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Neuro > Scrubs bits and pieces > Flashcards

Scrubs bits and pieces Flashcards

1
Q

Expressive aphasia

A

Broca’s (broken speech)

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2
Q

Receptive aphasia

A

Wernicke’s

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3
Q

Limbic system functions

A

Feeding, forgetting, fighting, family, fornicating

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4
Q

Broca’s stroke lesions

A

Middle cerebral artery, in posterior inferior frontal gyrus (left)

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5
Q

Wenicke’s stroke lesion

A

Middle cerebral artery (superior temporal gyrus)

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6
Q

Type of receptor in direct pathway

A

D1 GsGPCR

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7
Q

Type of receptor in indirect pathway

A

D2GiGPCR

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8
Q

Describe direct pathway

A

Cortex -Ex-> striatum-In->SNr/GPi (normally inhibit, but disinhibited)—>Thalamus -Ex- > Cortex

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9
Q

Describe indirect pathway

A

Cortex excites striatum, inhibits GPe, inhibits STN but this normally inhibits the thalamus so disinhibited

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10
Q

Fast glutamate

A

AMPA. Permeable to NA/K, impermeable to Ca2_

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11
Q

Slow Glutamate

A

Permeable to Ca/K/Na. Has Mg block. Needs AMPA depolarisation, glutamate and glycine

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12
Q

GABA A

A

Ionotropic chloride channel

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13
Q

GABA B

A

GPCR

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14
Q

Baclofen

A

GABA B agonist

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15
Q

Gabapentanoids

A

Alpha 2 delta Calcium channel subinit antagonist. Used as anticonvulsants, chronic pain

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16
Q

Clozapine

A

Last resort atypical antipsychotic, ADRS severe constipation, metabolic syndrome weight gain, agranulocytosis, Long QT

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17
Q

St John’s wort

A

SNRI (mild) CYP450 inducer

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18
Q

Hydrazine

A

MAO-I - do not combine with serotonin drugs

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19
Q

Difference between SNRI and TCA

A

TCA is 5HT/NA transporter inhibitor, also anticholinergic properties.
SNRI is 5HT/NA reuptake inhibitor

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20
Q

Buspirone

A

5HT1A agonist, presynaptic. Causes initial decrease in 5HT, then receptor gets desensitised,so has delayed onset and is anxiolytic that needs a few weeks to work.

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21
Q

Benzo/barb MAO

A

allosteric modulators of GABA A (increase GABA)

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22
Q

Catecholamines

A

DA/NA/Adrenaline

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23
Q

Parkinson’s disease genetic link

A

Parkin E3 ligase

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24
Q

Huntington’s symptoms

A

Chorea, depression, personality change

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25
Q

Brain tumour genes

A

NF1/NF2

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26
Q

GABA cycle

A

Can be reuptake by GAT-1 Can also be taken into glial cells, converted to glutamine, then glutamate, then transported to neuron and converted to GABA

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27
Q

Vagibitron

A

Last resort drug due to blindness risk. Inhibits GABA breakdown enzyme (GABA-AT)

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28
Q

Tiagabine

A

Blocks GAT-1

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29
Q

Autonomic dysreflexia

A

T6 or above lesion causes irritation of sympathetic, massive HT with bradycardia

30
Q

Dorsal column decussation

A

At nucleus FC/FG at medulla

31
Q

Auditory pathway

A

ECOLI
Nerve Eight goes to coclear and BIFURCATES- > superior olive - > lateral lemniscus- >inferior colliculi - > medial genitculate nucleus of the thalamus

32
Q

Where would audtory pathway lesion cause deafness?

A

Before the cochlear nucleus as otherwise it’s a bifurcating pathway and would need a lesion on both sides to be symptomatic

33
Q

CSF ventricle flow

A

Goes from lateral ventricle through IV foramen to 3rd ventricle, then cerebral aqueduct to 4th, then central canal

34
Q

Optic pathway

A

Retinal, CNII to optic chiasm. Then optic tracts. Synapse at medial geniculate nucleus of the thalamus. Then can either be superior pathway to occipital lobe, or meyer’s loop (via temporal lobe) to inferior aspect of occipital lobe.

35
Q

Light reflex pathway

A

Part of optic nerve goes to pretectal nucleus in upper midbrain, synapses with both EW nuclei which acts through CNIII (parasympathetic) to activate sphincter paillae

36
Q

Conjugate eye movements

A

PFEF (prefrontal eye fields) via paramedian pontine reticular formation or vestibuli nuclei can have input.
If vestibular then activation of semi circular canal goes through scarpas’s ganglion and synapses with contralateral CNVI nuclei and this then synapses with LR and contralateral CNIII (through medial longitudinal fasciculus) , moving a the MR

37
Q

Argyll robertson pupil

A

Has accomodation reflex but does not react to light. Historically seen in syphilis
The lesion is presumably near the pre-tectal nucleus where the pupillary fibres from the optic tract run to enter the Edinger Westphal nucleus from the dorsal aspect. The fibres for the accommodative pupillary response come from the occipital lobe via the internal capsule and enter the Edinger Westphal nucleus along a deeper course.

38
Q

Marcus Gunn Pupil

A

relative afferent pupillary defect (RAPD) - normal consensual response but impaired pupillary response.This occurs because of a decrease in afferent input reaching the pretectal pathway responsible for the pupillary light response in the midbrain via a damaged optic nerve, but efferent fibres to the affected eye are delivered via cranial nerve III.

39
Q

Dorsal nerve of the vagus

A

Lateral to Hypoglossal, medial to ambiguus. Enteric vagal (GI, heart etc)

40
Q

Vagus from ambiguus

A

muscles of palate, larynx and pharynx

41
Q

CNIX from ambiguus

A

stylopharyngeus

42
Q

CNIX difference between spinal and solitarius

A

Solitarius does taste (post 1/3 of tongue); spinal does visceral sensation from body

43
Q

Superior salivatory nucleus

A

CNVII for lacrimal, nasal, submandibular glands

44
Q

Inferior salivatory nucleus

A

CNIX to parotid

45
Q

Nystagmus naming

A

Named on fast (second) movement. Cold water causes slow movement towards, then fast opposite. Hot water causes slow movement opposite, then fast movement towards

46
Q

Anisocoria

A

Asymetric pupil size (physiological or pathological, e.g. horners)

47
Q

Adie’s tonic pupil

A

Pupil dilated, does not respond to direct light, Consensual light or accomodation

48
Q

hyaloid canal

A

Runs throught vitrious body of the eye

49
Q

ora serrata

A

Junction between retina and ciliary body

50
Q

Facial nerve runs

A

Pons - > internal acoustic meatus, out of the stylomastoid foramen then splits

51
Q

Nerve passing through ethmoid bone

A

CNI (crbriform)

52
Q

Bone for jugular canal

A

Temporal

53
Q

Bone for hypoglossal canal

A

occipital

54
Q

stretch reflex

A

Monosynaptic (2 neurons, 1 synapse). Group 1a myelinated axons (around intrafusal muscle) respond to stretch by activating alpha motorneuron. Shortens muscle in response

55
Q

gamma motorneurons

A

reset spindle mechanism to adjust sensitivity- faciliates stretch reflex.

56
Q

Golgi tendon organs

A

Sense tension in muscles. Preventws muscle from too much tension)Travel in 1 b afferent.
This is reversed myotatic/clasp. Polysynaptic as uses internneuron

57
Q

Flexor reflex

A

Nocicpetor mediated in response to pain, allows withdrawal. Polysynaptic. Works across several spinal segmented levels for rapid, coordinated limb withdrawal.

58
Q

Crossed extensor reflex

A

Polysynaptic path. Activated during flexor reflex to cause extension of opposite limb and maintain balance.

59
Q

Spinal cord lesion - reflex effect

A

Above would be preserved, at that level would be weak/absent. Below might initially be absent (spinal shock) then hyperactive due to lack of inhibition

60
Q

Significance of cetriazone/imipenem in meningitis

A

Can cross BBB as not effluxed

61
Q

Vaspodar

A

Experimental P-glycoprotein inhibitor

62
Q

MDR associated protein

A

Multidrug resistant protein - transports many drugs (inc. HIV antivirals/ chemotherapy) out of brain

63
Q

P glycoprotein

A

Efflux transporter. In CNS and enteric system. Examples of exploitation and loperamide (opioid but antitiarrhoeal as high p glyco affinity); domperidone can’t cross BBB, haloperidol can.
HIV protase inhibitors (tenofovir, ritoavir, atanavir) can’t cross BBB

64
Q

M/S symptoms

A

1) optical neuritis (painful loss of vision/colour vision - inflammation of optic nerve)
2) tranverse myelitis (often cervical, thoracic 0 rarely lumbar. weakness/sensory disturbance/UG issues)
3) cerebellar issue (ataxia)
4) Brain stem issue (vertigo, diplopia, nystagmus, dysphagia, vertigo)
5) Cerebral hemisphere issue (hemiparesis, sensory issue, depresion, fatigue)

65
Q

Diagnosis of M/S

A

DIS and DIT of 2+/ But CSG oligoclonal bands can negate the need for DIT
DIS by MRI (gadolinium )

66
Q

SPMS vs PPMS

A

SPMS is 6-12 month progression with no relapse. \
PPMS is 1 year of progression with no remission plus 2/3 of DIS in brain, DIS in spinal cord or positive CSF olgoclonal band

67
Q

Immunology of MS

A

T cell anti myelin is animal model. stimulate astrocytes and microglia B cells produce Myelin antibodies

68
Q

Gandolinium in CNS

A

In RRMS, BBB breakdown allows gadolinium into CNS and they travel to lesions

69
Q

PPMS and SPMS

A

Not inflammatory. Axons stripped of myelin and damaged. Not repairable.

70
Q

FLT in RRMS

A

FLT is Interferon (1/b/1a) and glatiramer acetate.
Teriflunomide (LFT regular)
Dimethylfumarate (better tolerated)

Antibody therapies:

  • Natalizumab (WBC entry blocker)
  • Fingolimod (peripheral lymphocyte depletion)
  • Alemtuzumab (binds B adn T cells to modulate immune system)

Steroids can be used in big relapse

71
Q

PPMS/SPMS therapy

A

SPMS - siponimod (reduces disability progression)

PPMS - Ocrelizumab (reduce disease progression)

Neuro (6 decks)

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