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mbchb - year 2 > Week 4 P&I > Flashcards

Week 4 P&I Flashcards

1
Q

What is cognition?

A

the process of thinking, knowing, understanding and making sense of the world around you

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2
Q

What 4 categories can attention be classified into?

A

Arousal, sustained attention, divided attention, selective attention

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3
Q

What are the 6 specific tests for attention?

A

Orientation in time and place, digit span, reciting months of the year, serial 7s, spell WORLD backwards, the STROOP test

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4
Q

What is the STROOP test?

A

Lots of multicoloured words on the page and the patient has to tell you what colour the word is rather than just reading the word

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5
Q

What is anterograde memory loss?

A

Memory loss for newly gained information (information gained after an injury occurs is forgotten)

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6
Q

What is retrograde memory loss?

A

Memory loss of old information (information from before the injury is lost)

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7
Q

What is Ribot’s gradient?

A

More recent material is forgotten first and then eventually they forget older information

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8
Q

What area of the brain is involved in short-term (working) memory?

A

The frontal lobe

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9
Q

What areas (3) of the brain is involved in implicit memory (a type of long term)

A

Basal ganglia, cerebellum, cortex

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10
Q

Where are episodic memory stores found?

A

medial temporal lobe

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11
Q

Where are semantic memory stores found?

A

anterior temporal lobe

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12
Q

What is dyspraxia?

A

Inability to move a body part despite having intact motor and sensory function.

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13
Q

What are 6 visuospatial deficits?

A

Topographical disorientation, difficulties with dressing, mis-reaching for objects, visual neglect, visual object agnosia, prosopagnosia

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14
Q

What is topographical disorientation?

A

Problems finding their way around

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15
Q

What is dressing apraxia?

A

When someone has difficulties with dressing. This is not a problem with praxis its an issue with visuospatial

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16
Q

What areas of the brain cause visuospatial deficits?

A

Parietal and temporal lobe

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17
Q

What is visual neglect?

A

patient could only eat half of their plate or dress half of their body

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18
Q

What is prosopagnosia?

A

Patients cant recognise familiar faces but might be able to recognise their voice

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19
Q

What is the ACE?

A

A 100 point test that is more sensitive than a MMSE and can pick up patients with mild impairment

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20
Q

What are the 2 cut off scores of the ACE?

A

88 and 82

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21
Q

What is a MMSE?

A

Mini-mental state examination gives a score out of 30. It is more reliable between different raters and you can expect similar scores from different doctors carrying it out.

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22
Q

What is the MMSE more heavily weighted towards?

A

memory and attention and is not very good for executive function

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23
Q

What are some hallmark feature of delirium?

A

Impaired consciousness, fluctuation, acute onset, visual hallucinations, affect changes.

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24
Q

What are the two possible subtypes of delirium?

A

hyperactive (can be violent) and hypoactive (sleepy and could be misdiagnosed as depression)

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25
Q

How can delirium be managed non-pharmacologically? (4)

A
  • Noise control and lighting
  • reality orientation
  • Limit variation in staff
  • avoid ward transfers
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26
Q

what are the options for pharmacological management of delirium?

A

Antipsychotics, benzodiazepines, specific treatment of underlying cause, melatonin, trazodone

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27
Q

Why is melatonin used in the treatment of delirium?

A

Melatonin levels are abnormal in delirium and dementia and supplementing it can help get a more normal sleep cycle

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28
Q

What are 2 examples of antipsychotics used in the treatment of someone who is actively hallucinating because of delirium?

A

Haloperidol, risperidone

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29
Q

What are the 2 classes of drugs used to treat dementia?

A

Cholinesterase inhibitors and partial glutamate antagonist

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30
Q

What do cholinesterase inhibitors do?

A

Block cholinesterase which breaks down Ach

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31
Q

What limits the efficacy of cholinesterase inhibitors?

A

Their toxicity

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32
Q

What are potential side effects of donepezil (cholinesterase inhibitor)?

A

Nausea and vomiting, diarrhoea, muscle cramps, dizziness, fatigue and anorexia

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33
Q

When is donepezil contraindicated?

A

In patients who have already had some kind of GI disease and is not usually given to patients who smoke

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34
Q

What types of dementia is donepezil used in?

cholinesterase inhibitor

A
  • Alzheimer’s mixed with vascular dementia

- PDD (NOT DLB)

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35
Q

What is rivastigmine licenced for?

A

DLB

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36
Q

What is glutamate?

A

An amino acid that is also the major excitatory transmitter

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37
Q

What are two receptors important in learning?

A

AMPA and NMDA

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38
Q

What are AMPA and NMDA permeable to?

A

Ions (Sodium and potassium) but AMPA is not permeable to calcium, only NMDA is.

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39
Q

What is excessive activation of the AMPA receptor called?

A

Excitotoxicity

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40
Q

What is the AMPA receptor mostly involved in?

A

Most Fast-synaptic transmission

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41
Q

What is the ion channel of the NMDA receptor blocked by?

A

Magnesium

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42
Q

What does memantine do?

A

Reduces the action potential of the NMDA receptor which prevents the hyperexcitation of it.

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43
Q

How is glutamate involved in AD?

A

Reduced glutamate clearance in AD brains so chronic overactivity could play a part in the pathological process

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44
Q

How does an NMDA receptor antagonist improve memory?

A

Restores homeostasis in the glutamatergic system - too little activation is bad but too much is even worse

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45
Q

What are potential side effects of memantine?

A

Dizziness, headache, constipation, somnolence and hypertension

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46
Q

What causes behavioural problems in dementia?

A

An interaction between an increasingly confused and vulnerable person and their environment and the reactions of carers.

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47
Q

What is melatonin licenced for?

A

Short term treatment of insomnia in people over 55 (when endogenous melatonin may be reduced)

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48
Q

Why are SSRIs used in dementia?

A

Useful for depression and apathy that can develop. sertraline and citalopram are associated with a reduction in agitation.

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49
Q

When do clinicians begin to consider prescribing memantine?

A

MMSE score below 20

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50
Q

What antipsychotics can be used in behavioural and psychological symptoms of dementia (BPSD)

A

atypicals like Risperidone and aripiprazole

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51
Q

When do clinicians move from donepezil to rivastigmine?

A

If there is side effects with donepezil or it doesn’t work, tend to move onto a rivastigmine patch

52
Q

When should antipsychotics be used (in dementia)?

A

Severe agitation that is a risk to themselves or others, psychosis

53
Q

when should antipsychotics NOT be used (in dementia)?

A

insomnia, wandering, abnormal vocalisations

54
Q

What drugs are most effective in the treatment of dementia?

A

Drugs that target the Acetylcholine system

55
Q

What happens when there is neurodegeneration in the basal ganglia?

A

Movement disorder e.g. Parkinson’s, Huntington’s

56
Q

What happens when there is neurodegeneration in the cerebellum and spinal cord?

A

Ataxia

57
Q

What happens when there is neurodegeneration in the cortex?

A

Alzheimer’s, FTD

58
Q

When does increased forgetfulness start?

A

Age 50

59
Q

What changes occur due to brain ageing?

A

Slowing of response times, physical changes (vision, hearing, sensory/motor impairment)

60
Q

What are the potential differential diagnoses for dementia like behaviour?

A 
A - Alzheimer's
V - Vascular disease
D - Drugs, Depression, Delirium
E - Ethanol
M - Metabolic
E - Endocrine 
N - Neurologic
T - Tumour, Toxin, Trauma
I - Infection 
A- Autoimmune
61
Q

What are some reversible causes of dementia? (5)

A

Hypothyroidism, Drugs, Tumours, neurosyphilis, chronic subdural haematoma

62
Q

How can a patient be described as potentially having Alzheimer’s?

A

Significant decline in cognition that interferes with independence in everyday activities

63
Q

What is the onset of AD like?

A

Insidious - family members can have varying opinions on when it started

64
Q

What are the initial and most prominent deficits in a patient with suspected AD?

A
  • Amnestic (episodic memory alteration)

- Non-amnestic - progressive aphasia, visuospatial deficit, executive dysfunction

65
Q

What can vary between patients with AD?`

A
  • Age of onset
  • Disease progression
  • Disease duration
  • Symptoms at onset
66
Q

What does the brain look like in AD?

A
  • A marked reduction in weight and you can see atrophy.
  • The ratio of the weight of the forebrain to the hind brain is different in Alzheimer’s
  • Ventriculomegaly
  • Sulcal spaces are enlarged as the Gyri have shrunk
67
Q

What protein is involved in neurofibrillary tangles?

A

Tau protein (an abnormal version)

68
Q

What is involved in the formation of neurytic plaques?

A

B-amyloid

69
Q

What symptoms can be seen in mild AD? (7)

A

memory loss, confusion, trouble handling money, poor judgment, mood changes, and anxiety.

70
Q

What symptoms can be seen in moderate AD? (7)

A

Increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements.

71
Q

What happens in severe AD?

A
  • Severe cortical atrophy.
  • Pathology throughout the neocortex.
  • Patients are completely dependent requiring nursing home care.
  • Weight loss, seizures, increased sleeping, loss of bladder and bowel control.
  • Death usually occurs from pneumonia
72
Q

What are the risk factors for (Alzheimer’s?) dementia?

A
  • Increasing age
  • Genetics
  • Downs syndrome
  • Female sex (2/3 of those with dementia are female)
  • Head injury
73
Q

What is the progression of vascular dementia like?

A

Stepwise - patient functions at a set level for a period of time and then this level drops of and they remain here for a period of time.
These are said to be in line with ischemic insults to the brain (more infarcts)

74
Q

What is one of the earliest histological signs of ischaemic insult?

A

Shrunken, red eosinophilic neurons.

These are usually bigger and more basophilic

75
Q

What are signs of dementia with Lewy bodies?

A
  • Progressive cognitive decline
  • fluctuating consciousness
  • Visual hallucinations
  • Parkinsonism
76
Q

What can be seen in the brainstem in DLB?

A

Pallor of brainstem pigmented nuclei

77
Q

What signs/ symptoms can be seen in a patient with Parkinson’s disease with dementia?

A
  • Bradykinesia, rigidity, tremor
  • Autonomic dysfunction
  • Cognitive impairment
78
Q

What protein causes Lewy body disorders?

A

A-synuclein

79
Q

What forms the tertiary structure of a protein?

A

Interactions between side chains of various amino acids - in particular disulphide bonds formed between cysteine groups

80
Q

What is protein conformation determined by?

A

Its primary structure

81
Q

What is an important determinant of final conformation?

A

Hydrophobicity - you want hydrophobic parts on the inside and the hydrophilic parts are on the outside

82
Q

Why is there an increased tendency for proteins to aggregate?

A

They don’t have the molecular space to fold (although they clearly do)

83
Q

What is a molecular chaperone?

A

Any protein that interacts with, stabilises or helps another protein to acquire its functionally active conformation, without being present in its final structure

84
Q

What are 5 proteome-maintenance functions?

A
  • de novo folding
  • refolding
  • oligomeric assembly
  • protein trafficking
  • proteolytic degradation
85
Q

What is the first thing that happens to a newly synthesised glycoprotein?

A

It is immediately glycosylated

86
Q

What happens to a newly synthesised glycoprotein after is it glycosylated?

A

A group of enzymes (glucosidases I & II) cleave off these sugar molecules which provides a binding site for the chaperones

87
Q

What happens after the chaperones have helped with protein folding?

A

Glucosidase II cleaves off the sugar group and this removes the chaperones too

88
Q

What happens if the protein is correctly folded?

A

It will be allowed to leave the ER and do its job

89
Q

What enzyme is responsible for deciding if proteins are correctly folded?

A

Glucosyltransferase

90
Q

How does glucosyltransferase check that proteins are folded correctly?

A

by checking if there are hydrophobic residues on the outside of the protein.

91
Q

What happens if glucosyltransferase detects hydrophobic residues on the outside of a protein?

A

it goes back to the start of the folding process

92
Q

How are proteins that need to be degraded sent to the proteasome?

A

They get a ubiquitin tag

93
Q

What are the 5 steps in a protein being tagged and degraded?

A
  1. Polyubiquitination
  2. polyUb-protein recognised by CAP
  3. polyUb removed; protein unfolded
  4. protein threaded through proteasome
  5. proteolysis
94
Q

How many ubiquitin molecules must be attached to a lysine residue?

A

at least 4

95
Q

What is a Proteinopathy?

A

accumulation of misfolded proteins resulting in aggregates, thereby gaining toxic activity or losing the normal function

96
Q

What is the common characteristic of all amyloidoses?

A

The collection of plaques of insoluble protein in the extracellular tissue which cannot be broken down by enzymes.

97
Q

What are amyloid plaques made up of?

A

Long filaments (fibrils) that are formed from densely packed B-sheets of identical proteins

98
Q

What is APP?

A

A transmembrane protein that has unknown function and is found in all neurons.

99
Q

What happens to APP once it is out of the transmembrane?

A

It is cleaved to form lots of different proteins with different functions

100
Q

Where is APP cleaved in the non-amyloidogenic state?

A

The extracellular domain just above the transmembrane domain

101
Q

What cleaves APP in the non-amyloidogenic state?

A

alpha-secretases

102
Q

What happens with cleaving of APP in the amyloidogenic state?

A

cleaves again just above the transmembrane domain this time by beta-secretases but is also cleaved within the transmembrane domain by gamma-secretases releasing a small part of the protein – amyloid beta peptide.

103
Q

What is the normal function of the tau protein?

A

as a bridge between the microtubules in axons, ensuring they run straight and parallel to each other

104
Q

Where is tau expressed?

A

Throughout the CNS

105
Q

Where is tau predominantly found?

A

Neuronal axons

106
Q

What happens if tau is phosphorylated?

A

it dissociates from microtubules meaning it destabilises it which means they can lengthen or shorten etc.

107
Q

What negatively regulates the binding of tau to microtubules?

A

Phosphorylation

108
Q

What happens if tau is hyper phosphorylated?

A

prevents tubulin binding and thereby results in the destabilization of microtubules. The hyperphosphorylation also leads to the tangles –> cell death

109
Q

What is the secondary structure of tau usually?

A

alpha helix but in abnormal cases it changes to beta sheets

110
Q

What are tauopathies characterised by?

A

Abnormal hyperphosphorylation of tau

111
Q

Where is alpha synuclein abundantly expressed?

A

The human brain - enriched at presynaptic terminals

112
Q

What does alpha synuclein do at presynaptic terminals?

A

binds lipids and regulates the release of synaptic vesicles

113
Q

What are alpha-synucleinopathies?

A

neurodegenerative diseases characterised by the abnormal accumulation of a-synuclein insoluble aggregates in neuronal or glial cells

114
Q

What are transmissible spongiform encephalopathies (TSEs)?

A

A family of rare, progressive & fatal neurodegenerative disorders

115
Q

What happens in transmissible spongiform encephalopathies (TSEs)?

A

loss of motor coordination and behavioural changes

116
Q

How can people get transmissible spongiform encephalopathies (TSEs)?

A

inherited, sporadic, acquired

117
Q

What does spongiform refer to in transmissible spongiform encephalopathies (TSEs)?

A

What the brain looks like

118
Q

What is the causative agent of transmissible spongiform encephalopathies (TSEs) believed to be?

A

Prions

119
Q

What are prions?

A

abnormal, pathogenic agents that are transmissible and are able to induce abnormal folding of specific normal cellular proteins called prion proteins

120
Q

Where are prion proteins most abundantly found?

A

In the brain

121
Q

What does the abnormal folding of the prion proteins lead to?

A

brain damage and the characteristic signs and symptoms of the disease

122
Q

What is the normal prion protein?

A

PrPc

123
Q

What is the infectious prion protein?

A

PrPsc

124
Q

What does the infectious prion protein go on to form?

A

prion rods which form plaques leading to neuron disease

125
Q

What characteristic of infectious prion proteins makes them so infectious?

A

They can self-aggregate and propagate

mbchb - year 2 (25 decks)

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