First Aid Psych 7-2 Cognitive Disorders

Front 1

26. Mini Mental State Exam (MMSE)?

Back 1

a. MMSE is a screening test used commonly due to its speed and ease of administration.

Front 2

27. What does the MMSE assess?

Back 2

a. Orientation to time and place, attention/concentration, language, constructional ability, and immediate and delayed recall.
b. Sensitive for dementia, particularly moderate to severe forms.
c. Lacks specificity; low scores may signal important changes in cognition.
d. Presence and nature of cognitive impairment should not be diagnosed. On the basis of MMSE scores alone.

Front 3

28. Perfect score and dysfunction on MMSE?

Back 3

a. Perfect score: 30.
b. Dysfunction: < 25

Front 4

29. What is dementia caused by hypothyroidism usually accompanied by (This is a reversible cause of dementia)?

Back 4

a. Depressed mood and lethargy.

Front 5

30. Alzheimer Disease?

Back 5

a. Most common type of dementia: affect 4.5 million in US.
b. F:M 3:1
c. Its presence in one first-degree relative ↑ the risk 4x.

Front 6

31. Neurotransmitter change in Alzheimer’s?

Back 6

a. These pts have a ↓ in Ach due to loss of noradrenergic neurons in the nucleus basalis and ↓ choline acetyltransferase (required for Ach synthesis).

Front 7

32. Clinical Manifestations of Alzheimer’s disease?

Back 7

a. Gradual progressive decline in cognitive functions, esp memory and language.
b. Personality changes, mood swings, and paranoia are very common.
c. Motor and Sensory sx are absent until late in the course of the illness.
d. Gradual and progressive course, typically 10 yrs from diagnosis to death.

Front 8

33. In addition to Alzheimer’s, in what other conditions are Senile plaques and neurofibrillary tangles found?

Back 8

a. Down syndrome and normal aging.

Front 9

34. Diagnosis of Alzheimer’s?

Back 9

a. Before death, it is a diagnosis of exclusions. (Can actually use PET Scan now).

Front 10

35. 3 primary Alzheimer’s genes?

Back 10

1. Presenelin I
2. Presenelin II
3. Amyloid Precursor Protein (APP)
b. Genes are rare accounting for only 5% of cases, usually early onset.
c. Most cases, especially after 65, are sporadic.

Front 11

36. Major susceptibility gene for Alzheimer’s?

Back 11

a. Apolipoprotein e4 (APOe4).

Front 12

37. Homozygous for APOe4?

Back 12

(2% of population):
b. 50-90% chance of developing dementia by age 85.

Front 13

38. Heterozygous for APOe4?

Back 13

a. 15 of population
b. 45% chance of developing dementia by age 85.
c. 20% chance in general population.

Front 14

39. Amyloid Cascade hypothesis for alzheimer’s (the dominant explanation for Alzheimer disease)?

Back 14

a. Excess of Aβ peptides either by overproduction or diminished clearance.
b. APP, presenilin I, and presenilin II pts are lifelong overproducers.
c. Sporadic cases result from failure of metabolism and degradation.

Front 15

40. Postmortem findings for alzheimer’s pts?

Back 15

a. Gross: diffuse atrophy w/enlarged ventricles and flattened sulci.
b. Microscopic: Senile plaques and neurofibrillary tangles
c. Neuritic plaques, but not neurofibrillary tangles, correlate w/severity of dementia.

Front 16

41. Tx of Alzheimer’s?

Back 16

a. No cure or truly effective tx.
b. Physical and emotional support, proper nutrition, exercise, and supervision.
c. Cholinesterase inhibitors
d. NMDA antagonists.

Front 17

42. Cholinesterase inhibitors for tx of Alzheimer’s use?

Back 17

a. Approved for mild-to-moderate disease
b. Able to slow cognitive decline for 6-12 months

Front 18

43. What are the 4 cholinesterase inhibitors approved for Alzheimer’s?

Back 18

1. Tacrine (Cognex)
2. Donepezil (Aricept)
3. Rivastigmine (Exelon)
4. Galantamine (Razadyne)

Front 19

44. 1 NMDA antagonist approved for Alzheimer’s and use?

Back 19

a. Memantine (Namenda)
b. Approved for moderate-to-severe Alzheimer’s.

Front 20

45. Vascular dementia?

Back 20

a. The second most common form of dementia.
b. It is caused by microvascular disease in the brain that produces multiple small infarcts.
c. A substantial infarct burden must accumulate before dementia develops.

Front 21

46. Course of vascular dementia?

Back 21

a. Typically chronically progressing dementia w/multiple small lacunar infarcts (small vessel disease) on CT.
b. Stepwise loss of function as the microinfarcts add up!!!

Front 22

47. Risk factors for Vascular Dementia?

Back 22

a. Stroke
b. DM
c. HTN
d. APOe4
e. 2x more likely in men than in women.

Front 23

48. A stroke to which area of the brain can cause sx of schizophrenia, bipolar I, and depression?

Back 23

a. Frontal lobe

Front 24

49. Clinical manifestations of vascular dementia?

Back 24

a. May follow a single strategic infarct, multiple cortical or lacunar infarcts, or a microvascular insult.
b. Step-wise deterioration.
c. No specific pattern of cognitive deficits define vascular dementia.
d. Neurophysiologic testing may not differentiate vascular fro Alzheimer dementia.

Front 25

50. Lateralizing signs of vascular dementia?

Back 25

a. Spasticity
b. Hemiparesis
c. Ataxia
d. Pseudobulbar palsy (extreme emotional lability, abnormal speech cadence, dysphagia, abnormal reflexes.
e. Depression, anger, and paranoia.

Front 26

51. Tx of Vascular dementia?

Back 26

a. No cure or truly effective tx.
b. Physical and emotional support, proper nutrition, exercise, and supervision.
c. Cholinesterase inhibitors have been used successfully in pt w/vascular dementia.
d. Antihypertensive therapy may prevent onset of vascular dementia.
e. Tx of sx as necessary.

Front 27

52. Lewy Body Dementia (LBD)?

Back 27

a. Lewy body dementia is the 3rd most common dementia (accounting for 10-15%).
b. Caused by Lewy bodies and Lewy neurites (pathologic aggregations of alpha-synuclein) in the brain, primarily in the basal ganglia.

Front 28

53. Clinical Manifestations of Lewy Body dementia?!?

Back 28

a. Progressive cognitive decline
b. Waxing and waning of cognition is Core feature!
c. Visual hallucinations!!! Usually vivid, colourful, and well-formed images of animals or people.
d. Paranoid delusions are common
e. Parkinsonism (without exposure to neuroleptics) is core feature (tremor, bradykinesia, rigidity, shuffling gait, masked facies, stooped posture, retropulsion.
f. Sensitivity to neuroleptics
g. Rapid eye movement (REM) sleep behaviour disorder is common.

Front 29

54. Diagnosis of Lewy Body Dementia (LBD)?

Back 29

a. Strong similarities to Parkinson disease dementia
b. Onset of dementia is w/in 12 months of parkinsonism symptoms.
c. Dementia that begins more than 12 months after the parkinsonism sx is classified as Parkinson disease dementia.
d. Lewy neurites are more closely linked w/clinical sx than are Lewy bodies.

Front 30

55. Tx of Lewy Body Dementia (LBD)?

Back 30

a. Cholinesterase inhibitors help improve visual hallucinations.
b. Psychostimulants, levodopa/carbidopa, and dopamine agonists may improve cognition, apathy, and psychomotor slowing.
c. Atypical neuroleptics have been slightly effective in stopping delusions and agitation.
d. Clonazepam (Klonopin) tx for REM sleep behaviour disorder.

Front 31

56. Pick Disease/Frontotemporal Dementia (FTD)?

Back 31

a. FTD includes a diverse group of clinical and pathological disorders that typically present between ages 45-65.

Front 32

57. With what gene are 20-30% of Pick disease (familial cases) association with?

Back 32

a. Mutations in the progranulin or MAPT gene.

Front 33

58. Mean duration of illness to death for Pick Disease?

Back 33

a. 4-6 yrs.

Front 34

59. Clinical manifestations of Pick Disease?

Back 34

a. Profound changes in personality and social conduct.
b. Usually present at the initial presentation of the pt.
c. Disinhibited verbal, physical, and sexual behaviour.
d. Echolalia, overeating, oral exploration of inanimate objects.
e. Lack emotional warmth, empathy, or sympathy

Front 35

60. Do pts w/Pick disease have insight to their condition?

Back 35

a. Not really, poor insight about behavioural alterations.

Front 36

61. In what areas are cognitive deficits seen w/Pick Disease?

Back 36

a. Attention, abstraction, planning, and problem solving.

Front 37

62. What areas of functioning are well preserved w/Pick Disease?

Back 37

a. Memory, language, and spatial functions.

Front 38

63. Pathology of Pick disease (Frontotemporal dementia)?

Back 38

a. Marked atrophy of the frontal and temporal lobes.
b. Neuronal loss, microvacuolization, and astrocytic gliosis in cortical layer II.
c. Only moderate correlation between clinical and pathological findings.

Front 39

64. Tx of Pick’s disease?

Back 39

a. Anticholinergic meds and antidepressants have consistently shown to improve behavioural sx but not cognition.

Front 40

65. HIV-associated dementia (HAD)?

Back 40

a. HAD is the most common dementia caused by infectious disease, and its prevalence is increasing as pts live longer will illness.
b. It is caused by infections due to neutropenia, as well as direct effects of the virus on cells.