Scrubs bits and pieces Flashcards
1
Q
Expressive aphasia
A
Broca’s (broken speech)
2
Q
Receptive aphasia
A
Wernicke’s
3
Q
Limbic system functions
A
Feeding, forgetting, fighting, family, fornicating
4
Q
Broca’s stroke lesions
A
Middle cerebral artery, in posterior inferior frontal gyrus (left)
5
Q
Wenicke’s stroke lesion
A
Middle cerebral artery (superior temporal gyrus)
6
Q
Type of receptor in direct pathway
A
D1 GsGPCR
7
Q
Type of receptor in indirect pathway
A
D2GiGPCR
8
Q
Describe direct pathway
A
Cortex -Ex-> striatum-In->SNr/GPi (normally inhibit, but disinhibited)—>Thalamus -Ex- > Cortex
9
Q
Describe indirect pathway
A
Cortex excites striatum, inhibits GPe, inhibits STN but this normally inhibits the thalamus so disinhibited
10
Q
Fast glutamate
A
AMPA. Permeable to NA/K, impermeable to Ca2_
11
Q
Slow Glutamate
A
Permeable to Ca/K/Na. Has Mg block. Needs AMPA depolarisation, glutamate and glycine
12
Q
GABA A
A
Ionotropic chloride channel
13
Q
GABA B
A
GPCR
14
Q
Baclofen
A
GABA B agonist
15
Q
Gabapentanoids
A
Alpha 2 delta Calcium channel subinit antagonist. Used as anticonvulsants, chronic pain
16
Q
Clozapine
A
Last resort atypical antipsychotic, ADRS severe constipation, metabolic syndrome weight gain, agranulocytosis, Long QT
17
Q
St John’s wort
A
SNRI (mild) CYP450 inducer
18
Q
Hydrazine
A
MAO-I - do not combine with serotonin drugs
19
Q
Difference between SNRI and TCA
A
TCA is 5HT/NA transporter inhibitor, also anticholinergic properties.
SNRI is 5HT/NA reuptake inhibitor
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.
21
Q
Benzo/barb MAO
A
allosteric modulators of GABA A (increase GABA)
22
Q
Catecholamines
A
DA/NA/Adrenaline
23
Q
Parkinson’s disease genetic link
A
Parkin E3 ligase
24
Q
Huntington’s symptoms
A
Chorea, depression, personality change
25
Brain tumour genes
NF1/NF2
26
GABA cycle
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
27
Vagibitron
Last resort drug due to blindness risk. Inhibits GABA breakdown enzyme (GABA-AT)
28
Tiagabine
Blocks GAT-1
29
Autonomic dysreflexia
T6 or above lesion causes irritation of sympathetic, massive HT with bradycardia
30
Dorsal column decussation
At nucleus FC/FG at medulla
31
Auditory pathway
ECOLI
Nerve Eight goes to coclear and BIFURCATES- > superior olive - > lateral lemniscus- >inferior colliculi - > medial genitculate nucleus of the thalamus
32
Where would audtory pathway lesion cause deafness?
Before the cochlear nucleus as otherwise it's a bifurcating pathway and would need a lesion on both sides to be symptomatic
33
CSF ventricle flow
Goes from lateral ventricle through IV foramen to 3rd ventricle, then cerebral aqueduct to 4th, then central canal
34
Optic pathway
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
Light reflex pathway
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
Conjugate eye movements
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
Argyll robertson pupil
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
Marcus Gunn Pupil
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
Dorsal nerve of the vagus
Lateral to Hypoglossal, medial to ambiguus. Enteric vagal (GI, heart etc)
40
Vagus from ambiguus
muscles of palate, larynx and pharynx
41
CNIX from ambiguus
stylopharyngeus
42
CNIX difference between spinal and solitarius
Solitarius does taste (post 1/3 of tongue); spinal does visceral sensation from body
43
Superior salivatory nucleus
CNVII for lacrimal, nasal, submandibular glands
44
Inferior salivatory nucleus
CNIX to parotid
45
Nystagmus naming
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
Anisocoria
Asymetric pupil size (physiological or pathological, e.g. horners)
47
Adie's tonic pupil
Pupil dilated, does not respond to direct light, Consensual light or accomodation
48
hyaloid canal
Runs throught vitrious body of the eye
49
ora serrata
Junction between retina and ciliary body
50
Facial nerve runs
Pons - > internal acoustic meatus, out of the stylomastoid foramen then splits
51
Nerve passing through ethmoid bone
CNI (crbriform)
52
Bone for jugular canal
Temporal
53
Bone for hypoglossal canal
occipital
54
stretch reflex
Monosynaptic (2 neurons, 1 synapse). Group 1a myelinated axons (around intrafusal muscle) respond to stretch by activating alpha motorneuron. Shortens muscle in response
55
gamma motorneurons
reset spindle mechanism to adjust sensitivity- faciliates stretch reflex.
56
Golgi tendon organs
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
Flexor reflex
Nocicpetor mediated in response to pain, allows withdrawal. Polysynaptic. Works across several spinal segmented levels for rapid, coordinated limb withdrawal.
58
Crossed extensor reflex
Polysynaptic path. Activated during flexor reflex to cause extension of opposite limb and maintain balance.
59
Spinal cord lesion - reflex effect
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
Significance of cetriazone/imipenem in meningitis
Can cross BBB as not effluxed
61
Vaspodar
Experimental P-glycoprotein inhibitor
62
MDR associated protein
Multidrug resistant protein - transports many drugs (inc. HIV antivirals/ chemotherapy) out of brain
63
P glycoprotein
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
M/S symptoms
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
Diagnosis of M/S
DIS and DIT of 2+/ But CSG oligoclonal bands can negate the need for DIT
DIS by MRI (gadolinium )
66
SPMS vs PPMS
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
Immunology of MS
T cell anti myelin is animal model. stimulate astrocytes and microglia B cells produce Myelin antibodies
68
Gandolinium in CNS
In RRMS, BBB breakdown allows gadolinium into CNS and they travel to lesions
69
PPMS and SPMS
Not inflammatory. Axons stripped of myelin and damaged. Not repairable.
70
FLT in RRMS
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
PPMS/SPMS therapy
SPMS - siponimod (reduces disability progression)
| PPMS - Ocrelizumab (reduce disease progression)
