NU 545 Unit 2 Study Guide questions with verified
answers
Characteristics of Alzheimer's disease. CH 17 Pg 520-522 Ans✓✓✓
There are three forms of AD: nonhereditary sporadic (late onset AD),
early onset familial AD (FAD) and early onset AD which is very rare
.
Occurs mostly in women
Greatest risk factors are age and family history
Other risk factors include diabetes, midlife hypertension,
hyperlipidemia, midlife obesity, smoking, depression, cognitive
inactivity, low educational attainment, female, estrogen deficit at time
of menopause, physical inactivity, head trauma, neuroinflammation,
high sodium homocysteine and cholesterol.
Clinical Manifestations: Has a long preclinical and prodromal course and
pathophysical changes can occur decades before the clinical symptoms
of dementia syndrome occur. Progresses from mild short term memory
deficits to total loss of cognition and executive functions. Initial clinical
symptoms are attributed to forgetfulness, emotional causes, and other
illness. A person becomes more forgetful over time more so in relation
to current events. Memory loss increases as the disorder advances and
the person becomes disoriented, confuses, and loses the ability to
concentrate. Abstraction, problem solving and judgment gradually
,deteriorate with failure in mathematical calculation ability, language
and visuospatial orientation.
Dyspraxia occurs, mental status changes causes behavioral changes
such as irritability, agitation and restlessness. Mood changes may also
occur with depression, hostility, anxiety, emotionally labile, and mood
swings.
Motor changes may occur if posterior frontal lobes are involved causing
rigidity flexion posturing.
Weight loss can be significant
Great variability in age of onset, intensity and sequence of symptoms
and location and extent of brain abnormalities is common.
See Table 17. 15 for progression of disease.
Define and describe the pathophysiology, clinical manifestations and
etiology of Guillian Barre Syndrome. CH 18 pg 583 Ans✓✓✓ Guillain-
Barre Syndrome - An acquired acute inflammatory demyelinating or
axonal polyneuropathy with four subtypes: Acute inflammatory
demyelinating polyneuropathy, acute motor axonal neuropathy, acute
motor and sensory axonal neuropathy, and fisher syndrome (only 5% of
cases).
Pathophysiology: Considered to be an autoimmune disease triggered by
a preceding bacterial or viral infection (Etiology). Molecular mimicry
(cross-activation of self-epitopes and pathogen-derived peptides by
autoreactive T and B cells) is associated with the immune injury.
Glycolipids, particularly gangliosides, are immune targets. The muscle
innervated by the damaged peripheral nerves undergoes denervation
,and atrophy. If the cell body survives, regeneration of the peripheral
nerve takes place and recovery of function is likely. If the cell body dies
from intense root involvement in the inflammatory-degenerative
process, no regeneration is possible. Collateral reinnervation from
surviving axons and regenerating axons may take place. In this case,
motor recovery is less complete and residual deficits persist.
Clinical Manifestations:Vary depending on subtype. Typically first
manifestations include numbness, pain, paresthesias, or weakness of
the limbs. Motor signs manifest as an acute or subacute progressive
paralysis. Proximal muscles may be involved earlier and more
significantly than distal muscles. Paresis/Paralysis may be in an
ascending pattern, involving the limbs, respiratory muscles, and bulbar
muscles. Only bulbar muscles may be involved resulting in dysphagia
and dysarthria. Weakness plateaus or improves by the fourth week in
90% of cases. Sensory symptoms include: paresthesias/dysthesias,
tingling, burning, shocklike sensations (particularly in the limbs), pain,
and numbness. Respiratory muscle weakness leads to vent support in
10-
Define and describe the pathophysiology, clinical manifestations and
etiology of Huntington disease. CH 17 pg 535- 536 Ans✓✓✓
Huntington Disease also known as chorea, is a relatively rare,
hereditary, degenerative hyperkinetic movement disorder diffusely
involving the basal ganglia and cerebral cortex.
Pathophysiology: The major pathologic feature of HD is severe
degeneration of the basal ganglia and the frontal cerebral cortex.
, Degeneration of the basal ganglia and the substantia nigra exhibit a
depletion of neurons that secrete GABA (an inhibitory
neurotransmitter). GABA depletion leads to an excess of dopaminergic
activity that causes hypotonia and hyperkinesia (involuntary,
fragmentary movements).
Clinical Manifestations:
Abnormal movement and progressive dysfunction of intellectual
processes (dementia) and emotional lability. Chorea (involuntary, quick
movements of the feet or hands comparable to dancing) is the most
common type of abnormal movement affecting individuals with HD. It
begins in the face and arms, eventually affecting the entire body.
Symptoms of frontal lobe dysfunction include attention deficits, short
term memory loss, reduced capacity to plan, organize, and sequence,
as well as bradyphrenia (slow thinking); and apathy.
Etiology:
HD (Chorea) is a rare, hereditary (autosomal dominant)-degenerative
disorder diffusely involving the basal ganglia and cerebral cortex,
commonly manifests between 25-45 years of age, and occurs in all
races. The abnormality is manifested on the short arm of chromosome
4.
Treatment: No known treatment is effective in halting the degenerative
process in HD. The chorea can be treated with dopamine receptor-
blocking or depleting agents, and medical and non- medical care for
depression and aggressive behavior may be required.
answers
Characteristics of Alzheimer's disease. CH 17 Pg 520-522 Ans✓✓✓
There are three forms of AD: nonhereditary sporadic (late onset AD),
early onset familial AD (FAD) and early onset AD which is very rare
.
Occurs mostly in women
Greatest risk factors are age and family history
Other risk factors include diabetes, midlife hypertension,
hyperlipidemia, midlife obesity, smoking, depression, cognitive
inactivity, low educational attainment, female, estrogen deficit at time
of menopause, physical inactivity, head trauma, neuroinflammation,
high sodium homocysteine and cholesterol.
Clinical Manifestations: Has a long preclinical and prodromal course and
pathophysical changes can occur decades before the clinical symptoms
of dementia syndrome occur. Progresses from mild short term memory
deficits to total loss of cognition and executive functions. Initial clinical
symptoms are attributed to forgetfulness, emotional causes, and other
illness. A person becomes more forgetful over time more so in relation
to current events. Memory loss increases as the disorder advances and
the person becomes disoriented, confuses, and loses the ability to
concentrate. Abstraction, problem solving and judgment gradually
,deteriorate with failure in mathematical calculation ability, language
and visuospatial orientation.
Dyspraxia occurs, mental status changes causes behavioral changes
such as irritability, agitation and restlessness. Mood changes may also
occur with depression, hostility, anxiety, emotionally labile, and mood
swings.
Motor changes may occur if posterior frontal lobes are involved causing
rigidity flexion posturing.
Weight loss can be significant
Great variability in age of onset, intensity and sequence of symptoms
and location and extent of brain abnormalities is common.
See Table 17. 15 for progression of disease.
Define and describe the pathophysiology, clinical manifestations and
etiology of Guillian Barre Syndrome. CH 18 pg 583 Ans✓✓✓ Guillain-
Barre Syndrome - An acquired acute inflammatory demyelinating or
axonal polyneuropathy with four subtypes: Acute inflammatory
demyelinating polyneuropathy, acute motor axonal neuropathy, acute
motor and sensory axonal neuropathy, and fisher syndrome (only 5% of
cases).
Pathophysiology: Considered to be an autoimmune disease triggered by
a preceding bacterial or viral infection (Etiology). Molecular mimicry
(cross-activation of self-epitopes and pathogen-derived peptides by
autoreactive T and B cells) is associated with the immune injury.
Glycolipids, particularly gangliosides, are immune targets. The muscle
innervated by the damaged peripheral nerves undergoes denervation
,and atrophy. If the cell body survives, regeneration of the peripheral
nerve takes place and recovery of function is likely. If the cell body dies
from intense root involvement in the inflammatory-degenerative
process, no regeneration is possible. Collateral reinnervation from
surviving axons and regenerating axons may take place. In this case,
motor recovery is less complete and residual deficits persist.
Clinical Manifestations:Vary depending on subtype. Typically first
manifestations include numbness, pain, paresthesias, or weakness of
the limbs. Motor signs manifest as an acute or subacute progressive
paralysis. Proximal muscles may be involved earlier and more
significantly than distal muscles. Paresis/Paralysis may be in an
ascending pattern, involving the limbs, respiratory muscles, and bulbar
muscles. Only bulbar muscles may be involved resulting in dysphagia
and dysarthria. Weakness plateaus or improves by the fourth week in
90% of cases. Sensory symptoms include: paresthesias/dysthesias,
tingling, burning, shocklike sensations (particularly in the limbs), pain,
and numbness. Respiratory muscle weakness leads to vent support in
10-
Define and describe the pathophysiology, clinical manifestations and
etiology of Huntington disease. CH 17 pg 535- 536 Ans✓✓✓
Huntington Disease also known as chorea, is a relatively rare,
hereditary, degenerative hyperkinetic movement disorder diffusely
involving the basal ganglia and cerebral cortex.
Pathophysiology: The major pathologic feature of HD is severe
degeneration of the basal ganglia and the frontal cerebral cortex.
, Degeneration of the basal ganglia and the substantia nigra exhibit a
depletion of neurons that secrete GABA (an inhibitory
neurotransmitter). GABA depletion leads to an excess of dopaminergic
activity that causes hypotonia and hyperkinesia (involuntary,
fragmentary movements).
Clinical Manifestations:
Abnormal movement and progressive dysfunction of intellectual
processes (dementia) and emotional lability. Chorea (involuntary, quick
movements of the feet or hands comparable to dancing) is the most
common type of abnormal movement affecting individuals with HD. It
begins in the face and arms, eventually affecting the entire body.
Symptoms of frontal lobe dysfunction include attention deficits, short
term memory loss, reduced capacity to plan, organize, and sequence,
as well as bradyphrenia (slow thinking); and apathy.
Etiology:
HD (Chorea) is a rare, hereditary (autosomal dominant)-degenerative
disorder diffusely involving the basal ganglia and cerebral cortex,
commonly manifests between 25-45 years of age, and occurs in all
races. The abnormality is manifested on the short arm of chromosome
4.
Treatment: No known treatment is effective in halting the degenerative
process in HD. The chorea can be treated with dopamine receptor-
blocking or depleting agents, and medical and non- medical care for
depression and aggressive behavior may be required.
