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Flashcards in dementia Deck (56):
1

dementia and age?q

it is a disease of aging. 50% chance of having dementia by 85

2

dementia continuum

normal aging decline > mild cognitive impairment > dementia

3

what are some normal age associated changes

difficulty retrieving words. slower processing speed. difficulty sustaining attention with distractions. learning something new takes more effort. there should be no functional impairment.

4

mild cognitive impairment

memory complaint corroborated. objective memory impairment for age and education. preserved general cognition. normal activities of daily living. not demented, although some do progress to dementia

5

amnestic MCI

memory loss, but not enough to meet dementia criteria. progresses to AD in 10-15%. maybe the earliest phase of AD>

6

what are the criteria for dementia

memory decline and impairment. at least one of the following: aphasia, apraxia. decline in memory, cognition, complex attention, executive function, learning/memory, language, perceptual/motor or social cognition.
this is an impairment.

7

early onset AD

between 30-60. rare. familial in most.

8

what genes/chromosomes associated with early onset AD.

1 - presinilin 2
14 - presinilin 1
21 - amyloid precursor.

9

late onset AD

most common form. develops after age 60. chromosome 19 seems to be involved. this is E4 gene.

10

alzheimers

most common cause of dementia. deficits in recent memory that progresses to global impairment of cognition. usually sporadic and late onset. neuronal and synaptic loss effects the cortical and subcortical areas.

11

gross affects of AD

cerebral atrophy, especially affecting the temporal, parietal, and frontal areas. this is found with ventricular enlargement. flattening of gyri enlarging sulci. the hippocampus is greatly atrophied.

12

microscopic affects of AD

amyloid plaques, neurofibrillary tangles, granulovacular degeneration. hirano bodies.

13

where are the A-beta plaques?

they are extracellular and often associated with dystrophic neurites.

14

where are the neurofibrilary tangles and what are they?

they are intracellular, in the cytoplasm. they are composed of hyperphosphorylated Tau. for AD they are in the shape of the neuron.

15

what is characteristic about the plaques?

they have apple-green birefringence this confirms the presence of amyloid. perivascualr causes bleeding.

16

what is Pick's disease?

this is a tauopathy. it is frontal-temporal lobe dementia. the occipital and parietal lobes are spared. typical knife-edge gyri

17

what are the risk factors for AD?

increasing age, females, family history, fewer years of education, lowr income, depression or emotional illnesses, head injury, low seri, folate/b12, elevated homocysteine, postop delirium, alcohol abuse.

18

what are three spheres of dementia

impairments in cognition, function, and behavior.

19

Pick's FTLD

insidious onset, gradual progression, early decline in social interpersonal conduct, loss of regulation of interpersonal conduct with loss of insight. early emotional blunting. behavioral abnormalities. memory loss may occur later but is not as pronounce as AD

20

treatments for FTLD

NO ACH -DOESNT WORK. use divalproex for behavior. SSRI for irritability.

21

AD psychopharm

ACH inhbitors, NMDA antagonists.

22

why does acetylchoine work?

nucleus basal is of maynert degeneration in AD causes widespread loss of ACH. replenishing that seems to resolve some symptoms.

23

common therapy

donepezil

24

why use NMDA antagonists?

remember blandens paper. this may be excitotoxicity issue.

25

what is a common NMDA antagonist used?

memantine

26

why do we not use antipsychotics?

because there are major risks involved. cardiovascular events

27

vascular dementia

multiinfarct dementia. cerebral amyloid angiopathy. HTN related small vessel disease. most common after AD. step-wise progression. can be abrupt after cerebrovascular event. emotional lability.

28

which arteries are affect the most by HTN in the brain?

the lenticulostriates.

29

how to treat vascular?

focus on reducing the risks. BP, smoking, blood sugar, diet and exercise.

30

treatment for vascular

donepezil. and other cholinesterase inhibitors.

31

lewy body dementia

intracellular fibrillary deposits of presynaptic protein alpha-syn. primarily sporadic. parkinsons and LBD. everyone that has one develops the other, if they live long enough.

32

cardinal symptoms of parkinsons

TRAP. tremor, rigidity, akinesia, postural instability. shuffling gait. dementia also occurs. this is caused by dopaminergic deficit. responds to L-dopa. substantia nigra pars compacta pallor.

33

characteristics of lewy body

they are intracellular inclusions of alpha-syn/

34

dementia with lewy bodies LBD.

sporadic, late onset, memory less affected than AD. frontal and subcortical features such as deficits in alertness and attention are common. there are also pronounced fluctuations in symptoms. common with vivid hallucinations and delusions. motor symptoms of PD are variably present. there is nigral pallor, with less cortical atrophy.

35

clinical aspects of LBD

short term memory loss with gradual onset. visual hallucinations, cognitive fluctuations, REM sleep disorder. frequent falls, autonomic dysfunction.

36

what to treat

Ach works here for support. dopa for movement. AVOID ANTIs for increased sensitivity. REM sleep can use clonazepam

37

traumatic brain injury incidence

1.7 million in the US.

38

causes of TBI

falls, MVA, assaults

39

what is TBI

efined as a blow or jolt to the head or a penetrating head injury that disrupts the function of the brain. Not all blows or jolts to the head result in a TBI. The severity of such an injury may range from "mild," i.e., a brief change in mental status or consciousness to "severe," i.e., an extended period of unconsciousness or amnesia after the injury. A TBI can result in short or long-term problems with independent function.

40

Compression Fracture

A depressed skull fracture in which the broken bone exerts pressure on the brain.

41

Concussion

The common result of a blow to the head or sudden deceleration usually causing an altered mental state, either temporary or prolonged. Physiologic or anatomic disruption of connections between some nerve cells in the brain may occur. Often used by the public to refer to a brief loss of consciousness.

42

Contrecoup

Bruising or damage to brain tissue on the side opposite where the blow was struck.

43

Diffuse Brain Injury

Injury to cells in many areas of the brain rather than in one specific location.

44

Hematoma

Rupture of a blood vessel leading to the collection of blood in brain tissues or empty spaces. There are several types of hematoma:

45

Epidural

– Outside the brain and its fibrous covering, the dura, but under the skull.

46

Subdural

– Between the brain and its fibrous covering (dura).

47

Intracerebral

– In the brain tissue.

48

Subarachnoid

– Around the surfaces of the brain, between the dura and arachnoid membranes.

49

how does the brain heal?

some parts of the brain adapt to take over other functions.

50

rehabilitation is focused on what?

relearning and adapting

51

normal MMSE

27-30

52

mild dysfunction MMSE

20-30

53

moderate MMSE

10-20

54

severe MMSE

<10

55

what is the acronym for activities of daily living and what does it stand for?

DEATH.
dressing, eating, ambulating, toileting, hygiene.

56

what is the acronym for iADLS and what does it stand for

SHAFT
shopping, housekeeping, accounting, food prep, transportation.