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Medicine Year 2 > Scenario 30 > Flashcards

Scenario 30 Flashcards

1
Q

What are the 5 main symptoms in Dementia?

A

Amnesia, Apraxia, Agnosia, Aphasia, Associated factors

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2
Q

What is meant by amnesia?

A

Forgetting recent events and new information, long term better

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3
Q

What is meant by apraxia?

A

Difficulty in performing co ordinated tasks despite intact motor and sensory systems such as eating, dressing

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4
Q

What is meant by agnosia?

A

Inability to understand the significance of sensory stimuli- misidentification of objects by feel, misidentification of faces, own body parts, R/L disorientation

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5
Q

What is meant by aphasia?

A

Simplified use of language, less description, word finding problems, naming difficulties, complete loss of communication

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6
Q

What are the other associated features?

A

Aggression, wandering, sexual disinhibition, eating, sleeping, delusion, hallucinations, mood disorders

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7
Q

What is anterograde amnesia?

A

Inability to form new memories after the event

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8
Q

What are the steps in memory formation?

A

Sensory register, short term memory and then long term memory

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9
Q

How long is information stored in the sensory register

A

500ms

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10
Q

How can you test the function of the sensory register?

A

Use the probe memory test (grid of numbers then disappear and put a probe at a line want to recall) Remember if early

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11
Q

What is the function of the sensory register?

A

Selective attention, filling in gaps of saccadic eye movements

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12
Q

What is the storage capacity of short term memory?

A

7+/- 2 and forget in 30 seconds if we dont do anything with it

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13
Q

What are the components of short term memory?

A 
Phonological loop (acoustic code)- phonological similarity, word length etc 
VSSP (visuospatial sketchpad)- visual and spacial information
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14
Q

How is the information from these two parts integrated?

A

Episodic buffer- capacity, rehearsal maintenance and access to conscious awareness

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15
Q

What is stored in the long term memory?

A

Declarative memory and non declarative memory- flexible and accessible
Episodic or semantic (facts

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16
Q

What is declarative memory?

A

knowing what something is, life experiences, comparison

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17
Q

What is non declarative memory?

A

procedural, skills and habits, perceptual learning, habitation or sensitisation

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18
Q

How to test short term memory?

A

Ask to recall a list of words- first and last remembered but after a delay forget the last- STM lost
Ask to read out a sequence with increasing number of digits, as soon as over the STM limit cannot be remembered

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19
Q

What do we see in patients with medial temporal lobe lesions?

A

Succeed in remembering what they have encountered as long as the material can be supported by the limited capacity of the STM system

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20
Q

What happens in hippocampal damage?

A

Problems with new declarative memory

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21
Q

Where does the initial perception and processing and the LT storage of a memory happen?

A

Neocortex

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22
Q

Where is reactivation of a memory first seen?

A

Hippocampus then neocortex

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23
Q

What is the prose passage recall test and what brain area is it testing?

A

Reading out a story and asking the patient to recall it- tests temporal lobe function (left)

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24
Q

What is digit span test and what brain area does it test?

A

Working up and repeating a sequence of digits (held in phonological loop)- frontal lobe

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25
Q

What is the card sorting test

A

Trying to work out the pattern of the cards being chosen- dorsolateral prefrontal cortex (executive function)

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26
Q

What is the verbal fluency test and what brain area is being tested?

A

Find words for a category- frontal in phoemic category, temporal in semantic category, Broca’s area and number of switched is dorsolateral prefrontal cortex

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27
Q

What is the Rey Osterreith complex figure and what area of the brain does it test?

A

Diagram that must be shown then drawn- temporal lobe (right)

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28
Q

What is the Kendrick object learning test and what area of the brain does it test?

A

Remember objects from a grid- temporal (test for dementia)

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29
Q

What is stroop and what area of the brain is involved?

A

Asked to read out colour of words not the words- frontal lobe

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30
Q

How many dementia sufferers have AD?

A

66% (of 750,000)

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31
Q

What are the main pathologies of AD?

A

Gross cerebral atrophy, senile plaques, neurofibrillary tangles

32
Q

Which areas of the brain are most atrophied?

A

Typically primary sensory/ motor areas and hippocampus

Cerebellum relatively spared

33
Q

What are the components of the plaques?

A

Central core of beta amyloid surrounded by abnormal swollen distorted neuronal processes called neuritis, start as non-aggregated no neurotoxic beta amyloid but the enzyme butyrycholinesterase may play an essential role in maturation

34
Q

What are neurofibrillary tangles?

A

Mainly affect glutamatergic neurone composed of abnormal fibrils measuring 10nm in diameter

35
Q

What do NF tangles consist of?

A

Abnormally phosphorylated tau and ubiquitin, cholinesterase’s and beta-amyloid 4 in neuronal cytoplasm

36
Q

Where are NF fibres found?

A

Layer II neurons of enterohinal cortes, hippocampus, amygdala and deeper layers of neocortex. In hippocampus involved in loss of ST memory
Basal forebrain neurons that provide most of cholinergic innervation to the cortex

37
Q

Why is there increased phosphorylation of tau in AD?

A

Due to underactivation of PP2 so it doesnt interact with microtubules and self aggregates instead- microtubule system no longer works

38
Q

What are the genetic factor contributing to AD?

A

APP on chromosome 21 which gives rise to Abeta in AD(found in plaques)
A beta is metabolised by alpha secretase then gamma secretes- non amyloidogenic but if beta secretes then gamma secretes can be amyloidogenic (forming an oligomer)

39
Q

What codes for the gamma secretase?

A

Presenilin 1 and 2 mutations account for the gamma secretase balance and also the delivery of synaptic vesicles to preseynaptic terminals (NT defect)

40
Q

What is a genetic risk factor for late onset AD?

A

Gene for APOE- synaptic repair and neuronal structure and cholinergic function E4 allele increases risk E4/E4- 95% chance

41
Q

What is the effect of AD on cholinergic transmission?

A

Although receptors well preserved ChAT activity, AChE activity Ach synthesis and choline uptake are reduced

42
Q

What is the effect of AD on glutamate-glutamine cycle?

A

Stains less for glutamine and glutaminase and neurons contain tangles. Difficult to treat as ubiquitous and too much glutamate is harmful. There is less production and less uptake, cause memory problems

43
Q

Other problems which could cause AD pathology?

A

Free radical production and mRNA mutations in beta amyloid

44
Q

What are anti dementia drugs based on?

A

Ach deficiency (aricept, exelon and remencyl- AchE inhibitors) or glutamate deficiency (Ebixa- NMDA anatagonist)

45
Q

What % of sufferers gain a benefit from anti dementia drugs?

A

60%

46
Q

What are important body changes during sleep?

A

Decrease alertness, temperature and potassium in urine and increase growth hormone, cortisol

47
Q

What are the features of REM sleep?

A

Frequent dreams, high levels of cortical activity and metabolic rate, increased brain temp but reduced body temp, irregular autonomic activity but net parasympathetic dominance, selective paralysis and loss of muscle tone and loss of some homeostatic reflexes

48
Q

What are some features of nREM sleep?

A

Few dreams, low levels of cortical activity and reduced metabolic rate, reduced brain temperature, autonomic output is dominated by parasymp tone, muscle tone normal, reflexes intact

49
Q

How many cycles of REM and nREM sleep are there?

A

4 sleep cycles

50
Q

How many stages of nonREM sleep are there?

A

4

51
Q

What is the pontine switch mechanism?

A

Upper brain nuclei mutually excite and inhibit each other. REM-on neurons are mutually inhibitory with the aRAS and the REM-on condition activates the thalamus and cholinergic basal forebrain arousal system (activates the cortex) and inhibits motor output causing paralysis by glycinergic interneurons in the spinal cord

52
Q

What are the role of orexins?

A

From the hypothalamic nuclei negatively regulate REM-on state and positively regulate REM-off neurons of the aRAS

53
Q

What are the mental signs of sleep loss?

A

Reduced motor control, paranoia, hallucinations, memory and learning difficulties

54
Q

What are the physical signs of sleep loss?

A

Increased metabolic rate, reduced immune function, weight changes

55
Q

What are the cellular purposes of sleep?

A

Metabolic reconstitution (restoring glycogen levels for energy, refilling NT stores, clearance of unwanted metabolic products), Neuroplasticity (consolidation or dissasembly of new synaptic connections), repair and reconstruction (tissue repair, immune regulation)

56
Q

What neuronal activity occurs during sleep and wakefulness?

A

Depends on the relationship between the activity in the cortex and thalamus when relatively hyperpolarised thalamic neurons fire in phasic bursts driving low freq cortical activity- sleep
The opposite in wakefulness- desynchronised and high freq

57
Q

What is the neuronal mechanism of arousal?

A

Excitatory input to cortical neurons or directly by thalamocortical projections
Direct cortical input to cortex from basal forebrain nuclei (cholinergic), hypothalamic nuclei, upper brainstem nuclei (dorsal raphe nuclei, locus correleus- monoamine) and reticular formation (NA and ACh)

58
Q

What is insomnia?

A

Insufficient quantity and/or quality of sleep- delayed onset, freq awakenings- transient, short term or chronic

59
Q

What is narcolepsy?

A

Excessive daytime sleepiness with or without cataplexy and often hypagogic hallucinations and sleep paralysis- rapid entry to REM sleep, often triggered by emotional stimuli

60
Q

What causes narcolepsy?

A

Good evidence that functional defect in orexin signalling system and may be autoimmune

61
Q

What is the treatment for narcolepsy?

A

stimulant drugs that potentiate monoamine systems but also including the CNS depressant sodium oxybate

62
Q

What are GABA PAMs?

A

Work by binding to an allosteric site on GABAa receptor and increasing its infinity for GABA so the associated cl channel opens more frequently

63
Q

What are the cons of GABA PAMs?

A

Dont mimic sleep exactly, cause drug dependence and withdrawal symptoms, safe in overdose alone but dangerous with other drugs

64
Q

What is the role of melatonin?

A

Act at melatonin receptors in SCN causing resetting of circadian clock rhythm

65
Q

What is the role of alcohol?

A

enhanced GABAa, inhibits NMDA, opens two pore domain K channels, reduced quality of sleep

66
Q

What are the role of orexin antagonist?

A

Blocks the orexin stimulation for arousal- high proportion of REM sleep

67
Q

What are the role of amphetamine like drugs in stimulation?

A

Inhibit uptake of monoamines reversing so uptakers release monoamines potentiating monoamine outputs from the aRAS system

68
Q

What are the symptoms of a coma due to?

A

resembles sleep usually a consequence of CNS malfunction including aRAS system

69
Q

What are the symptoms of locked in syndrome due to?

A

Cortical damage

70
Q

What are the symptoms of locked in syndrome due to?

A

Brain stem injury, usually extensive damage to the pons but the aRAS and cerebrum are spared

71
Q

What mechanism excites the brain stem and aRAS nuclei?

A

LNH and PNH using orexin

72
Q

How do the aRAS and brain stem respond?

A

Positive feedback exciting the hypothalamic neurons using monoamines, NA and 5-HT

73
Q

What is the function of the VLPO?

A

Inhibits aRAS using GABA

74
Q

What does inhibition of aRAS cause?

A

disinhibition of VLPO and increased VPLO activity- more inhibition of aRAS

75
Q

What is the role of the SCN/

A

Generates a circadian rhythm by innervating the PNH

76
Q

What is the tubomamillary nucleus?

A

Promotes wakefulness via histamine release by exciting aRAS and inhibiting VPLO neurons

77
Q

What is the role of adenosine?

A

Accumulates in the brain during wake periods and excited VPLO promoting sleep

Medicine Year 2 (19 decks)

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