During an interview with a male client who has Parkinson's disease (PD), the nurse notices that he is drooling and mumbling. Which pathophysiological factor contributes to the client's inability to express himself?
Damage to Broca's area in temporal lobe of brain.
Degeneration of dopaminergic neurons of the basal ganglia.
Brain atrophy with diffuse amyloid plaques disposition.
Paralysis of the pharyngeal and epiglottal area.
The Correct Answer is B
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra of the basal ganglia. This degeneration leads to a deficiency of dopamine, a neurotransmitter involved in the regulation of movement and coordination. The inability to express oneself, as seen in the client's mumbling, can be attributed to the motor symptoms of PD, particularly bradykinesia (slowness of movement) and hypomimia (reduced facial expression), which result from dopaminergic neuron degeneration.
A) Damage to Broca's area in the temporal lobe of the brain:
Damage to Broca's area typically results in expressive aphasia, which is characterized by difficulty speaking and forming coherent sentences. While speech difficulties can occur in PD, they are primarily due to motor dysfunction rather than damage to specific language centers in the brain.
B) Degeneration of dopaminergic neurons of the basal ganglia:
Correct. Degeneration of dopaminergic neurons in the basal ganglia, particularly the substantia nigra, is the primary pathological factor in Parkinson's disease. This degeneration leads to motor symptoms such as bradykinesia, tremor, and rigidity, which can affect the client's ability to speak clearly and express himself.
C) Brain atrophy with diffuse amyloid plaques disposition:
This description is more characteristic of Alzheimer's disease, a different neurodegenerative disorder characterized by brain atrophy and the deposition of amyloid plaques. While cognitive impairment can occur in PD, the primary motor symptoms are related to dopaminergic neuron degeneration rather than amyloid plaque deposition.
D) Paralysis of the pharyngeal and epiglottal area:
Paralysis of the pharyngeal and epiglottal area can lead to dysphagia (difficulty swallowing) rather than difficulty expressing oneself verbally. While dysphagia can occur in PD, it is not typically the primary factor contributing to speech difficulties in this condition.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
A) Flank pain and profound hypotension:
Correct. Flank pain, often described as a deep, constant, gnawing, or throbbing sensation in the abdomen or back, can be a sign of impending rupture or dissection of an abdominal aortic aneurysm (AAA). Profound hypotension may occur if the AAA ruptures, leading to massive internal bleeding and shock. Prompt recognition of these signs is crucial for early intervention and surgical repair to prevent catastrophic consequences.
B) Acute shortness of breath and chest pain:
Acute shortness of breath and chest pain are more indicative of cardiovascular or pulmonary conditions such as myocardial infarction, pulmonary embolism, or acute coronary syndrome rather than an abdominal aortic aneurysm. While aortic dissection can present with chest pain, it is typically described as severe, tearing, or ripping pain that radiates to the back, not as acute shortness of breath.
C) Absent pedal pulses and darkened toes:
Absent pedal pulses and darkened toes may indicate peripheral vascular disease or critical limb ischemia but are not specific signs of an abdominal aortic aneurysm. While AAA can lead to peripheral ischemia in advanced cases, it is not typically associated with acute changes in pedal pulses or toe discoloration.
D) Tea-colored urine and decreased output:
Tea-colored urine and decreased urine output may indicate acute kidney injury or rhabdomyolysis but are not specific signs of an abdominal aortic aneurysm. While a ruptured AAA can lead to renal ischemia and acute kidney injury due to hypoperfusion, these symptoms are not the primary manifestations of AAA
Correct Answer is A
Explanation
Gout is a type of inflammatory arthritis caused by the deposition of monosodium urate crystals in the joints and surrounding tissues. Here's an explanation of the pathophysiological process producing the symptoms of gout:
A) Deposition of crystals in the synovial space of the joints produces inflammation and irritation:
Correct. In gout, elevated levels of uric acid in the blood lead to the formation and deposition of monosodium urate crystals in the synovial fluid of joints, particularly in the big toe joint (first metatarsophalangeal joint) in many cases. These crystals trigger an inflammatory response, activating immune cells and causing swelling, redness, warmth, and severe pain in the affected joint. The inflammation and irritation result from the body's immune response to the presence of these crystals.
B) Chondrocyte injury destroys joint cartilage, producing osteophytes and joint inflammation:
This option describes a process more characteristic of osteoarthritis, where degeneration of joint cartilage leads to the formation of osteophytes (bone spurs) and joint inflammation. Gout involves the deposition of urate crystals rather than direct chondrocyte injury.
C) An immune complex and autoantibody deposition in connective tissue results in inflammation:
This process describes the pathophysiology of autoimmune diseases such as rheumatoid arthritis, where immune complexes and autoantibodies contribute to inflammation and tissue damage. In gout, the inflammation is primarily triggered by the deposition of urate crystals rather than immune complex deposition.
D) An autoimmune inflammation involving IgG response to an antigen causes joint destruction:
This option describes the autoimmune process seen in diseases like rheumatoid arthritis, where antibodies target specific antigens, leading to joint destruction. Gout is not an autoimmune disease, and joint destruction in gout is primarily due to inflammation caused by urate crystal deposition rather than autoimmune mechanisms.
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