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DVM2 > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the main structural divisions of the brain?

A

Forebrain- prosencephalon (telencephalon (cerebrum) and diencephalon (thalamus and its regions))
Midbrain- mesencephalon (tectum, tegmentum, cerebral peduncles)
Hindbrain- rhombencephalon (metencephalon (cerebellum and pons) and myelencephalon (medulla oblongata))

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2
Q

What comprises the brainstem?

A

Mesencephalon, pons, medulla oblongata +/- diencephalon

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3
Q

What is the most caudal part of the brain and what are it’s margins?

A

Medulla oblongata.

Caudal margin= spinal cord
Rostral margin= prominent transverse ridge of the pons

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4
Q

Where can the piriform lobes be found?

A

Ventral aspect of cerebral hemispheres

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5
Q

The superficial origins of all cranial nerves (except for which one?) are visible on the ventral surface of the brain.

A

Trochlear nerve (CN IV)

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6
Q

The roof of the skull is the ________
The bones of the brain case include ___________
The membranous fold arising from the midline of the skull roof is the __________
The cerebellum and cerebrum are separated by what?

A

Calvaria
Frontal, parietal, occipital, temporal, sphenoid and ethmoid
Falx cerebri
Tentorium osseum and tentorium cerebelli

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7
Q

The optic canal lies immediately rostral to what?

A

The optic chiasm

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8
Q

Describe the position of the pituitary gland.

A

It lies in the hypophyseal fossa which lies caudal to the optic chiasm on the ventral aspect of the brain

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9
Q

Where can the cochlea and the vestibular apparatus be found?

A

Housed within the petrous temporal bone

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10
Q

What comprises the ventricular system?

A

Paired lateral ventricles (one within each cerebral hemisphere)
Third ventricle
Mesencephalic aqueduct
Fourth ventricle

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11
Q

What is the reticular formation? What does it do?

A

Region of mixed grey and white matter from the medulla oblongata to the thalamus

Modulates HR, BP and resp and protective reflexes (eg. Vomiting) and arousal

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12
Q

Which animals have lissencephalic telencephalons?

A

Rodents, rabbits, birds

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13
Q

Describe the following 2 landmarks:
Cruciate sulcus
Lateral rhinal sulcus

A

Cruciate sulcus- transverse groove between frontal and parietal lobes
Lateral rhinal sulcus- separates the rhinencephalon from main part of cerebral hemispheres

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14
Q

What are the three types of cerebral cortex and where do they occur?

A

Paleocortex- olfactory lobe
Archeocortex- medial aspect of each hemisphere dorsal to the corpus callosum
Neocortex- frontal, parietal, occipital and temporal lobes

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15
Q

What is a choroid plexus?

A

Tangled networks of blood vessels, Pia and ependyma protruding into the ventricles. It is responsible for the production of cerebrospinal fluid (ultrafiltration of blood plasma)

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16
Q

Describe the flow of CSF. How is it absorbed?

A

Flow is in a caudal direction through brain’s ventricular system. It leaves the brain via the lateral apertures under the cerebellum which take the csf into the subarachnoid space.

Absorbed by the arachnoid villi as well as by lymphatics around the origins of the cranial and spinal nerves, and veins around the brain and within the meninges.

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17
Q

What are the three layers of meninges from external layer to internal? Between which layers is the epidural space?
Which layer encloses the spinal roots as they leave the spinal cord?

A

Dura mater, arachnoid mater, Pia mater

Epidural space is external to dura mater and contains fat and vertebral venous plexi

Dura mater encloses spinal roots

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18
Q

What are the leptomeninges?

A

Arachnoid mater and Pia mater

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19
Q

In which areas is the dura mater folded to form a double membrane?

A 
Falx cerebri (ethmoid bone to osseous tentorium)
Tentorium cerebelli (petrosal crest to osseous tentorium)
Diaphragma sella (dorsum sella  to caudal chinois process of sphenoid bone near optic canal area)
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20
Q

Briefly describe the vascular supply and drainage of the spinal cord.

A

Supply:

  • longitudinal arteries (2 dorsolateral and the ventral spinal artery)
  • radicular arteries
  • collateral circulation

Drainage:
-internal vertebral venous plexus (on floor of vertebral canal)

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21
Q

Briefly list the main arterial supply to the brain.

A
  • left and right internal carotid
  • basilar (continuation of ventral spinal artery)
    • > circle of Willis
  • rostral cerebral artery (rostromedial half of cerebral hemispheres)
  • middle cerebral artery (lateral part and rostral brain stem)
  • caudal cerebral artery (caudomedial part)
  • rostral and caudal cerebellar arteries
  • rostral, middle and caudal meningeal arteries
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22
Q

What is responsible for connecting each lateral ventricle to the centrally located third ventricle?

A

Interventricular foramina

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23
Q

Where do the lateral apertures of the fourth ventricle occur?

A

Between the fourth ventricle and subarachnoid space at the level of CNVIII

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24
Q

Describe the two clinically important CSF cisterns.

A
  1. Cerebellomedullary cistern (lies between caudal cerebellum and medulla oblongata)
  2. Lumbar cistern ((caudal end of spinal cord -L7)
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25
Q

List the arrangement of cranial nerves.

A 
Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducens 
Facial
Auditory (vestibulocochlear)
Glossopharyngeal
Vagus
Accessory
Hypoglossal
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26
Q

In regards to the cranial nerves, no nerve is purely sensory but some nerves are purely motor. True or false?

A

False! No nerve is purely motor but some nerves are purely sensory (I, II, VIII)

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27
Q

Which cranial nerves exit together through the internal acoustic meatus? Why is this important clinically?

A

CN VII and VIII exit together. Therefore may bothe be affected by otitis externa

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28
Q

Describe the innervation of the pharynx and larynx.

A

Pharynx:

  • sensory CN IX
  • motor CN IX and X

Larynx

  • sensory CN X and XI
  • motor CN X and XI
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29
Q

Which cranial nerves have meningeal coverings which extend out into the periphery?

A

I, II and VIII

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30
Q

a) Anosmia (lack of smell) can be a sign of dysfunction of which nerve?
b) strabismus (lateral/medial rotation of the dorsal aspect of the eye)
c) balance problems

A

a) CN I
b) CN IV and CN VI
c) CN VIII

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31
Q

Which cranial nerves may the following signs of dysfunction be associated with?

a) dysphagia and respiratory noise
b) visual and PLR deficits
c) dropped jaw and facial sensory deficits
d) paralysis and deviation of the tongue

A

a) IX and X
b) II
c) V
d) XII

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32
Q

Which cranial nerves may the following signs of dysfunction be associated with?

a) facial muscle paralysis, decreased lacrimation and taste
b) atrophy/ dysfunction of trapezius, brachio- and sterno-cephalicus
c) PLR deficits and strabismus

A

a) VII
b) XI
c) III

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33
Q

The sympathetic division of the autonomic nervous system arises from which spinal nerves?

A

C8 to L3/4

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34
Q

What are the three major ganglia called through which the sympathetic and vagus pass through?

A

Cervicothoracic (only sympathetic)
Middle cervical
Cranial cervical

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35
Q

Where can the hypogastric nerves be found? What do they supply?

A

Distal to the caudal mesenteric ganglion. Structures of the pelvis

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36
Q

Where does parasympathetic supply to the head arise?

A

From the parasympathetic nuclei of cranial nerves III, VII and IX

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37
Q

What does the parasympathetic nucleus of CN III in the mesencephalon supply? (This is called the Edinger-Westphal nucleus) Where does it run?

A

Supplies the iris and ciliary body.

Travels to the eye via the orbital fissure

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38
Q

What does the parasympathetic nucleus of CN VII and IX supply?

A

Salivary glands

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39
Q

What are two roles of the parasympathetic nucleus of CN X?

A

Innervates the pharynx and larynx

Innervates the thorax and abdomen

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40
Q

Touch, pressure and proprioception respond to purely mechanical stimulation and is transmitted in which part of the spinal cord along which tract?

A

Dorsal funiculus

Fasciculus gracilis and fasciculus cuneatus

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41
Q

Pinprick pain, heat and cold are transmitted in which part of the spinal cord and along which tract? What about deep pain?

A

Lateral funiculus along the spinothalamic tract

Deep pain: diffusely. Sent to the ascending reticular formation in the brain stem

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42
Q

What is sensory and motor ataxia?

A

Sensory ataxia= incoordination of motor coordination due to lack of proprioceptive input
Motor ataxia= incoordination of motor action due to lack of UMN input

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43
Q

What are some LMN deficit signs as opposed to UMN deficit signs?

A

LMN: flaccid paralysis, hyporeflexia, atonia, neurogenic atrophy to specific muscles

UMN: extensor rigidity, hyper-reflexia, general hypertonia, mild generalised disuse atrophy

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44
Q

Name the 5 spinal cord motor tracts that we learnt about and specify where each one originates.

A
  1. Corticospinal (motor cortex of cerebrum)- only pyramidal one
  2. Rubrospinal (red nucleus of the midbrain)
  3. Vestibulospinal (vestibular nuclei)
  4. Tectospinal (tectum)
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45
Q

Which tract is found entirely within the spinal cord?

What does it do?

A

Propriospinal tract
Has ascending and descending fibres for reflex activity within and between spinal cord segments

(Surrounds grey matter)

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46
Q

The fasciculus gracious conveys proprioceptive information to the brain from _______ whereas the fasciculus cuneatus conveys proprioceptive information to the brain from ________

A

Gracilis: from body caudal to T8
Cuneatus: from body cranial to T8

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47
Q

What is the main tract responsible for carrying pain and temperature sensibility? Does it have ipsi- or contra- lateral projection?

A

Lateral spinothalamic tract in the ventral part of the lateral funiculus
Both ipsi and contralateral projection

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48
Q

Which pathways are involved in conveying proprioceptive info for posture and adjustment of posture after movement? Do these pathways have contralateral or ipsilateral projection?

A
  • dorsal and ventral spinocerebellar (caudal 1/2 of body)
  • cranial spinocerebellar (cranial 1/2 of body)
  • spinovestibular (head and neck junction)
  • dorsolateral fasciculus

All have ipsilateral projection

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49
Q

What is the major extrapyramidal tract and a major voluntary motor pathway in animals?

A

Rubrospinal tract

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50
Q

What is the lateral (medullary) reticulospinal tract?

A

Extrapyramidal tract from the reticular formation of the medulla oblongata.

It is facilitatory to the contralateral proximal flexors. It suppresses standing and other antigravity activities

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51
Q

What is the lateral vestibulospinal tract?

A

Originates from the lateral vestibular nuclei of the medulla oblongata. It facilitates ipsilateral extensor and inhibits ipsilateral flexors

Always active

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52
Q

What is the medial vestibulospinal tract responsible for?

What about the medial longitudinal fasciculus?

A

Maintaining balance with head movements

Coordinates trunk movements with head and neck movements

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53
Q

Where does the ventral (pontine) respticulospinal tract originate? What does it do?

A

Reticular formation of the pons

Maintains standing posture (facilitatory to ipsilateral LMNs of prox extensor muscles)

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54
Q

the eyeball consists of three tunic layers. What are they and what are they comprised of?

A
  1. Outer fibrous tunic
    - collagenous tissue
    - sclera and cornea which meet at the limbus
  2. Vascular tunic (uvea)
    - choroid, ciliary body and iris
  3. Retina
    - pigmented epithelial layer
    - neuroepithelial layer
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55
Q

How does the cornea receive its nutrients? What provides sensory perception to it?

A

Via lacrimal fluid and aqueous fluid of anterior chamber

Opthalmic branch of CNV

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56
Q

What is the choroid? What does it do? Is it vascular or avascular?

A

Part of the vascular tunic that lines the sclera from the optic nerve almost to the limbus.
Provides nutrients for outer layers of retina.
It has a vascular and avascular part. Blood vessels are found in the pigmented part of it. It also has an avascular tapetum lucidum dorsally which is reflective/iridescent

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57
Q

What is the ciliary body? What is its role?

A

Thickening of choroid dorsally. It provides an anchoring point for zonular fibres which suspend the lens. It also produces aqueous humour

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58
Q

The iris is under both parasympathetic and sympathetic supply. Explain this further.

A

Smooth muscle sphincter responsible for pupillary constriction is under PS supply. the radial muscle responsible for dilation is under sympathetic supply

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59
Q

What are the cells (from outer to inner) comprising the neuroepithelial layer of the retina?

A 
Photoreceptor cells (rods and cones)
(Horizontal cells)
Bipolar cells
(Amacrine cells)
Ganglion cells (light hits these first)
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60
Q

What are the roles of rods and cones?

A

Rods- night vision

cones- colour vision

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61
Q

Which cells of the neuroepithelial layer of the retina feed into the optic nerve?

A

The ganglion cells

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62
Q

What do horizantal and amacrine cells do?

A

Horizontal: modify transmission between bipolar and photoreceptor cells
Amacrine: modify transmission between bipolar and ganglion cells

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63
Q

what is the eye lens comprised of? Where does it get its nutrients from?

A

Epithelial cells and lens fibres

Aqueous and vitreous humour

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64
Q

Where does the aqueous humour drain? Where is it produced?

A

Into venous sinuses at iridocorneal angle

Cells of ciliary body

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65
Q

Describe the periorbita fascia of the eye

A

fibrous fascial sheath which blends medially and dorsally with periosteum. Inserts in eyelids and surrounds eyeball and extrinsic muscles of the eye. It also contains smooth muscle which helps to keep the eyeball slightly protruded under normal sympathetic tone

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66
Q

What is the puncta lacrimalia?

A

Minute slits on the upper and lower lids adjacent to the lacrimal caruncle. They are the openings to the canaliculi leading too nasolacrimal duct.

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67
Q

Lacrimal sceretions consist of 3 layers. What are they?

A
  1. outermost lipid layer
  2. aqueous layer form
  3. inner mucoid layer
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68
Q

What is the vascular supply of the eye?

A

External opthalmic artery (from maxillary)
Internal opthalmic artery (supplies CNII)

Venous drainage is via several vorticose veins emerging through sclera

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69
Q

Which nerve innervates the auricular muscles of the pinna?

A

CNVII

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70
Q

What is the external acoustic meatus?

A

Canal running from narrow part of auricular cartilage to tympanic membrane

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71
Q

Describe the tympanic membrane?

A

Thin complete membrane separating external acoustic meatus from middle ear. Fibrous tissue. Attached to osseous tympanic ring. Covered laterally by epidermis and medically by mucosa

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72
Q

The tympanic (middle ear) cavity is connected to the inner ear by…?

A

The vestibular and cochlear windows

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73
Q

What are the auditory ossicles? What muscles are they associated with?

A

Malleus, incus and stapes.

Stapedius muscle and tensor tympanum muscle (they act to dampen transmission)

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74
Q

What components comprise the bony and membranous labyrinths of the inner ear?

A

Bony: vestibule, semicircular canals, cochlea
Membranous: urticaria/ saccule, semicircular ducts, cochlear duct

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75
Q

Which plexus is responsible for control of gut secretion? Which is responsible for control of gut motility?

A

Submucosal

Myenteric

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76
Q

What layers make up the eyelids?

A

Skin
Musculofibrous layer (with orbicularis oculi and tarsal glands)
Conjunctiva ( lines posterior surface of eyelids -palpebral- and reflects onto sclera-bulbar)

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77
Q

What is the nerve supply to the eye?

A

CNII- light perception
CNIII- motor to dorsal, medial and ventral recti; ventral oblique and lavatory palpebrae superioris. PS innervation to iris and ciliary body
CNIV- dorsal oblique
CNV- sensory to eyeball, eyelids and conjunctiva
CNVI- lateral rectus, retractor bulbi
CNVII- motor to orbicularis oculi, lacrimal gland
Sympathetic innervation- periorbita, pupillary dilation (radial m.), eyelids open, and retraction of third eyelid

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78
Q

What is the vestibular system and how does it work (briefly)?

A

=organ responsible for sensing body position
Movement of cilia towards or away from static kinocilium results on depolarisation or hyperpolarization of hair cell, and excitation or inhibition of firing of neutron at base of hair cell

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79
Q

Describe where the utricle and saccule are located and how they are positioned.

A

Utricle- base of semi-circular canals. Oriented in horizontal plane
Saccule- ventral to utricle, connected to endolymphatic duct. Oriented in vertical plane

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80
Q

What are maculae?

A

Sensory hair cells in saccule and utricle which sense static position. They project into the otolithic membrane.

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81
Q

In the semicircular ducts, hair cells are located on (a)… and project into (b)…

A

a. Crista

b. Cupula

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82
Q

What is the basilar membrane?

A

Part of cochlear duct adjacent to the Scala tympani. It transducers sound into nerve impulses and has hair cells with cilia tips that are embedded into the tectorial membrane.

83
Q

How does hearing occur? (10 main steps)

A

Vibration of tympanic membrane ➡️ vibration of auditory ossicles (malleus, incus and stapes) ➡️ vibration of stapes against vestibular window ➡️ waves in perilymph of Scala vestibuli ➡️ vibration of vestibular membrane ➡️ waves in endolymph of cochlear duct ➡️ vibration of basilar membrane ➡️ distortion of hair cell cilia in tectorial membrane ➡️ depolarisation of hair cells ➡️ impulse in cochlear nerve.

84
Q

What is the innervation associated with the ear and hearing?

A

CNVIII
CNVII: supplies m. stapedius
CNV: supplies m. tensor tympani

85
Q

What is the difference between a neurotransmitter, neuromodulator and neurotropic factor?

A

NT: released by presynatic terminals and produce rapid excitatory resposes in post synaptic neurons
NM: released by neurons and produce slower pre- or post-synaptic responses (G-protein coupled receptors)
NTF: released mainly by non-neuronal cells. Act on tyrosine kinase linked receptors that regulate gene expression

86
Q

PGE2 and PGI2 are hyperalgesic. What does this mean?

A

Increase sensitivity of receptors to painful stimuli

87
Q

What are some examples of excitatory neurotransmitters? What about some inhibitory?

A

glutamate, substance P, neurokinin A, prostaglandins

beta-endorphins, NA, adenosine, GABA

88
Q

What classes of analgesics are used in vet med?

A 
local anaesthetics
NSAIDs
opioid analgesics
centrally acting non-opioid analgesics
alpha2 adrenergic agonists
89
Q

What are the 2 types of nociceptive afferent neuron fibres?

A

C fibres: non-myelinated, low conduction veocity. Sense dull pain
A-delta fibres: myelinated, fast transmission. sense sharp localised pain

90
Q

What are the different opioid receptors?

A
  1. mu-receptors: mu1 mediate most analgesic effects. mu2 mediate undesirable side-effects
  2. kappa: spinal cord analgesia (fewer side effects)
  3. delta: peripheral analgesia
91
Q

In most species, opioids cause pupillary constriction. In which species do they cause mydriasis?

A

Cats!

92
Q

What is the difference between opioid peptides, opiates and opioids?

A

Opioid peptides: endogenous
Opiates: derived from opium
opioids: any substance with morphine-like effects that are blocked by antagonists.

93
Q

How may opioids be classified? Give examples.

A

Pure agonists: morphine, codeine, fentanyl
Partial agonists: buprenorphine (temgesic)
Mixed agonists/antagonists: butorphanol
Antagonists: Naloxone, naltrexone

94
Q

What class of dub is gabapentin? What about ketamine?

A

Anticonvulsant

NMDA receptor blocker

95
Q

Opioid receptors are linked to…?

A

G-proteins.

96
Q

What are the main effects of alpha2 adrenergic agonists?

A

Analgesia, Muscle relaxation, dose-dependent sedation

97
Q

What are the pre and post synaptic effects of alpha2 adrenergic agonists?

A

Pre-synaptic: inhibits release of NA

Post: ontraction

98
Q

What are some contraindications for alpha2 adrenergic agonists?

A

Heart disease, arterial hypotension and shock, renal or hepatic impairment, epilepsy, late stage pregnancy…

99
Q

What is the main alpha2 adrenergic agonist used in dogs/cats and horses? What is used for reversal?

A

Dogs and cats: medetomidine (domitor)
Horses: detomidine or romifidine

Reversal agents:
Yohimbine (for xylazine sedation in cattle)
Atipamezole (for medatomidine)

100
Q

What is an example of a phenothiazine derivative? What are the main actions of such drugs?

A 
Example: acepromazine, chlorpromazine
Activity:
1. block dopamine receptors
2. block peripheral alpha adrenoceptors
3. inhibit adenosine uptake
4. block emesis at CRTZ
101
Q

What class of drugs does diazepam belong to? What are the principal effects of these drugs?

A

Benzodiazepine

  • hypnotic
  • sedative
  • anxiolytic
  • anticonvulsant
  • skeletal muscle relaxant
  • amnesic
102
Q

What are some features of a good anaesthetic?

A

Should render the patient unconscious
Induction and recovery should be rapid and smooth
Depth of anaesthesia should be easily adjusted
Should be non irritant and non toxic

103
Q

What are some signs that allow us to monitor the depth of anaesthesia in a patient?

A
  • Eyeball nystagmus
  • Pupil dilation/ constriction
  • CV depression
  • Respiratory depression
  • Muscle relaxation
104
Q

What are the stages of anaesthesia?

A

Stage 1: amnesia/ euphoria
Stage 2: excitement, delirium, resistance to handling
Stage 3: unconsciousness, regular respiration, decreasing eye movement
Stage 4: resp arrest, cardiac depression/ arrest

105
Q

What is blood/gas PC? What about oil/gas PC?

A

Blood/ gas PC= measure of the spreed of anaesthetic induction and recovery, and the rapidity of changes in anaesthetic levels
Oil/gas PC= correlates with lipid solubility and therefore measures the potency of the anesthetic. Influences kinetics of distribution and recovery.

106
Q

What is a partition coefficient in reference to anaesthtics?

A

A measure of solubility. It’s the concentration ratio of anaesthetic in 2 phases. (blood/gas for example). ie. how a drug will partition itself following equilibrium.

107
Q

What is the MAC of an anaesthetic?

A

Minimum alveolar concentration=concentration that prevents gross powerful movement in 50% of subjects exposed to a supramaximal noxious stimulus.
Deep anaesthesia= 2xMAC

108
Q

What is a side effect of halothane as a inhaled anaesthetic?

A

Causes decreased cardiac output and sensitises the myocardium to adrenaline. This increases the risk of arrythmias.
Halothane hepatitis has also been recorded

109
Q

Why is isoflurane preferable to something like halothane?

A

It’s:

  • less depressive on HR, SV
  • 4x less arrythmogenic than halothane
  • less than 1% is metabolised
110
Q

What are some classes of injectable anaesthetics? Provide examples.

A
  1. Barbiturate (eg. thiopental, pentobarbitol)
  2. Propofol
  3. Dissociative anaesthetics (eg. ketamin and tiletamine)
  4. Steroid anaesthetics (eg. alfaxan)
  5. Benzodiazepines (eg. diazepam)
111
Q

What is sevoflurane?

A

An inhaled anaesthetic very similar to isoflurane but it is:

  • less soluble
  • less irritant to airways
  • less smell
  • not gentle
112
Q

What are some drug interactions to be aware of when thinking about anaesthetics?

A

Do not mix thiopentone with other drugs. It will precipitate out.

113
Q

How do barbiturates work?

A

Allosteric modulators of GABA receptor. They enhance the efficacy of the inhibitory neurotransmitter GABA-> increased duration of chloride channel opening thus permitting a greater influx of chloride ions-> hyperpolarisation and decreased excitability of target cell.

Note: some also act at glutamate receptors to decrease activity of excitatory receptors

114
Q

What are some side effects of barbiturates?

A

Increase HR, decreased SV

Respiratory depressant

115
Q

What is the difference between thiobarbiturates and oxybarbiturates in terms of how they stop working?

A

Thio: termination of effects depends on redistribution (cff. hepatic metabolism)

116
Q

Which anaestetic is useful for short procedures?

A

Thiopental sodium
Methohexital
Propofol

117
Q

What are some precautions/contraindications for the use of barbiturates?

A 
Thin patients
Obese patients
Hepatic dysfunction
Respiratory depression
Strictly IV.
118
Q

How does ketamine work? What are its side effects? What would you combine it with?

A

It’s a dissociative anaesthetic. It’s a specific antagonist at glutamate NMDA receptor and at CNS muscarinic Ach receptors.
An agonist to opioid receptors- analgesic properties.
It causes functional dissociation between the thalamus and cortex
Side effects: resemble symp NS stimulation
Benzos

119
Q

What is propofol? What are its side effects?

A

A GABA-mimetic. Rapidly metabolised by liver.

Side effects like thiopentone (myocardial depressio, vasodilation, hypotension, apnoea)

120
Q

How does alphaxalone work?

A

Modulates GABA transmission

121
Q

What are the principle actions of benzodiazepines on the CNS?

A
  • hypnotic
  • sedative
  • anxiolytic
  • anticonvulsant
  • skeletal muscle relaxant
  • amnesic
122
Q

How do benzodiazepines work?

A

An allosteric modulator of the GABA receptor

123
Q

Which anaesthetics provide analgesia?

A

Ketamine
Nitrous oxide
Methoxyflurane

124
Q

How do local anaesthetics work?

A

They inhibit conduction of APs in efferent and afferent nerve fibres, either in peripheral nerves or in the spinal cord.

125
Q

To increase the effect of local anaesthetics, a greather length of nerve is infiltrated rather than an increased dose being given locally. Why is this?

A
  • Transmission of APs depends on opening of voltage gated Na channels. LAs are Na channel blockers (bind in active state).
  • Myelinated fibres are only blocked at nodes. Therefore, smaller unmyelinated fibres are easier to block.
  • Pain fibres (small and unmyelinated) are first to be blocked
  • Motor fibres are last to be blocked
126
Q

Ester-linked LAs are metabolized _________ in _______. They have a ?long/short? duration.
Amide-linked LAs are metabolized _________ in _______. They have a ?long/short? duration.

A

Rapidly in tissue/ plasma
Short

Slowly in liver
Medium to long

127
Q

What are some examples of LAs?

A 
Lignocaine
Bupivacaine
Mepivacaine
Amethocaine
Ropivacaine
128
Q

What is the term for inflammation of the grey/ white matter? What about for inflammation of the brain/ spinal cord?

A

Polioencephalitis
Leukoencephalitis

Encephalomyelitis

129
Q

What is the difference between ependymitis and ventriculitis?

A

ependymitis- infl. of lining of ventricles

ventriculitis- infl. of ventr. cavities

130
Q

Why is inflammation of the CNS particularly bad?

A
  1. brain is vital for survival
  2. space limitations
  3. ventricular/ meningeal system promotes spread of infection
    4, few barriers to spread of infection through neuropil (no stroma, no fibrocytes)
131
Q

What are some features of CNS infl.?

A
  • Perivascular cuffing
  • leptomeningitis (expansion of subarachnoid space)
  • gliosis
132
Q

Which organism enters the CNS via retrograde neuronal transport?

A

Listeria monocytogenes

133
Q

What type of cellular response is typical for bacterial infection within the CNS? Virus infection? Fungal? Protozoa? Paraasitic?

A 
Bact: neutrophilic/ pyogranulomatous
Viral: lymphocytic/ lymphoplasmacytic
Fungal: granulomatous/ pyogranulomatous
Prot: lymphoplasmacytic and granulomatous
Para: granulomatous and eosinophilic
134
Q

What is granulomatous meningoencephalitis?

A

A common disease in dogs (toy and terrier breeds esp) in which lesions are seen in the white matter of the brain and spinal cord. Poor prognosis.

135
Q

WHat is necrotizing meningoencephalitis?

A

Possibly an autoimmune disease directed against astrocytes. Most common in pugs. Lesions occur in grey matter of cerebral cortex and overlying meninges

136
Q

In which animal is steroid-responsive meningitis-arteritis mostly seen? What is this?

A

young beagles

necrotizing infl. in small to medium sized arteries.

137
Q

What is TSE?

A

A non-infl disease of the CNS

138
Q

What are the main types of cells found in pancreatic islets? What do these cells secrete?

A

Endocrinocytus alpha (secrete glucagon), beta (secrete insulin and amylin), delta (secrete somatostatin), gamma (pancreatic polypeptide) and epsilon (ghrelin).

139
Q

The pituitary gland lies within the …(a)… which lies caudal to the …(b)…?

A

a) hypophyseal fossa

b) optic chiasm

140
Q

Hyperadrenocorticism is the most common endocrinopathy in dogs. TRUE or FALSE?

A

FALSE. It is the third most cmmon (pseudopreg and Hypothyroidism are more common)

141
Q

What is the innervation of the adrenal glands?

A

Sympathetic pre-ganglionic axons arising from splanchnic and adrenal ganglia.

142
Q

Which cell organelles/ inclusions are important for steroidogenesis?

A

ER, mitochondria, lipid

143
Q

What does the adrenal medulla produce?

A

Noradrenaline and adrenaline

144
Q

What do the different zones of the adrenal cortex produce?

A

Zona glomerulosa- mineralocorticoids (eg. aldosterone)
Zona fasciculata- glucocorticoids (eg. cortisol)
Zona reticulata- androgens (eg. testosterone)

145
Q

Where is aldosterone produced? What are the effects of aldosterone?

A

Zona glomerulosa of the adrenal cortex.
Effects:
-increased transcription/translation of Na Channel components and Na/K pump components
-targets distal tubules and collecting ducts
-Increased Na reabsorption from kidneys-> water retention

146
Q

What is atrial natriuretic peptide?

A

Hormone released from the cardiac atrial myocardium. does the opposite of aldosterone.

147
Q

What is the main glucocorticoid produced in reptiles, birds and rodents?

A

Corticosterone.

148
Q

What are the general effects of glucocorticoids?

A

Slow down growth and shift resources to maintaining the body under stressful conditions. Metabolic effects, psychoneural effects, reduced inflammation and other.

149
Q

What are the specific effects of glucocorticoids?

metabolic 5, Infl. 5, phychoneural 3, other 4

A

Metabolic:

  • protein catabolism
  • gluconeogenesis
  • decreased insulin sensitivity
  • lipolysis
  • increased effect of glucagon and adrenalin

Inflammation/ immunosuppression:

  • decreased prostaglandin synthesis
  • decreased histamine release
  • decreased phagocytosis and Ab production
  • decreased release of proteolytic enzymes
  • decreased egress of neutrophils and lymphocytes

Pyschoneural:
-euphoria, depression and increased appetite

Other:

  • delayed wound healing
  • decreased bone formation
  • increased bone resorption
  • decreased ADH release
150
Q

What androgens are produced by the zona reticularis?

A

Dehydro-epi-andro-sterone

Androstenedione

151
Q

What controls release and synthesis of adrenal androgens? How do adrenal androgens work?

A

Adrenal androgen-stimulating hormone
They act through nuclear receptors. Hormone binds cytosolic receptor and translocates to the nucleus where regulation of target genes occurs.

152
Q

How is cortisol transported in blood?

A

Bound to corticosteroid-binding globulin (aka transcortin) and albumin

153
Q

What is the half life of glucocorticoids in the blood?

A

60-90 mins

154
Q

Most sex hormones are transported in the blood via ___a___, ___b___, or ____c____. Dehydroepiandrosterone and androstenedione however are mainly transported by ___d___

A

a. transcortin
b. albumin
c. sex-hormone binding globulin
d. albumin

155
Q

How and where are catecholamines made?

A

Post-ganglionic neurons of the adrenal medulla hydroxylise amino acid tyrosine to produce adrenlaine and NA which are then stored in cytoplasmic granules

156
Q

What is Addison’s disease? What are the common clinical signs? What are potential causes?

A 
Hypoadrenocorticism.
Causes:
-autoimmune disease (attack of cortex)
-iatrogenic
-tumour

Consequences:

  • lower Na to K ratio
  • high ACTH levels
  • skin darkening
157
Q

What is Cushing’s disease? What are potential causes? Signs?

A 
Hyperadrenocorticism
Causes:
- pituitary neoplasia
-adrenal neoplasia
- iatrogenic

Consequences:

  • high blood glucose
  • muscle loss
  • immnuosuppression and risk of infection
  • polyphagia, PU/PD
  • delayed wound healing
  • bone loss
158
Q

How are adrenocortical steroids degraded/excreted?

A

The steroid core does not breakdown. The hormones are inactivated by the liver and conjugated with sulphates and glucuronides. this makes them more water-soluble for excretion in bile and urine.

159
Q

Alpha adrenoceptors have an affinity for…?

Beta adrenoceptors have an affinity for …?

A

Alpha- NA

Beta- adrenaline

160
Q

What adrenal pathologies involve excessive adrenocortical tissue?

A

Adrenocortical hyperplasia, adenoma or carcinoma

161
Q

What might adrenocortical hyperplasia represent?

A
  1. pituitary hyperstimulation (too much ACTH)
  2. sustained physiological stress
  3. Idiopathic/ incidental
162
Q

How might one differentiate nodular hyperplasia of the adrenal cortex vs an adenoma?

A
  • Nodular hyperplasia is a response to a stimulus (adenomas occur independently of stimulus)
  • multiple foci (single)
  • bilateral (often unilateral)
  • not encapsulated (often encapsulated)
  • small <1cm (large)
  • don’t compress surrounding tissue (may compress)
163
Q

What are some characteristics of an adrenocortical carcinoma?

A
  • rare
  • large, poorly defined against normal tissue
  • metastatic
  • functional or not
  • vascular invasion and thrombosis
164
Q

What are the five forms of hyperadrenocorticism? How do these affect the size of the adrenal glands?

A
  1. Pituitary dependent- bilateral cortical hyperplasia
  2. Adrenal dependent- bilateral adrenocortical atrophy
  3. Iatrogenic- bilateral adrenocortical atrophy
  4. Ectopic ACTH secretion- bilateral cortical hyperplasia
  5. Food responsive- bilateral cortical hyperplasia
165
Q

What are some signs of hyperadrenocorticism?

A

Alopecia, dermal atrophy, hyperpigmentation, calcinosis cutis, muscle catabolism, pot belly, enlarged liver, Pu/PD, polyphagia…

166
Q

What are some effects of primary hyperaldosteronism? When may secondary hyperaldosteronism occur

A

Hypernatraemia
hypokalaemia
increased H secreation

Secondary may occur due to chronic kidney hypoperfusion or due to overactivation of RAAS

167
Q

What are some diseases involving loss of adrenocortical tissue?

A 
Aplasia
Atrophy
Haemorrhage/ necrosis (exertional death)
Toxicity 
Inflammation
168
Q

What is Pheochromocytoma?

A

Neoplasia of the adrenal medulla mostly seen in dogs and cattle (but rarely). May be benign or malignant. It’s a dark coloured tumour. It may secrete catecholamines

169
Q

How does hyperadrenocorticism differ in ferrets?

A

Secretes sex hormones instead of corticosteroids.

170
Q

What are the differences in hyperadrenocorticism symptoms in horses, dogs and cats?

A

Dogs: PPP and BBB
Cats: thin skin, diabetes(insulin resistant), PPP. Note: VERY RARE
Horses: mostly due to Pituitary pars intermedia dysfunction. Hirsutism, PU/PD, recurrent laminitis, muscle wasting. pot belly

171
Q

What would you find on haematology in a patient with HyperA? Explain each of these findings.

A

Stress leukogram

  • Lymphopenia (sequstration and lysis due to cortisol)
  • Mature neutrophilia (Increased release from storage pool, decreased emigration to tissues and shift from marginating to circ)
  • Mild monocytosis (shift from marg->circ)
  • Eosinopenia (margination or sequestration, inhibition of marrow release and inhibition of IL-5)
  • Mild thrombocytosis
  • Lipaemic sample
172
Q

What might you find on biochem in a patient with HyperA? Explain each of these findings.

A
  • Elevated ALP (induction of corticosteroid isoform and steroid hepatopathy)
  • Elevated ALT (steroid hepatopathy)
  • Elevated GGT (steroid hepatopathy)
  • Hypercholesterolaemia/ hypertriglyceridaemia (stim of VLDL synthesis in liver/ hormone sensitive lipase, inhibition of lipoprotein lipase through insulin antagonism)
  • Hyperglycaemia (insulin antagonism, decreased GLUT4 transporters, stimulation of gluconeogenesis/ glucagon release)
  • Low TT4
  • Mild elevation in urea (prerenal azotaemia)
173
Q

What might you find on routine urinalysis in a patient with HyperA? Explain each of these findings.

A

Poorly concentraed urine (inhibited ADH action and release)

Mild proteinura (glomerular hypertension)

UTIs (immunosuppression, poorly concentrated urine)

174
Q

The urinary creatinine cortisol ratio screening test used to rule out a diagnosis of HyperA is highly sensitive but poorly specific/ How might one increase the specificity of this test? What is a normal UCCR?

A

Test free catch sample of urine tested at home to minimise stress

<17.5

175
Q

How does the low dose dexamethasone suppression test work?

A

Patient is given low dose of dexamethasone IV and cortisol levels are tested at 0, 4 and 8 hrs post admin (in horse its a o hr sample and 19-24hr sample). Dex should cause neg feedback to pituitary -> reduced ACTH -> reduced cortisol. It does not cross react with cortisol assay.

176
Q

How might the following dogs show up on a low dose dex test?

  1. dogs with adrenal tumours
  2. dogs with pituitary dependent HyperA
  3. stressed dogs
A
  1. lack of suppression
  2. partial suppression, escape from suppression or no suppression
  3. partial or no suppression
177
Q

What test is the best for diagnosis of iatrogenic hyperA? How does this test work?

A

ACTH stim test.

Take 0hr cortisol then admin ACTH 5ug/kg IV or IM then 1hr later test cortisol (in dog. in cats do 0, 30 min and 60 min)

178
Q

What is the rationale behind an endogenous ACTH test for localising hyperA?

A

Dogs with pituitary hyperA will have normal to high ACTH levels. Dogs with adrenal ACTH will have very low levels. Iatrogenic hyperA cases have very low levels also

(Horses with PPID will have high levels)

179
Q

How might you expect the adrenals to look with imaging in a dog with:

  1. Pituitary dep hyperA
  2. Adrenal tumours
A
  1. bilateral adrenal enlargement

2. one large and one small adrenal

180
Q

What are some potential causes of hypoadrenocorticism?

A
  1. Adrenal gland failure
  2. Failure of ACTH secretion by pituitary
  3. Iatrogenic (corticosteroid therapy withdrawal or Lysodren/Trilostane treatment with is used for hyperA)
  4. Critical illness/ relative adrenal insufficiency
181
Q

What are some symptoms one might see with hypoadrenocorticism in a dog? What might be some DDx?

A

Vague signs (vomiting, diarrhoea, abdominal pain, collapse, bradycardia, PU/PD, dehydration, tremors, GIT haemorrhage)

DDx:
Acute renal insufficiency, urinary obstruction, GIT disease. hypercalcaemia of malignancy

182
Q

What are some clinical pathology findings one might see with hypoadrenocorticism in a dog?

A
  1. electrolyte abnormalities
  2. Low Na:K ratio
  3. lack of stress leukogram
  4. lymphocyte count <2.4 x 10^9
  5. Azotaemia
  6. Hypercalcaemia
  7. Hypoglycaemia
  8. Erythrocytosis/ anaemia
  9. Hypoalbuminaemia
  10. elevated liver enzymes
  11. USG<1.030
183
Q

How do you test for hypoadrenocoticism?

A

ACTH stim test (0 and 1hr)

Cortisol: ACTH ratio

184
Q

What are the effects of calcitonin and where is it produced?

A

Secreted by parafoliiclular (C cells) of thyroid gland.

It decreased blood calcium and phosphate concentrations by inhibiting osteoclastic bone resorption. It also increases the renal excretion of calcium and phosphate.

185
Q

What is the extracellular calcium-sensing receptor and what is it role?

A

G protein coupled receptor expressed by parathyroid gland chief cells, thyroid gland C cells and several types in kidney. It mediates effects of low and high calcium on PTH and mediates effects on calcium reabsorption on kidney.

186
Q

What are the two ways in which activated vitamin D stimulates calcium absorption in the intestine?

A
  1. Active transcellulat (mainly duodenum)

2. Diffusional (through tight junctions and intercellular spaces. Throughout intestines).

187
Q

How do birds cope with the increased demand for calcium during egg-laying?

A

They form medullary bone on endosteal surfaces prior to and during egg-laying in response to sex steroids, it provides calcium reservoir.

188
Q

Explain milk fever:

A

High [Ca] in milk->decreased [Ca] in plasma-> detected by calcium-sensing receptor -> PTH secretion

189
Q

How are blood glucose levels sensed and responded to?

A

GLUT2 receptor on beta cells allows unimpeded glucose entry. When intracellular glucose reaches a threshold, cell membrane depolarises, get a Ca influx and consequent exocytosis of insulin granules which go into portal vein and then systemic circ. =positive feedback loop

190
Q

What is the half life of insulin and how is it cleared?

A

4-6mins. Cleared by enzymatic degradation by insulinase mainly in the liver and a little bit in kidney and muscles

191
Q

What does growth hormone inhibiting hormone (somatostatin) do?

A

2 things

  1. Inhibits release of GH from somatotropin of anterior pituitary
  2. Inhibits release of TSH by thyrotrophs of anterior pituitary
192
Q

What is the term to describe the physical representation of uncontrolled GH secretion? What bones does it primarily affect?What might cause it?

A

Acromegalia. Bones of the limbs, skull and jaw (not long bones because growth plates have closed)
Functional anterior pituitary tumour (in dogs)
Hyperplastic/ hypertrophic somatotrophs (in cats)

193
Q

What might stimulate GH release? What might inhibit it?

A

Stimulate: hypoglycaemia, stress, high dietary protein, low fatty acids, exercise, ghrelin, deep sleep

Inhibit: high carbs, neg feedback (from IGF-1and GH)

194
Q

What two toxins are of particular importance relative to the adrenal glands?

A

Mitotane and trilostane

195
Q

What is the blood supply and innervation of the pancreas?

A

Cranial and caudal pancreatoduodenal arteries
Branches of splenic and hepatic artery
Drainage: cranial and caudal pancreatoduodenal veins, splenic vein (drain into portal vein)
Innervation: sympathetic (coeliac and cranial mesenteric plexuses) and parasympathetic (CNX)

195
Q

What are the five effects of insulin on carbohydrate metabolism?

A
  1. Glucose influx (via glut 4 receptors)
  2. Increased glycogen synthase activity
  3. Decreased liver phosphorylase activity
  4. Decreased glucose phosphatase activity
  5. Increased glucokinase activity
196
Q

What are the five effects of insulin on protein metabolism?

A
  1. Increased aa uptake
  2. Increased gene transcription into RNA
  3. Inhibits lysosomal protein degradation
  4. Inhibits enzymes important in gluconeogenesis
  5. Needed for ribosomal function
197
Q

What are some positive and negative regulators of glucagon?

A

Positive:

  • low BG
  • high blood aa
  • beta adrenergic stimulation

Negative:

  • insulin
  • amylin
  • somatostatin
  • high BG
198
Q

Briefly explain how glucagon works.

A

Exocytosed by alpha cells of the pancreas in response to low BG.

Binds to GPCR ➡️ activation of adenylate cyclase ➡️ increased IC cAMP ➡️ range of metabolic effects (eg. Increased glycogenolysis)

199
Q

What is somatostatin?

A

Aka growth hormone inhibitory hormone released from delta cells. It suppresses the secretion of insulin and glucagon (paracrine), inhibits it’s own secretion and inhibits upper GIT motility. Extends period of food and nutrient availability

200
Q

Explain how glucagon malfunction works in diabetes patients.

A

Alpha cells rely on insulin to uptake glucose. Therefore in diabetic patients, low insulin means low intracellular concentration so less glucagon release despite high blood glucose levels

201
Q

What are some pathophysiological consequences of diabetes? (6)

A
  1. Hyperglycaemia
  2. Glucosuria
  3. Polyuria, dehydration and thirst
  4. Tissue injury (structural changes in blood vessels)
  5. Metabolic ketoacidosis
  6. Protein depletion
202
Q

What is DKA?

A

Diabetic ketoacidosis. Results from insulin not working. Sugar is not used and body switches to lipid metabolism. Increased beta oxidation of fatty acids leads to ketone formation and ketonaemia.

Ketonaemia + high BG ➡️ CTZ - emesis - further dehydration
Ketonaemia + dehydration ➡️ acidosis - diabetic coma
Dehydration ➡️ hyperviscosity, thromboembolism and hypovolaemic

203
Q

What are some Ddx for glucosuria?

A 
Diabetes
Tubular abnormalities
Fanconi syndrome
Cephalosporin
Increased [vit C]
Increased progesterone

DVM2 (13 decks)

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