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26 Cards in this Set
- Front
- Back
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65. HIV-associated dementia (HAD)?
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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. |
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66. Risk factors for HIV-associated dementia?
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a. Duration of Illness
b. Low CD4 c. High Viral loads |
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67. Clinical manifestations of HIV-associated dementia (HAD)?
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a. Rapid decline in cognition, behaviour, and motor abilities.
b. Poor memory and impaired concentration c. Psychomotor retardation d. Apathy and social withdrawal e. Depression f. Language usually preserved. |
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68. Course of Pick vs. Alzheimer’s?
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a. Picks is a much more rapid progression to death.
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69. Tx of HIV-associated Dementia?
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a. HAART improves cognition and prolongs life.
b. Psychostimulants target fatigue and psychomotor retardation. |
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70. Note: a ↓ in viral load is often accompanied by an improvement in AIDS-related dementia.
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70. Note: a ↓ in viral load is often accompanied by an improvement in AIDS-related dementia.
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71. Huntington Disease (HD)?
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a. Autosomal-dominant genetic disorder.
b. Results in progressively disabling cognitive, physical, and psychosocial functioning, ultimately resulting in death. |
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72. Onset of HD?
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a. 35-50.
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73. Clinical manifestations of Huntington disease?
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a. Progressive dementia that typically begins 1 yr before or 1 yr after chorea
b. Pts are often aware of deteriorating mentation. c. Choreiform movements (dance-like) d. Muscular hypertonicity e. Psychiatric manifestations include depression, psychosis, and alcoholism. f. ↑ rate of suicide. |
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74. Diagnosis of Huntington’s?
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a. MRI shows caudate atrophy (and sometimes cortical atrophy).
b. Genetic testing. |
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75. Cause of HD?
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a. Expanded trinucleotide (CAG) repeats.
b. The longer the CAG repeat, the earlier age of onset. |
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76. HD gene?!?
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a. Trinucleotide repeat on short arm of chromosome 4.
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77. Lilliputian hallucinations?
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a. Disturbances in size appearance of objects. I.e. small or large.
b. Can occur in Temporal lobe epilepsy |
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78. Parkinson Disease?
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a. PD is a progressive disease w/prominent neuronal loss in substantia nigra, which provides dopamine to the basal ganglia, causing physical and cognitive impairment.
b. Approximately 30-40% of pts w/Parkinson disease develop dementia. c. 50% of pts will suffer from depression. d. Occurs slightly more in men than in women. |
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79. Etiology of PD?
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a. Idiopathic (most common)
b. Traumatic (eg, Muhammad ali) c. Drug or toxin-induced d. Encephalitic (as in the book/movie Awakening) e. Familial (rare). |
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80. Clinical manifestations of PD?
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a. Dementia sx resemble Alzheimer’s type.
b. Dementia rarely occurs as an initial sx. c. Parkinsonism (bradykinesia, cogwheel rigidity, resting tremor, mask-like facial expression, shuffling gait, dysarthria). |
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81. Pathology of PD?
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a. Loss of cells in the substantia nigra of the basal ganglia –> a ↓ dopamine and loss of the dopaminergic tracts.
b. Similar to Alzheimer disease: Senile plaques and neurofibrillary tangles, loss of neurons, and a ↓ in choline acetyltransferase. |
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82. Creutzfeldt-Jakob Disease (CJD)?
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a. CJD is a rapidly progressive, degenerative disease of the CNS caused by accumulation of abnormal forms of prions (proteinaceous infectious particles that are normally expressed by healthy neurons of the brain).
b. Affects older pts, and may be inherited, sporadic, or acquired. c. A small percentage of pts have become infected through corneal transplants. |
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83. Clinical manifestations of CJD?
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a. Rapidly progressive dementia 6-12 months after onset of sx.
b. More than 90% of pts have myoclonus (sudden spasms of muscles). c. Basal ganglia and cerebellar dysfunction is common. d. Personality changes, immature behaviour, and paranoia are early signs. e. Rapid progression to stupor, coma, death in a matter of months to a few yrs. |
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84. Diagnosis of CJD?
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a. Definitive: Pathological demonstration of spongiform changes in brain tissue.
b. Probable: The presence of both rapidly progressive dementia and periodic generalized sharp waves on EEG plus at leat 2 of the following clinical features: 1. Myoclonus 2. Cortical blindness 3. Ataxia 4. Pyramidal signs or extrapyramidal signs. 5. Muscle atrophy 6. Mutism. |
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85. Other prion diseases:
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1. Kuru
2. Gerstmann-Sträussler syndrome 3. fatal familial insomnia 4. BSE |
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86. Normal Pressure hydrocephalus (NPH)?
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a. NPH is a potentially reversible cause of dementia
b. These pts have enlarged ventricles w/↑ CSF pressure. c. The etiology is either idiopathic or secondary to obstruction of CSF reabsorption sites due to trauma, infection, or haemorrhage. |
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87. Clinical manifestations?
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a. Clinical Triad:
1. Gait disturbance: Apraxia (often appears first) 2. Urinary incontinence 3. Dementia (mild, insidious onset). |
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88. Tx of NPH?
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a. Relieve ↑ pressure w/shunt.
b. Of the clinical triad, dementia is least likely to improve. |
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89. The 3 W’s of NPH?
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a. Wobbly = gait disturbance
b. Wet = Urinary incontinence c. Wacky = Dementia |
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90. Complete.
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90. Complete.
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