it will go towards the same ear

Question 390

What is the dix hallpike test?

Answer 390

This tests the posterior semicircular canal. The patient lies down with their head haning back- turn their head to one side. BPPV will show nystagmus in the side turned to the ground.

Question 391

Define pain

Answer 391

An unpleasant sensory and emotional experience associated with actual or potential tissue damage

Question 392

What are the components of pain?

Answer 392

- Affective: mood and emotion - Autonomic: Increased HR, RR, BP, sweating - Motor: withdrawal, immobilization, vocalising - Sensory: Actual feeling of pain

Question 393

Define pain threshold and give factors that affect where it sits

Answer 393

The point at which a stimulus is perceived as pain | - Factors include personality, stress, anxiety, culture, emotion etc

Question 394

What is pain tolerance? Give factors that will increase or decrease it

Answer 394

Pain tolerance is the duration or intensity of pain that an individual will tolerate before initiation of overt pain responses Tolerance can increase due to distraction, alcohol, faith etc It can decrease due to repeated exposure, fatigue, or sleep deprivation

Question 395

Define allodynia, paraesthesia, causalgia and nociception

Answer 395

Allodynia: Pain due to stimulus that is not normally painful Paresthesia: Abnormal sensation of burning, numbness, tingling etc Causalgia: Sustained burning pain and allodynia after traumatic nerve lesion Nociception: Sensory process of detecting tissue damage

Question 396

What are nociceptors?

Answer 396

Free nerve afferents. They can be A delta or C fibres. They are distributed throughout the body, and are stimulated by noxious mechanical, thermal or chemical stimuli

Question 397

What are the four basic processes of nociception?

Answer 397

Transduction Transmission Perception Modulation

Question 398

What are C vs A delta fibres?

Answer 398

C fibres are small, unmyelinated and slow, whereas A delta are fast, myelinated and medium. These are quick intense pain, whereas C are slow throbbing pain Both are primary afferent fibres

Question 399

What is transduction of pain?

Answer 399

Sensory cells convert external painful stimuli into electrical signals, which occurs in primary sensory cells

Question 400

What is transmission of pain?

Answer 400

Pain is transferred from primary afferents to the dorsal horn, to brain stem, to thalamus, to sensory cortex. It can be done with electrical or neurotransmitter signals

Question 401

Describe the classes of second order neurons in the dorsal horns

Answer 401

Nociceptive specific fibres are in laminae I and II, activated only by noxious stimuli Wide dynamic range are in lamina V, activated by noxious and innocuous stimuli

Question 402

What are neurotransmitters?

Answer 402

Chemical substances that allow nerve impulses to move from one neuron to another across a synapse. They can be excitatory or inhibitory

Question 403

What structures are involved with pain perception?

Answer 403

The reticular system- autonomic and motor responses The limbic system: emotional and behavioural responses Somatosensory cortex- perception and interpretation of sensation

Question 404

Describe the Gate control method of pain dampening

Answer 404

1. Segmental inhibition: AKA gate control theory- a non painful stimulus can block transmission. Pain fibres open the gate, while A beta fibres carrying light touch closes the gate. The brain itself can also open or close the gate This is due to inhibitory interneurons in the sminal cord that make enkephalin, which blocks pain transmission

Question 405

Describe the descending inhibitory nerve system

Answer 405

Descending axons transmit impulses from brain stem to spinal cord to reduce painThe stimulus stimulates periaqueductal gray area, which activates neurons to LC and NRM. This causes release of enkephalin in the spinal cord

Question 406

Describe the theory of pain amplification

Answer 406

It's also called windup. This is the process of increased AP output by DH cells in response to sustained low frequency input from nociceptive afferents via C fibres to the DH neurones It causes increased ca2+ in DH cells, leading to them becoming more responsive- leading to hyperalgesia

Question 407

Describe nociceptive pain

Answer 407

Due to stimuli from somatic and visceral structures after tissue damage. Mediateors such as K+, prostaglandins, bradykinin etc are released and act on nociceptors They usually are opioid sensitive

Question 408

Describe neuropathic pain

Answer 408

Due to damaged neuronal structure. usually opioid resistant, but sensitive to co-analgesics, such as tricyclics, electrical pulses etc It can be peripheral (pains and needles, burning, shooting, stinging) or central (thalamic sensory relay nuclei affected after stroke, spinal cord compression) Can also be complex regional pain syndrome

Question 409

Describe CRPS

Answer 409

Caused by ajor injury or minor trauma Shows as severe debilitating pain with abnormal circulation, temp, sweating, functionolaesa, atrophy and hair/skin changes Treatment invovles PT, SNS blocks and meds

Question 410

Describe inflammatory pain

Answer 410

Post traumatic pain including tissue damage and inflammatory mediators Non neurogenic inflammation is due to inflam substance release from BV and CT due to tissue damage Neurogenic damage is due to inflammatory cells releasing mediators that act on other areas, causing primary and secondary hyperalgesia

Question 411

Describe referred pain

Answer 411

Somatic structures have nerves that feed into the same DH inputs as internal structures, so pain feels like it's coming from a dermatome level

Question 412

Describe the mechanism of chronic pain

Answer 412

Pain and inflammation causes neurotransmitter release onto second order neurons. However, if not treated in time,, they can also cause activation of nearby glial cells, which release their own cytokines to keep the pain going. As a result, pain can be generated in the DH even after the periphery has healed

Question 413

What are the behavioural and psychological changes assoc with chronic pain

Answer 413

``` Depression Sleeping disorders fear unpleasent sensation anxiety ```

Question 414

What is the most useful method of assessing pain?

Answer 414

Scale of 1 to 10 Mild is less than four Moderate if five to six Severe is more than seven

Question 415

What are some causes of spinal cord injuries?

Answer 415

Most frequently it is traumatic injuries Can also be malignant tumours, demyelination, disc protrusion or syringomyelia. The cervical region is the most vulnerable

Question 416

Describe the consequences of T8 spinal cord left side hemisection

Answer 416

Motor issues: Monoplegia in left leg due to loss of inputs from corticospinal and rubrospinal tract Hyperreactive reflexes in left leg due to increased motoneuron excitability from imbalance of symp inputs from reticulospinal and vestibulospinal tracts Sensory issues: Loss of pain and temp on RHS Loss of discriminative sensation in LHS

Question 417

Describe spinal schock

Answer 417

Occurs for first 1-3 days after complete spinal cord transection: A temporary period of areflexia due to loss of facilitatory inputs from reticulospinal and vestibulospinal tracts Includes: - Flaccid paralysis in both legs - All conscious sensation lost - Areflexia - Decreased BP due to loss of sympathetic tone - Absence of thermal sweating (but red skin) - Atonic bladder and bowels - Sexual organ dysfunction

Question 418

Describe te symptoms of spinal cord transection after spinal shock is over

Answer 418

Recovery of muscle tone and hyperreflexia (spastic) Spontaneous bladder.rectum voiding Variable or increased BP due to disrupted baroreception Flexor reflex returns after months Extensor babinski reflex Paraesthesia from affected regions

Question 419

What are the two methods of recovery of CNS systems after transection

Answer 419

Sprouting of presynaptic terminals | Denervation supersensitivity due to increased receptor expression on post synaptic membrane

Question 420

What are ways of managing resp/motor skills in quad/paraplegic patients?

Answer 420

Quads- may need artificial ventilation or resp pacemaker if lesion is above C3 Para: Can use parasetp (microcomputer muscle control)or rewalk (exoskeleton) to gain mobility

Question 421

How do you stimulate CNS regeneration?

Answer 421

Antibodies to neutralise growth inhibithing MAG or NOGO-A Neurotriphin 3 Tissue bridges with fetal spinal cord, peripheral nerve grafts, schwann cells or olfactory glial cells- allows potential recovery of function, but harder than in PNS due to oligodendrocytes being used instead of schwann cells Neural stem cell use