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Years 1+2 > S3C5 (2.0) > Flashcards

S3C5 (2.0) Flashcards

1
Q

What is a UMN lesion?

A

Lesion along the descending motor pathways

Typically before the anterior horn cell of the spinal cord or motor nuclei of the cranial nerves

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2
Q

What is a LMN lesion?

A

Lesions anywhere along the nerve fibres between the ventral horn of the spinal cord and relevant muscle tissue

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3
Q

Which motor neuron lesion would lead to atrophy and fasciculations?

A

Lower motor neuron

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4
Q

What are fasciculations?

A

A twitching of muscle caused by involuntary, asynchronous contraction of muscle fascicles within a single motor unit

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5
Q

What are the characteristics of UMN lesion?

A

Central paresis (spastic paresis): pyramidal tract signs
Increased tone, spasticity and clonus
Decreased power
Increased reflexes Increased muscle tone

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6
Q

What are the characteristics of LMN lesion?

A

Peripheral paresis (flaccid paresis): absent pyramidal tract signs
Decreased tone
Decreased power in single muscle fibres
Decreased reflexes / areflexia

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7
Q

What effect does a UMN lesion have on the bladder?

A

Detrusor hyperreflexia and detrusor/external sphincter dyssynergia (A disturbance of muscular coordination that causes uncoordinated and abrupt movements)

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8
Q

What effect does a LMN lesion have on the bladder?

A

Overflow incontinence - An involuntary leakage of urine secondary to overfilling of the bladder

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9
Q

Which motor neuron lesion would lead to the babinski sign and pronator drift?

A

Upper motor neuron

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10
Q

What is clonus?

A

Involuntary contractions and relaxations of muscles in response to stretching

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11
Q

What causes spasticity?

A

Removal of inhibitory influences exerted by the cortex on the postural centres of vestibular nuclei and reticular formation

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12
Q

What is memory?

A

The mental capacity to store and later recall or recognise event that were previously experienced
Memory is an active mental system the received, encodes, modifies and retrieves info

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13
Q

What is recall?

A

Reproducing info to which you were previously exposed to without linked stimulus

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14
Q

What is recognition?

A

Uses a stimulus to retrieve something you have seen or heard before (cue dependent)

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15
Q

What did Bartlett say on the constructive nature of memory?

A

Serial reproduction of stories

People who perform a memory task do no simply repeat what they have learned but actively reconstruct what they remember

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16
Q

What are the main models of memory?

A

Multistore model
Working memory theory
Levels of processing model

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17
Q

What are the 3 types of memory in the multistore model?

A

Sensory
Short term
Long term

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18
Q

What is sensory memory in the multistory model?

A

Lasts about 0.1 to 0.5 of a second
Holds quite an accurate and complete representation
Encoding is sense-specific - different sensory memory stores for the different sensory modalities

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19
Q

What is short term memory in the multistory model?

A

Lasts seconds to minutes
Involves frontal and parietal lobes
Capacity is limited to 7 (the rule of 7) - chunking can improve capacity
Uses an acoustic engram

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20
Q

What is long term memory in the multistory model?

A

Duration potentially unlimited
Much greater capacity
Activity spread throughout brain but hippocampus is essential to consolidation
Sleep essential to consolidation and especially 7 days for emotional processing involving the amygdala
Mainly semantic encoding

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21
Q

What are the different elements of the working memory theory?

A

Central executive
Phonological loop
Visuo-spatial sketchpad

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22
Q

What is the central executive of the working memory theory?

A

Allocates limited attention resources to other components of working memory. Performs cognitive tasks such as problem solving

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23
Q

What is the phonological loop of the working memory theory?

A

Stores auditory info by silently rehearsing sounds and words in a continuous loop - the articulatory process

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24
Q

What is the visuo-spatial sketchpad of the working memory theory?

A

Stores visual and spatial info -engages when performing spatial tasks and visual ones

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25
Q

What is the levels of processing model?

A

Memory is a function of processing activity
Superficial vs deep processing
Stronger memories through elaborative rehearsal - more extensive neuronal connections

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26
Q

What is the epidemiology of GAD?

A

More common in women

Median age 30

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27
Q

When does anxiety become abnormal?

A 
Excessively intense
Disproportionate to the stimulus
Occurs without a cause
Continues beyond exposure to danger
Cant be controlled
Causes distress
Impairs functioning
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28
Q

How does the risk increase is a firist-degree family member has GAD?

A

risk x2.5

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29
Q

What can cause GAD?

A 
Molecular genetics (Serotonin transporter gene affected?)
Overactive amygdala
Childhood trauma
Parental rejection or over-control
Major life stress - threat events
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30
Q

What is GABA?

A

Inhibitory neurotransmitter

Main inhibitory neurotransmitter in CNS

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31
Q

What % of brain synapses is GABA present?

A

30%

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32
Q

How is GABA made?

A

Synthesised by decarboxylation of glutamic acid

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33
Q

What is the role of GABA?

A

Regulating neuronal excitability and muscle tone

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34
Q

What are the 2 main receptors where GABA is an endogenous agonist?

A

GABA-A - multiple ligand binding sites

GABA-B

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35
Q

What is baclofen?

A

GABA analogue which acts as a selective agonist

Used clinically as a muscle relaxant

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36
Q

What is the GABA-A receptor?

A 
Transmembrane, ligand-gated ion channel receptor
5 subunits (pentameric) arranged around a central chloride channel
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37
Q

What are the subunits of GABA-A receptor?

A

α, β, γ, δ, ρ

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38
Q

What is the most common structure of GABA-A

A

(α1)2 (β2)2 (γ2)

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39
Q

Where does GABA bind?

A

binding pocket Between α and β subunits

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40
Q

What does GABA binding cause?

A

Cl- ions to flow into the neuron, leading to a decreased chance of action potential - hyperpolarisation

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41
Q

What is the diagnosis criteria for GAD?

A

At least six months with predominant tension, worry, and feelings of apprehension about everyday events and problems
Restlessness or feeling keyed up or on edge; being easily fatigued; difficulty concentrating or mind going blank; irritability; muscle tension; and sleep disturbance

42
Q

What are the psychological symptoms of GAD?

A

Constant worries, intrusive thoughts
Feeling of apprehension and dread
Poor concentration
If severe - depersonalisation and derealisation

43
Q

What are the physical symptoms of GAD?

A 
Tremor
Sweatiness
Palpitations
Muscular tension
Tension headache
Hyperventilation
	Difficulty taking breaths
	Atypical chest pain
	Paresthesias in hands, feet and lips
44
Q

What are the behavioural symptoms of GAD?

A

Putting things off because of anxiety
Avoidance of particular situations
Self-medication - misuse of drugs and/or alcohol to relieve anxiety

45
Q

What are side effects of SSRIs?

A 
Drowsiness
Nausea
Dry mouth
Insomnia
Diarrhea
Nervousness, agitation or restlessness
Dizziness
Sexual problems, such as reduced sexual desire or difficulty reaching orgasm or inability to maintain an erection (erectile dysfunction)
Headache
Blurred vision
46
Q

Where do benzodiazepines bind?

A

Benzodiazepine receptors which mediate sleep, affects muscle relaxation, anticonvulsant activity, motor coordination, and memory.

47
Q

What is the moa of mirtazapine?

A

Blocks pre synaptic alpha-2 auto-receptors

48
Q

What is duloxetine and venlafaxine?

A

SNRI

49
Q

What is imipramine?

A

TCA

50
Q

What is the MOA of pregabalin?

A

Binds to alpha-2-delta (α2d) subunit of the voltage-dependent calcium channel in CNS. This decreases the release of neurotransmitters including glutamate, noradrenaline and substance P.

51
Q

Where is broca’s area located?

A

Left hemisphere, frontal lobe

52
Q

Where is Wernicke’s area located?

A

Posterior superior temporal lobe

53
Q

What is the role of the angular gyrus?

A

Associate a perceived word with different images, sensations and ideas.

54
Q

What is CVA?

A

The sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is impaired by blockage or rupture of artery to the brain.

55
Q

What are the histological features 12-24 hours after ischemia?

A

Red neurones

Eosinophillic cytoplasm and pyknotic nucleus

56
Q

What are the histological features 1-3 days after ischemia?

A 
Neutrophils 
Liquefactive necrosis (partial or complete dissolution of dead tissue and transformation into a liquid)
57
Q

What are the histological features 3-5 days after ischemia?

A

Macrophages (microglia, CD40 positive)

58
Q

What are the histological features 5-15 days after ischemia?

A 
Reactive gliosis (astrocytes)
Vascular proliferation
59
Q

What are the histological features >15 days after ischemia?

A

Glial scarring

60
Q

What does the anterior cerebral artery supply?

A

Medial portions of the frontal lobes (including medial sensorimotor cortex).
Superior medial parietal lobes.
Anterior four-fifths of the corpus callosum.
Anterior portions of the basal ganglia and internal capsule.
Olfactory bulb and tract.

61
Q

What are the two major branches of the anterior cerebral artery?

A

Pericallosal artery – this forms an anastomosis with the posterior cerebral artery.
Callosomarginal artery

62
Q

What is the pathway of the middle cerebral artery?

A

turns laterally to enter the depths of the Sylvian fissure.
Bifurcates into superior division and inferior division.
Form loops as they pass over the insula (insular branches) and then around and over the operculum (opercular branches) to exit the Sylvian fissure onto the lateral convexity.

63
Q

What does the middle cerebral artery supply?

A

Most of the cortex on the dorsolateral convexity of the brain.

64
Q

What is the pathway of the posterior cerebral artery?

A

Curves back after arising from the top of the basilar and sends branches over the inferior and medial temporal lobes and over the medial occipital cortex.

65
Q

What does the posterior cerebral artery supply?

A

The inferior and medial temporal and occipital cortex.

66
Q

What are the lenticulostriate arteries?

A

Arise from the initial portions of the middle cerebral artery before it enters the Sylvian fissure, and they supply large regions of the basal ganglia and internal capsule.

67
Q

What is the anterior choroidal artery?

A

Arises from the internal carotid artery. Its territory includes portions of the globus pallidus, putamen, thalamus, and the posterior limb of the internal capsule.

68
Q

What is the recurrent artery of Heubner?

A

Arises from the initial portion of the anterior cerebral artery to supply portions of the head of the caudate, anterior putamen, globus pallidus, and internal capsule.

69
Q

What is a TIA?

A

Temporary, focal cerebral ischemia that results in brief neurologic deficits lasting <24 hours
No permanent loss of CNS function

70
Q

What is a stroke?

A

Acute neurological conditions caused by an acute cerebrovascular event

71
Q

What is an ischemic stroke?

A

Cerebral infarction due to insufficient cerebral blood flow, which results in ischemia and neuronal injury

72
Q

What is an haemorrhagic stroke?

A

Cerebral infarction due to haemorrhage; either intracerebral or subarachnoid

73
Q

What % of stroke deaths are female?

A

60% of stroke deaths are female - potentially because women on average are older when stroke occurs

74
Q

What age are stroke patients?

A

2/3rds of patients are <65

75
Q

What ethnicities are at higher risk of stroke?

A

African Americans and Hispanics

76
Q

How many strokes happen p/a in England and Wales?

A

80,000

77
Q

What % of stroke patients die within 30 days?

A

15%

78
Q

What are the symptoms of stroke?

A 
Limb weakness
Numbness
Speech disturbance (aphasia/dysarthria)
Visual loss/ disturbance/ visual field defect
Disturbance of balance
Inability to swallow safely
79
Q

What are the risk factors for stroke?

A 
BP
Cholesterol
High Blood sugar
Abnormal sinus rhythm
Smoking
Obesity
Stress
80
Q

What % of strokes are ischaemic?

A

85%

81
Q

What is the management of stroke in A+E?

A

Initial assessment an handover from paramedics
Exclude Hypoglycaemia if BM <3.5 treat urgently and reassess
Urgent scan
Early ASU admission reduces mortality

82
Q

What are the clinical features by a stroke affecting the MCA?

A

Contralateral sensory loss and paralysis in the arms, lower half of the face, and lower limbs
Gaze deviates towards side of infarction
Contralateral homonymous hemianopia without macular sparing
Aphasia - The inability (or difficulty) to comprehend and/or formulate language due to damage to specific brain regions; refers to a variety of disorders and etiologies (left MCA territory; dominant hemisphere)

83
Q

What are the clinical features by a stroke affecting the ACA?

A

Contralateral paralysis in the lower limbs&raquo_space; upper limbs
Minimal sensory loss in the lower limbs&raquo_space; upper limbs
Dysarthria
Aphasia
Abulia (lack of motivation)
Limb apraxia
Urinary incontinence

84
Q

What are the clinical features by a stroke affecting the PCA?

A

Visual field defects: Contralateral homonymous hemianopia with macular sparing
Contralateral hemisensory loss: due to lateral thalamic involvement
Touch, pinprick, positional sense may be reduced
Memory deficits
Vertigo, nausea
Left PCA territory: alexia without agraphia, anomic aphasia, visual agnosia
Right PCA territory: prosopagnosia
Thalamic syndrome

85
Q

What artery is most commonly affected in stroke?

A

Middle cerebral artery

86
Q

What is a watershed infarct?

A

A border-zone infarct in the region between two major arteries
Usually as a result of a sudden decrease in blood pressure or cessation of blood flow through both vessels. This occurs because the region between the two territories is most susceptible to ischemia.

87
Q

What are the clinical features of a watershed infarct?

A 
Signs of symptomatic hypoperfusion
	Tachycardia
	Low BP
	Pallor
	Sweating
Diffuse neurological deterioration
Bilateral symptoms
	Visual loss
	Proximal limb weakness with face, hands and feet spared
88
Q

What scan is used to diagnose a stroke?

A

Non contrast cranial CT : detects acute hemorrhage but cannot reliably identify early ischemia

89
Q

What can MRI show about a stroke?

A

Diffusion-weighted imaging (DWI) identifies ischemia earlier than CT (within 3–30 minutes after onset)
Detects hyper acute haemorrhage

90
Q

What is the pathology of ischemic stroke?

A

Infarction
Liquefactive necrosis - due to increased lysosomes and decreased connective tissue support in the brain - Caused by neutrophilic release of lysosomal enzymes that digest tissue. Characterized histologically by macrophages and cellular debris (early) followed by cystic spaces (late)
Cystic cavity formation

91
Q

What is the mechanism for selective neuronal necrosis?

A

Transient ischemia with subsequent reperfusion (e.g., resuscitation following cardiac arrest)
Increased metabolic demand and neurotoxicity due to the release of excitatory neurotransmitters (e.g., status epilepticus)
Certain neurons are more susceptible to ischemic injury as a result of cell-specific features (e.g., higher metabolic demand, absence of heat shock proteins)
Pyramidal cells of the hippocampus: damage causes anterograde amnesia
Purkinje cells of the cerebellum: damage causes intention tremor, nystagmus, and ataxia
Pyramidal cells of neocortex: symptoms depend on the affected brain region

92
Q

What is the mechanism for reperfusion injury?

A

Injury which increases the permeability of cell membranes so you get more diffiusion across membranes and so more oedema and swelling
Reintroducing oxygen turn causes production of more reactive oxygen species which leads to further inflammation and therefore tissue damage and you enter a vicious circle that gets exponentially worse as both mechanism feed back to into each other to cause more tissue damage
The breakdown of the cell membrane further causes the release of intracellular potassium which can then lead to high serum potassium causing hyperkalaemia

93
Q

What is IV thrombolytic therapy?

A

Intravenous recombinant tissue plasminogen activator (rtPA) alteplase

94
Q

What are the complications of thrombolytic therapy?

A

Intracranial and extracranial hemorrhage

Angioedema

95
Q

What is the criteria for IV thrombolytic therapy?

A

Onset of symptoms ≤ 4 hours (therapeutic window of thrombolytic therapy )
Age ≥ 18 years

96
Q

What is the exclusion criteria for IV thrombolytic therapy?

A

Previous intracranial hemorrhage
Head trauma or stroke (within the past 3 months)
Recent intracranial or intraspinal surgery
Arterial puncture at noncompressible site (within the past 7 days)
Intracranial neoplasm, arteriovenous malformation, or aneurysm
Intracranial bleeding
Active internal bleeding or bleeding diathesis
Hypertension > 185/110 mm Hg
Anticoagulation (prolonged PTT or INR > 1.7)
Low platelet count
Hypoglycemia < 50 mg/dL or hyperglycemia > 400 mg/dL
Minor stroke or TIA

97
Q

What is the procedure for IV thrombolytic therapy?

A

Fibrinolysis, preferably with recombinant tissue-type plasminogen activator (tPA), e.g., alteplase
Most commonly systemic infusion via IV catheter

98
Q

What is Intra-arterial thrombolysis?

A

Indicated in patients who are not eligible for IV thrombolytic therapy
Procedure: intra-arterial administration of tPA close to the vessel occlusion within 6 hours of symptom onset

99
Q

When would a mechanical thrombectomy be appropriate?

A

Indicated in patients with proximal large artery occlusion in the anterior cerebral circulation (usually in addition to IV thrombolytic therapy)

100
Q

How many stroke survivors leave hospital with a disability?

A

2/3

101
Q

What is the WHO definition of a stroke?

A

A clinical syndrome characterised by the rapid onset of focal or global cerebral deficit lasting over 24 hours

Years 1+2 (21 decks)

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