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RRCCPA Clinical Medicine I > Dementia (Exam 2) > Flashcards

Dementia (Exam 2) Flashcards

1
Q

Dementia is defined as a decline from prior functioning, interfering with ADLs when it isn’t better explained by _______ or __________ ________

A

Delirium or psychiatric disorder

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2
Q

T/F To be considered cognitively impaired you need 4/5 symptoms.

A

F. You need 2

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3
Q

What are the 5 diagnostic symptoms associated with dementia

A
  1. Visuospatial skills
  2. Language skills
  3. Memory
  4. Judgment, reasoning, or handling complex tasks
  5. Personality/ behavior changes
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4
Q

DDx for most dementias

A

(Alzheimer’s, Lewy Body, Vascular, Frontotemporal) Dementia/ CJD/ normal pressure hydrocephalus/ hypothyroidism/ depression/ Wernicke’s encephalopathy/ delirium/ Hepatic encephalopathy/ drug or EtOH intoxication/ Brain tumor or metastasis/ Pseudodementia/ Uremia/ Syphilis/ Intracranial hemorrhage

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5
Q

What is the MC type of dementia?

A

Alzheimer’s disease (AD)

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6
Q

What is the biggest risk factor for AD?

A

Older age (6th-7th decade)

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7
Q

Old people get AD: what are other risk factors?

A

FH (autosomal dominant genetic mutations - Down Syndrome), lower education level, being a woman

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8
Q

The Pathophys of AD is caused by what 2 proteins? What formations do they make?

A 
Beta-amyloid - Neuritic plaque
Hyperphosphorylated tau (p-tau) - neurofibrillary tangles
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9
Q

What neuro transmitter is decreased in AD?

A

Acetylcholine

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10
Q

What part of the brain is first to be affected by AD?

A

Hippocampus

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11
Q

What is the hippocampus involved in?

A

Memories, learning, emotions

explicit (declarative) memory declines first in AD

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12
Q

The ability to make an egg or ride a bike is a certain kind of memory. What is it?

A

Implicit (procedural) memory. This is spared in AD

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13
Q

AD patients present with declines in their executive function, especially when out of their safe, predictable environment. What are these deficits?

A

Less motivated, organized, and abstract thinking
Finances
Driving, shopping, housekeeping
Following instructions on the job

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14
Q

Memory is tricky because how do you know if you have lost it? And if you do know, will you remember? What is it called when you aren’t aware of your own deficits?

A

Anosognosia

Most patients are aware of their memory loss

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15
Q

T/F Behavioral/ neuro psychiatric abnormalities are common in mild, moderate, severe, and end stage AD

A

F: it isn’t common in mild. They only have slight recent memory issues

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16
Q

The common first behavioral/ neuropsychiatric symptoms of AD are what 3 things?

A

Apathy, irritable, socially disengaged

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17
Q

The common later behavioral/ neuropsychiatric symptoms of AD are what 4 things?

A

Overt agitation, aggression, psychosis, wandering

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18
Q

Define dyspraxia/ apraxia

A

difficulty/ inability to execute a motor task

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19
Q

What are the 6 main clinical presentations of AD?

A 
Dyspraxia/ apraxia
Olfactory dysfunction
Sleep disturbances
Visuospatial deficits (read a clock)
Seizures
Destabilization caused by changes
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20
Q

AD is a progressive disease. It starts mild and eventually will progress to death. What is the MCC of death?

A

Aspiration

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21
Q

From mild it first goes to Mod. What are the main deficits of AD that show up here?

A 
Impaired language
Easily lost and confused
Not able to work
Apraxia emerges
Visuospatial
ADL deficits become more prominent
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22
Q

From Mod the obvious progression is to Severe. What marks this stage of AD?

A 
Either wandering away or stuck in bed since they can't walk.
Delusional
Disinhibited
Disturbed sleep cycle
Withdrawn
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23
Q

The definitive diagnosis is histological so we have to do it before the patient dies. What labs and imaging would you get to rule out other diagnosis?

A

CBC, CMP, TSH, B12, RPR, UA C&S

CT or MRI

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24
Q

You can get labs and imaging, but what else should you do to diagnose AD clinically?

A

Cognition assessment

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25
Q

What are three Cognition assessments?

A

MMSE, MoCA, SLUMS

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26
Q

There are 2 main drug treatments, 2 mixed drug treatments, and 2 treatments with no shown benefits. What are they?

A

Cholinesterase inhibitors and NMDA receptor antagonist
Vitamin E and Selegiline (antidepressant)
Anti-inflammatory drugs, Ginkgo biloba

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27
Q

Cholinesterase inhibitors work by slowing the progression of AD by increasing the amount of ACh in the CNS so it would benefit what stages of people with AD?

A

Mild- Mod

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28
Q

What are the 3 Cholinesterase Inhibitors from most to least common?

A

Donepezil (Aricept), Rivastigmine( Exelon), Galantamine (Razadyne)

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29
Q

What 2 side effects do every cholinesterase have?

A

N/V

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30
Q

What drug is used on patients with mod-severe AD?

A

NMDA receptor antagonists
Memantine (Namenda)
The drug name on this one is nice if you remember NMDA - N(a)M(end)DA

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31
Q

T/F Pts with AD could have delirium; you should consider other causes before you treat their neuropsychiatric symptoms.

A

True.

Consider medical causes, medication side effects, or pain they can’t express.

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32
Q

What are the 4 medication classes used to treat neuropsych symptoms in AD?

A

Antidepressants - Citalopram (Celexa)
Anti-seizure - Carbamazepine (Tegretol), Valproate (Depakote) Gabapentin (Neurontin)
Dextromethorphan-quinidine (Nuedexta)

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33
Q

When do you need to give antipsychotics to AD pts? Why should you be careful about using them?

A

Increases mortality. Not approved for treatment of behavioral disturbance in those with dementia.

Safety of caregiver necessitates use.

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34
Q

Which is not an antipsychotic used to help in AD?

a. Seroquel
b. Risperidone
c. Gabapentin
d. Zyprexa

A

c. Gabapentin is an anti-seizure med.

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35
Q

When antipsychotics are used with AD, what are some side effects and how would you prevent them?

A

Tapering helps lessen S/E

EPS/TD, somnolence, Increased risk for: CVA, MI

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36
Q

AD is a progressive, incurable disease: what is the typical course from diagnosis?

A

8-10 years

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37
Q

What are the 5 most common causes of death in AD?

A

Aspiration (MCC), malnutrition, secondary infections, PE, heart disease

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38
Q

What is the second most common form of dementia?

A

VaD - Vascular Dementia

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39
Q

T/F There is a significant overlap of VaD with AD.

A

True. 15-20% have both

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40
Q

Men over the age of 65 get VaD the most. What are 5 other risk factors?

A

Cardiovascular disease, high glucose levels, DM, HTN, afib

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41
Q

The prognosis is fair for AD (8-10 yrs). Is it better or worse for VaD, and how much?

A

Worse. Survival ~ 5 years

Severe likelihood for CVA/ MI

42
Q

VaD is caused by atheroslerotic plaques in the vasculature. These can grow and/or break and cause multiple infarctions of the brain. What are the three kinds of infarcts?

A

Large infarct, Lacunar infarct, chronic subcortical ischemia

43
Q

Where is a large infarction?

A

At the level of major cerebral vessels (usually cortical)

44
Q

Where is a lacunar infarct?

A

In a small artery infarction (subcortical)

45
Q

Where is a chronic subcortical ischemia?

A

In distribution of small arteries of periventricular white matter

46
Q

The clinical presentation of a patient with Cortical VaD is dependent on and specific to what?

A

The specific area affected

47
Q

What are some common clinical presentations of Cortical VaD?

A 
Speech difficulty
Trouble preforming routine tasks
Sensory interpretation difficulty
Confusion
Amnesia
Executive dysfunction
(Stepwise of fluctuant course common)
48
Q

What are some common clinical presentations of Subcortical VaD?

A 
Gait dysfunction
Personality & mood changes
Urinary frequency, urgency, or symptoms not from urologic disease
Cognitive dysfunction
(Gradual or stepwise)
49
Q 
What shows VaD infarcts the best?
a. CT w/o
b CT w/
c. CTA
d. MRI
A

MRI

50
Q

VaD has associated risk factors, what can be done to alleviate these?

A

Antihypertensive, DM management, Statins, Antiplatelet agents, smoking cessation, diet/ exercise

51
Q

What are the three classifications of meds you can give to help with symptoms of VaD?

A

Acetylcholinesterase inhibitors
NMDA antagonists (Memantine)
Calcium Channel blockers (looks promising, more trials needed)

52
Q

Name 3 acetylcholinesterase inhibitors used on VaD.

A

Donepezil
Galantamine
Rivastigmine

53
Q

What is Pseudodementia and what patient population is it seen in?

A

It is a psychiatric illness who appears to be demented

It is commonly seen in an episode of major depression. (dementia syndrome of depression)

54
Q

Think about the differences between depressed and demented patients. What were three differences given to us?

A

(Dementia/ Depression)
Answering questioning (confabulation/ “I don’t know” or correct)
Accomplishments (Delight in/ emphasizes failures)
Memory (tried to cover up/ complains)
[see slides for table]

55
Q

What are the treatments for Pseudodementia?

A

Antidepressants (SSRI’s preferred)

ECT

56
Q

What should you avoid giving to Pseudodementia patients?

A

Acetylcholinesterase inhibitors

NMDA antagonists

57
Q

What is the umbrella term for a group of neurodegenerative diseases that result in degeneration of the frontal and/ or temporal lobe?

A

Frontotemporal dementia (FTD)

58
Q

What is Frontotemporal dementia characterized by changes in?

A

Personality, language, and behavior

59
Q

FTD is caused by degeneration of the frontal and/or temporal lobes: what 4 diseases are associated with these areas?

A

Pick disease, dementia associated with ALS, coritcobasal degeneration, and genetic mutations.

60
Q

If you look at some brain under a microscope of someone with FTD, what are you going to see?

A

Neuronal loss, loss of myelin, astrocytic gliosis, and abnormal protein inclusions in neuronal or glial cells.

61
Q

FTD as a 2 variants and 3 subtypes. What are they?

A

Behavioral (MC)
Primary Progressive Aphasia (PPA)
PPA has three subtypes: nonfluent, semantic, logopenic

62
Q

The behavioral subtype of FTD is marked by what?

A

Disinhibition, apathy, loss of empathy, hyperorality, compulsive behaviors

63
Q

Primary Progressive Aphasia (PPA) is a language impairment varient of FTD: what brain functions are preserved in these patients?

A

Episodic memory and other cognitive functions.

64
Q

Nonfluent variant PPA

A

Motor speech deficit - effort to produce words/ articulate
Effortful, halting speech
Distortions
Agrammatism (not grammatically correct)

65
Q

Semantic variant PPA

A

Impaired: single word comprehension, object naming, spelling, word finding (earliest symptom)
Preserved: fluency, repetition. and grammar

66
Q

Mispronouncing/ misspelling words with irregular spelling is called what?

A

Surface dyslexia or surface dysgraphia

67
Q

Logopenic variant PPA

A

Impaired: single word retrieval, repetition, speech/naming errors
Preserved: single word comprehension, object knowledge, motor speech
“Empty” patients - vague stories w/o detail

68
Q

Motor syndromes happen in conjunction with FTD and are correlated with what?

A

Shorter survival

69
Q

What are the three main motor syndromes associated with FTD?

A
  1. Motor neuron disease (upper&lower)
  2. Corticobasal syndrome
  3. Progressive supranuclear palsy
70
Q

How do you diagnose FTD?

A

Neuroimaging (SPECT, PET, Perfusion MRI, others…)
Many will show focal frontal or temporal atrophy
Functional imaging shows hypoperfusion or hypometabolism

71
Q

Imaging is helpful for FTD, but you can also clinically diagnose. Name the 6 criteria.
T/F: You need 5/6 to be considered FTD

A 
F: 3/6 required
Disinhibition
Apathy/ inertia
Loss of sympathy/ empathy
Perseverative/ compulsive behaviors
Hyperorality
Dysexecutive neurological function
(have an idea, don't memorize)
72
Q

What are the diagnostic criteria for the PPA subtype of FTD?

A

1-3 inclusion criteria must be answered positive
1-4 exclusion criteria must be answered negatively
(have an idea, don’t memorize)

73
Q

What is the main treatment of FTD and the last resort med used?

A

SSRI trial - Paroxetine (Paxil) 10 mg PO daily
Atypical atipsychotic trial (last resort) - Seroquel 12.5 mg PO daily
Cholinesterase inhibitors no evidence, but reasonable if nothing else
(No effective disease modifying treatments exist - symptoms treated)

74
Q

What is the prognosis for FTD pts?

A

8-10 yrs from onset-death (slightly more rapid than AD)
2 years from onset for pts with Motor Neuron Disease
(Paulson noted a 3 yr average)

75
Q

Lewy Body Dementia (LBD or DLB) is characterized by dementia with or preceding _________ ___________

A

Parkinsonian symptoms

76
Q

What Parkinsonian symptoms are seen in LBD?

A 
Hallucinations
Fluctuations in cognition/ alertness
Dysautonomia (ANS nerves dysfunction)
!Parkinsonism (Parkinson's has Lewy Bodies)!34
Disordered sleep
77
Q

T/F: When you get PD before dementia it is considered PD, and when you get dementia before PD it is considered LBD.

A

True

78
Q

VaD is the 2nd most common form of dementia. What is the 2nd most common form of degenerative dementia?

A

LBD

79
Q

What kind of picture do you have in your mind of a typical LBD patient?

A

A 75 y/o male with a FH of PD, does NOT drink caffeine, has gone to college, and is a monozygotic twin.

80
Q

What plays a role in developing LBD as a monozygotic twin?

A

Environment/ epigenetics and triplication of SNCA gene, and autosomal dominant inheritance of LBD.
(Didn’t talk about but is on slides)

81
Q

Lewy bodies are round, ________ ____________ neuronal inclusions.

A

Eosinophilic intracytoplasmic

82
Q

Where in the brain is LBD most commonly found?

A 
Deep cortical layers, especially:
Anterior frontal and temporal lobes
Cingulate gyrus
Insula
Substantia nigra
Locus Ceruleus
83
Q

LBD - 3 Neuro-transmitter deficits

A

Acetylcholine
Dopamine
Serotonin
(probably play a pathological role)

84
Q

LBD has dementia before PD, what comes before dementia in LBD?

A

Cognitive dysfunction, often presenting symptom

(Impaired: attention, exec. fxn., visuospation fxn.

85
Q

What are the 2/3 core clinical features needed in LBD?

A 
Cognitive fluctuations (Course of a day/seconds from lucid-comatose/ pleasant-difficult) [60-80%]
Visual hallucinations (can be auditory)
PD-ism
86
Q

Feature of LBD that lasts seconds to days and happens in 60-80% of cases. Can be subtle or quite dramatic

A

Cognitive fluctuations

87
Q

PD symptoms

A 
Bradykinesia
Limb rigidity
Shuffling gait
Resting tremor
Postural instability
[70-90% of those with LBD]
88
Q

There are 2 other clinical features than the main 3 in LBD. What are they?

A 
REM sleep disorder (REM=dreams. looks purposeful)
Neuroleptic Sensitivity (aka. anti psychotic sensitivity. Severe state, Dopamine is inhibited)
89
Q

Supportive features of LBD

A 
Falls
Syncope, LOC
ANS dysfunction
Hallucinations
Delusions
Depression
90
Q

T/F Imaging is necessary for LBD

A

False. Only a clinical diagnosis

91
Q

LBD - treatment

A

Cholinesterase inhibitors.
First line - Rivastigmine (Exelon)
Donepezil (Aricept)

Melatonin or clonazepam (REM sleep disorder)

Levodopa

92
Q

Rivastigmine (Exelon)

A

Treatment for LBD. PO or patch.
Less anxiety, delusions, hallucinations AND better performance on neuropsych testing
S/E: nausea, vomiting, dizziness, HA, diarrhea, falling

93
Q

LBD - Prognosis

A

Progressive, Variable (generally faster than AD)

94
Q

The last dementia! This is associated with a progressive virus.

A

HIV-Associated Dementia (HAD)

95
Q

HAD is mostly in untreated patients with advanced HIV. What are the Sx/Ssx?

A 
Subacute onset that may wax/wane
Attention concentration
Memory deficits
Behavioral/ mood changes
Impaired psychomotor speed/precision
96
Q

What is the expected finding on the brain scan of HAD?

A

Cerebral atrophy

Mainly basal ganglia and white matter

97
Q

T/F HAD can be explained by other conditions or pre-existing causes other than HIV.

A

F

98
Q

HAD - management

A

Antiretroviral (get one that goes into CNS)

If they are compliant - LP and investigate

99
Q

Do you think cerebral atrophy from a pt not taking their meds is a marker for increased mortality among HIV pts?

A

Duh

100
Q

Is this the 100th card?

A

Yes!

RRCCPA Clinical Medicine I (49 decks)

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