NB2 - Pathophysiology
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Material
, NB2 - Pathophysiology
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1. Loss of auditory function due to damage of conductive Acquired hearing loss
structures (eg. tympanic membrane; conductive hear-
ing loss), sensory receptors (eg. hair cells in the organ
of Corti; sensorineural hearing loss), or neural path-
ways. Causes include infections, trauma (conductive),
ototoxic medications, or chronic (sensorineural) noise
exposure.
2. Progressive and degenerative changes in the mac- Age-related macular de-
ula lutea, leading to painless central or pericentral generation (AMD) (de-
visual impairment and reduced visual acuity. Fun- posits?)
doscopy may show accumulation of extracellular de-
posits (drusen bodies; small, yellow deposits of lipid
and calcium) and dysfunction of retinal pigment ep-
ithelium. Risk factors include advanced age (>55), fam-
ily history, CVD, smoking, obesity.
3. Loss of visual motion perception, resulting from vascu- Akinetopsia
lar, traumatic, or degenerative damage to the human
visual motion area (V5/MT) on the lateral cortex at the
occipital/parietal/temporal junction. Few cases from
bilateral lesions have been well described; unilateral
lesions are either asymptomatic or more subtle.
4. Chronic alcohol exposure leads to selective atrophy of Alcoholic cerebellar de-
the superior vermis and lateral aspects of the anteri- generation (atrophy? pre-
or lobe, leading to postural instability, truncal ataxia, sentation?)
ataxic gait, and nystagmus. Degeneration of Purkinje
cells disrupts inhibitory output, impairing coordina-
tion and balance.
5.
, NB2 - Pathophysiology
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Chronic alcohol use causes damage to peripheral Alcohol-related peripheral
nerves through demyelination or thiamine (B1) defi- neuropathy (which modal-
ciency. The condition presents with symmetric sen- ities are lost first?)
sory loss (occurs first; distal to proximal, decreased
proprioception, paresthesia, burning feet syndrome)
and motor losses (occurs second; typically starts in the
lower leg). Autonomic involvement can occur in more
advanced cases.
6. A lowered threshold for nociceptor activation, caus- Allodynia
ing non-noxious stimuli to be abnormally perceived
as painful. Often involves sensitization mechanisms.
Altered NT signaling and changes in synaptic connec-
tivity contribute.
7. Black widow neurotoxin that causes massive ACh re- Alpha-latrotoxin
lease from presynaptic terminals by disrupting vesic-
ular exocytosis. This leads to excessive stimulation of
muscle fibers and hyperactivity. Sustained exposure
results in potential paralysis.
8. Progressive and fatal neurodegeneration of UMNs and Lou Gehrig's disease /
LMNs in the brain and spinal cord, targeting the soma Amyotrophic Lateral Scle-
and causing a combination of spasticity, weakness, rosis (ALS)
muscle atrophy, and abnormal reflexes. Typical on-
set is characterized by initial weakness in one limb
(within a few days/weeks) and less frequent bulbar
onset (starting with speech and swallowing problems)
and respiratory muscle onset (death due to respiratory
paralysis occurs within a few years). Cognitive function
may remain intact in many cases. Median age of onset
~55yrs. No cure.
| Complete Exam Study
Guide, Practice Questions,
Answers & ATI Review
Material
, NB2 - Pathophysiology
Study online at https://quizlet.com/_jafntt
1. Loss of auditory function due to damage of conductive Acquired hearing loss
structures (eg. tympanic membrane; conductive hear-
ing loss), sensory receptors (eg. hair cells in the organ
of Corti; sensorineural hearing loss), or neural path-
ways. Causes include infections, trauma (conductive),
ototoxic medications, or chronic (sensorineural) noise
exposure.
2. Progressive and degenerative changes in the mac- Age-related macular de-
ula lutea, leading to painless central or pericentral generation (AMD) (de-
visual impairment and reduced visual acuity. Fun- posits?)
doscopy may show accumulation of extracellular de-
posits (drusen bodies; small, yellow deposits of lipid
and calcium) and dysfunction of retinal pigment ep-
ithelium. Risk factors include advanced age (>55), fam-
ily history, CVD, smoking, obesity.
3. Loss of visual motion perception, resulting from vascu- Akinetopsia
lar, traumatic, or degenerative damage to the human
visual motion area (V5/MT) on the lateral cortex at the
occipital/parietal/temporal junction. Few cases from
bilateral lesions have been well described; unilateral
lesions are either asymptomatic or more subtle.
4. Chronic alcohol exposure leads to selective atrophy of Alcoholic cerebellar de-
the superior vermis and lateral aspects of the anteri- generation (atrophy? pre-
or lobe, leading to postural instability, truncal ataxia, sentation?)
ataxic gait, and nystagmus. Degeneration of Purkinje
cells disrupts inhibitory output, impairing coordina-
tion and balance.
5.
, NB2 - Pathophysiology
Study online at https://quizlet.com/_jafntt
Chronic alcohol use causes damage to peripheral Alcohol-related peripheral
nerves through demyelination or thiamine (B1) defi- neuropathy (which modal-
ciency. The condition presents with symmetric sen- ities are lost first?)
sory loss (occurs first; distal to proximal, decreased
proprioception, paresthesia, burning feet syndrome)
and motor losses (occurs second; typically starts in the
lower leg). Autonomic involvement can occur in more
advanced cases.
6. A lowered threshold for nociceptor activation, caus- Allodynia
ing non-noxious stimuli to be abnormally perceived
as painful. Often involves sensitization mechanisms.
Altered NT signaling and changes in synaptic connec-
tivity contribute.
7. Black widow neurotoxin that causes massive ACh re- Alpha-latrotoxin
lease from presynaptic terminals by disrupting vesic-
ular exocytosis. This leads to excessive stimulation of
muscle fibers and hyperactivity. Sustained exposure
results in potential paralysis.
8. Progressive and fatal neurodegeneration of UMNs and Lou Gehrig's disease /
LMNs in the brain and spinal cord, targeting the soma Amyotrophic Lateral Scle-
and causing a combination of spasticity, weakness, rosis (ALS)
muscle atrophy, and abnormal reflexes. Typical on-
set is characterized by initial weakness in one limb
(within a few days/weeks) and less frequent bulbar
onset (starting with speech and swallowing problems)
and respiratory muscle onset (death due to respiratory
paralysis occurs within a few years). Cognitive function
may remain intact in many cases. Median age of onset
~55yrs. No cure.
