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Pretest Patologi Anatomi Blok 2.2 Neurobehavior

Total questions: 10

Worksheet time: 10mins

Name
Class
Date
1.

A 68-year-old patient develops progressive memory loss and confusion. MRI reveals cortical atrophy, especially in the hippocampus. Histological examination shows extracellular plaques and intracellular tangles. Which combination best describes the molecular components of these lesions?

a)

α-synuclein and TDP-43

b)

Aβ peptide and phosphorylated tau

c)

Polyglutamine and ubiquitin

d)

Amyloid precursor protein and α-synuclein

e)

Tau protein and neurofilament light chain

2.

In most neurodegenerative diseases, abnormal protein aggregation causes both “toxic gain-of-function” and “loss-of-function.” What mechanism best explains this dual effect?

a)

Reduced neurotransmitter release in surviving neurons

b)

Inhibition of neuronal firing by GABAergic dominance

c)

Misfolded proteins interfere with normal protein activity and damage neurons

d)

Increased degradation of normal proteins via lysosomal pathways

e)

Enhanced synaptic pruning by microglia

3.

Which feature most clearly distinguishes Alzheimer’s disease from Parkinson’s disease at the cellular pathology level?

a)

Lewy bodies in the substantia nigra

b)

α-synuclein inclusions in cortical neurons

c)

Amyloid plaques and neurofibrillary tangles

d)

Neuronal loss in the basal ganglia

e)

Mitochondrial dysfunction in dopaminergic neurons

4.

Which of the following mechanisms contributes most directly to neuronal loss in Parkinson’s disease?

a)

Excessive β-amyloid production

b)

Autoimmune attack on acetylcholine receptors

c)

Misfolding and aggregation of α-synuclein

d)

Failure of cerebrovascular autoregulation

e)

Hyperphosphorylation of tau protein

5.

A 60-year-old man presents with resting tremor, rigidity, and bradykinesia. Which structure is primarily affected and what neurotransmitter is most depleted?

a)

Substantia nigra pars compacta – dopamine

b)

Basal nucleus of Meynert – acetylcholine

c)

Hippocampus – glutamate

d)

Cerebellum – GABA

e)

Prefrontal cortex – serotonin

6.

Which statement best explains why ischemic stroke commonly produces “liquefactive necrosis” in brain tissue?

a)

Brain tissue lacks myelin and is rich in fibrous proteins

b)

The brain has abundant lysosomal enzymes and little structural stroma

c)

The inflammatory response is primarily granulomatous

d)

Cerebral vessels rapidly regenerate after injury

e)

The infarcted region undergoes coagulative necrosis followed by fibrosis

7.

Which neuropathological feature is most likely observed one week after an ischemic stroke?

a)

Presence of red neurons with eosinophilic cytoplasm

b)

Gliosis and formation of microglial nodules

c)

Cystic cavity with reactive astrocyte wall

d)

Perivascular hemorrhage and necrosis

e)

Neuronal vacuolization and nuclear pyknosis only

8.

An infarct in the left middle cerebral artery (MCA) territory is most likely to result in:

a)

Contralateral leg weakness with behavioral changes

b)

Homonymous hemianopia without motor deficit

c)

Aphasia and contralateral hemiplegia

d)

Ataxia and intention tremor

e)

Bilateral sensory loss of face and body

9.

A researcher finds that α-synuclein aggregates in Parkinson’s disease can spread between neurons and induce further aggregation in recipient cells. This process is best described as:

a)

Autoimmune synaptic degeneration

b)

Prion-like propagation

c)

Excitotoxic apoptosis

d)

Demyelination

e)

Lysosomal overload

10.

Which feature differentiates vascular cognitive impairment (multi-infarct dementia) from Alzheimer’s disease?

a)

Accumulation of α-synuclein in cortical neurons

b)

Amyloid plaques and tangles in hippocampal neurons

c)

Gradual onset without stepwise decline

d)

Stepwise deterioration following repeated ischemic episodes

e)

Symmetric cortical atrophy sparing subcortical areas