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Psychiatry > Dementia > Flashcards

Dementia Flashcards

1
Q

What is subcortical dementia?

A

Subcortical dementia is a clinical syndrome characterized by slowness of mental processing, forgetfulness, impaired cognition, apathy, and depression.

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2
Q

Which blood tests are first line in investigating delirium?

A

FBC (anaemia), U&Es (hyponatraemia and hypercalcaemia, dehydration, porphryia), Urine dip (INFECTION), MSU, CXR and ECG (cardiac failure). See next question for causes of delirium!

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3
Q

What are the causes of delirium (random ones that you wouldn’t think of- obvious ones not included)?

A

Anxiolytics-hypnotics, anticholinergics, diuretics, steroids, digoxin, TCAs, MAOIS, L-dopa, polypharmacy, renal failure, hepatice/resp/cardiac failure, porphyria, malaria, HIV, Cushings, DKA, hypo perfusion states eg stress and sleep deprivation, faecal impaction etc etc.

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4
Q

What is the drug of choice when patient is agitated, anxious or aggressive or psychotic?

A

Haloperidol (because of its minimal anticholinergic side-effects) Should be kept to a minimum 0.5mg pRN

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5
Q

What is dementia?

A

Syndrome due to disease of the brain, progressive nature where disturbance of multiple higher cortical functions. CONSCIOUSNESS IS NOT CLOUDED.

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6
Q

What is dyscalculia?

A

Difficulties with maths

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7
Q

What is Diogene’s syndrome?

A

Is a disorder characterized by extreme self-neglect, domestic squalor, social withdrawal, apathy, compulsive hoarding of garbage or animals, and lack of shame. Sufferers may also display symptoms of catatonia. (SENILE SELF-NEGLECT)

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8
Q

What perceptional abnormalities are seen in patients with dementia?

A

Visual and auditory agnosia, visuospatial difficulties, body hemineglect, inability to recognise faces (proopagnoais), illusions, hallucinations (often visual), cortical blindness.

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9
Q

What is cortical blindness?

A

Is the total or partial loss of vision in a normal-appearing eye caused by damage to the brain’s occipital cortex. Cortical blindness can be acquired or congenital, and may also be transient in certain instances.

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10
Q

Where is Brocas area and what does it control?

A

Frontal lobe- expressive language

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11
Q

Where is wernickes area and what does it control?

A

Temporal lobe- language comprehension so you can get receptive dysphasia. And parietal lobe!

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12
Q

Which lobe controls voluntary movements?

A

Frontal

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13
Q

Which lobe controls spatial orientation, perception?

A

Parietal

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14
Q

Which lobe controls INITIAL cortical processing of tactile and proprioceptive information?

A

Parietal

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15
Q

Which lobe controls vision?

A

Occipital

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16
Q

Which motor impairments can happen in dementia?

A

Apraxia, spastic paresis, urinary incontinence

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17
Q

Name the PRIMARY dementias?

A

Alzheimers, dementia with lewy bodies and parkinsons, picks and other frontotemporals and huntington’s.

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18
Q

Name the SECONDARY dementias?

A

Vascular, AIDS, lyme, neurosyphilis, cranial arteritis, encephalopathy, MS, tumours, metabolic causes, endocrine, toxic, trauma, NPH, radiation, anoxia (no o2)

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19
Q

What is the neuropathology for alzheimer’s disease?

A

Cholinergic deficit, symmetrical cortical atrophy. Extracellular senile plaques and intracellular neurofibrillary tangles- (seen in normal ageing but more numerous in alzheimers!!) Other abnormalities include glial proliferation, granulovascular degeneration and Hirano inclusion bodies.

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20
Q

Where is the cortical atrophy initially more pronounced in alzheimer’s?

A

Temporal and parietal lobes

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21
Q

What do the senile plaques consist of?

A

They consist of core beta-amyloid surrounded by filamentous material.

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22
Q

What do the neurofibrillary tangles consist of?

A

Coiled filaments of abnormally phosphorylated microtubule-associated protein tau (tau is also found in picks bodies).

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23
Q

Who is alzheimer’s more common in men or women?

A

Women 2:1

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24
Q

Which may be protective factors in alzheimer’s?

A

Healthy life style, high educational attainment, NSAIDS, HRT and vitamins C& E

25
Q

Is head injury a risk factor for alzheimer’s?

A

yes

26
Q

Which genetic factors are there for alzheimer’s?

A

Inheritance of the e4 allele of apoliprotein E on chromosome 19- risk factor for the common sporadic late-onset form of the disease.
Also, mutations in the beta-amyloid precursor protein APP gene on chromosome 21, in the presenilin-1 gene on chromosome 14, and in the presenilin-2 gene on chromosome 1 are involved in rare, early onset autosomal dominant forms of the disease.

27
Q

Which inherited allele is protective?

A

e2

28
Q

From this, why could alzheimer’s be more common in Down’s?

A

Having an extra copy of the APP gene on chromosome 21 may increase production of beta-amyloid, triggering the chain of biological events leading to Alzheimer’s.

29
Q

What is the second most common dementia’s?

A

Dementia with lewy bodies. (DLB)

30
Q

What are lewy bodies?

A

Intracellular eosinophilic inclusions consisting of abnormally phosphorylated neurofilament proteins aggregated with ubiquitin and alpha-synuclein.

31
Q

What other neuropathology in seen in DLB?

A

Associated neuronal loss leading to cholinergic deficit but MINIMAL cortical atrophy.

32
Q

Compare alzheimer’s and DLB neuropathology.

A

Senile plaques may be present in DLB but neurofibrillary tangles are not marked feature in DLB like in alzheimer’s.

33
Q

Where are lewy bodies commonly found in DLB?

A

Numerous in the cortical areas (esp layers 4 & 5), the cingulate gyrus and the insular cortex.

34
Q

Where are lewy bodies found in the brain in parkinsons?

A

More numerous in the basal ganglia.

35
Q

What are the clinical features of DLB?

A

Marked fluctuation in cognitive impairment and alertness, vivid visual hallucinations, early parkinsonism and neuroleptic sensitivity, frequent fails and faints. (NB memory loss may NOT be a marked feature in the early stages of DLB!)

36
Q

What is the peak onset for Picks dementia (fronto-temporal)?

A

45-60 years of age. Also more common in females.

37
Q

What is the neuropathology in Picks?

A

Selective often asymmetrical ‘knife-blade’ atrophy and neuronal loss and gliosis affecting the frontal and temporal lobes. There are characteristic ‘ballooned’ neurons called pick cells and tau-positive neuronal inclusions called pick bodies but NO senile plaques or neurofibrillary tangles as seen in alzheimer’s.

38
Q

What are the clinical features seen in Picks?

A

Personality disturbances, eating disturbances, cognitive impairment, language difficulties (expressive Brocas is in frontal lobe) and (receptive in temporal), mood changes and motor signs. Memory is relatively SPARED

39
Q

When is the usual onset of Huntingtons?

A

Fourth or fifth decade

40
Q

What is the neuropathology in Hungtintons?

A

Abnormal huntington protein leads to the degeneration of neurone, especially in the caudate nucleus and putamen and in the cerebral cortex. Degeneration in the caudate and putamen leads to movement disorder, degeneration in the cerebral cortex leads to dementia.

41
Q

How does the abnormal huntington protein develop?

A

Expansion of CAG (cytosine-adenine-guanine) triplet repeats in the gene coding for the Huntingtin protein results in an abnormal protein

42
Q

What is the genetic picture with huntingtons?

A

Autosomal dominant neuro-degenerative disorder involving 36 or more CAG trinucleotide repeats encoding the glutamine in the hungtintin gene on chromosome 4. As the number of CAG increases, (one gen to the next in the paternal line), the age of onset decreases.

43
Q

What are the clinical features seen in huntington’s?

A

Choreiform movements, progressive dementia and other psychiatric disturbances, notable early depression and behavioural problems.

44
Q

Which is the third most common type of dementia?

A

Vascular. more common in men.

45
Q

What is mixed dementia?

A

Vascular and alzheimers

46
Q

What is the neuropathology seen in vascular?

A

Focal disease resulting from single or multiple thrombotic or embolic infarcts. Small vessel disease leads to diffuse disease (binswanger disease and lacunar state)

47
Q

What are the clinical features associated with vascular dementia?

A

Abrupt onset and stepwise progression. Clinical features obviously depend on where the infarcts happen. Insight is usually retained until late.

48
Q

Why has vascular dementia a shorter survival time than alzheimer’s?

A

Increased comorbidity associated with vascular.

49
Q

What is mild cognitive impairment?

A

Subtle but measurable memory difficulties seen in normal ageing but less severe than those in alzheimer’s. No deterioration in overall thinking and judgement or in the level of functioning. Risk of conversion to alzheimer’s is 15%

50
Q

What is paraphrenia?

A

Paraphrenia is a mental disorder characterized by an organized system of paranoid delusions with or without hallucinations (the positive symptoms of schizophrenia) without deterioration of intellect or personality (its negative symptom).

51
Q

What is pseudo dementia?

A

Pseudodementia is a situation where a person who has depression also has cognitive impairment that looks like dementia.

52
Q

What is amnestic syndrome?

A

a mental disorder characterized by impairment in short- and long-term memory, with anterograde and sometimes retrograde amnesia, occurring in a normal state of consciousness. Disorientation, confabulation, and a lack of insight into the memory deficit may be present. The most common cause is thiamine deficiency associated with chronic alcohol abuse (alcohol amnestic disorder, korsakoff’s syndrome), but the syndrome may result from any pathologic process causing bilateral damage to certain structures in the medial temporal lobe and diencephalon, including head trauma, brain tumors, infarction, cerebral hypoxia, carbon monoxide poisoning, and herpes simplex encephalitis. Basically brain damage causing amnesia

53
Q

Which imaging tool is best to suggest normal pressure hydrocephalus?

A

CT

54
Q

Random but what are the clinical features of selenium deficiency?

A

Selenium is necessary for the conversion of the thyroid hormone thyroxine (T4) into its more active counterpart, triiodothyronine, and as such a deficiency can cause symptoms of hypothyroidism, including extreme fatigue, mental slowing, goiter, cretinism, and recurrent miscarriage.

55
Q

What is selegiline?

A

Selective irreversible monoamine oxidase type B inhibitor

56
Q

What are the cholinesterase inhibitors used to treat dementia?

A

Donepezil, rivastigmine and galantamine

57
Q

How do cholinesterase inhibitors work?

A

Increasing cholinergic neurotransmission and can temporarily improve cognitive performance and behavioural problems in alzheimer’s and DLB

58
Q

What is memantine?

A

NMDA agonist that may protect neurone from glutamate mediated neurotoxicity.

Psychiatry (24 decks)

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