which of the following causes hepatic encephalopathy
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ATI RN

ATI Pathophysiology Exam 1

1. What causes hepatic encephalopathy?

Correct answer: B

Rationale: Hepatic encephalopathy is caused by increased ammonia levels in the bloodstream. Ammonia, a byproduct of protein metabolism normally processed by the liver, accumulates in the bloodstream when the liver is unable to function properly. This excess ammonia affects brain function, leading to symptoms of hepatic encephalopathy. Choices A, C, and D are incorrect because they do not directly relate to the pathophysiology of hepatic encephalopathy.

2. In Guillain-Barre syndrome, what pathophysiologic process underlies the deficits that accompany the degeneration of myelin in the peripheral nervous system (PNS)?

Correct answer: C

Rationale: In Guillain-Barre syndrome, the destruction of myelin leads to axonal damage. If remyelination does not occur, the axon will eventually degenerate and die, impacting nerve function. Choice A is incorrect because the destruction of myelin does not affect Schwann cell production. Choice B is incorrect as the lack of myelin directly affects the conduction of nerve impulses, not the axonal transport system. Choice D is incorrect as a deficit of myelin does not predispose the client to infections by potential pathogens.

3. A client with a diagnosis of depression has been prescribed a medication that ultimately increases the levels of the neurotransmitter serotonin between neurons. Which process will accompany the actions of the neurotransmitter in a chemical synapse?

Correct answer: D

Rationale: When serotonin levels increase, more neurotransmitters will cross the synaptic cleft and bind with postsynaptic receptors, facilitating enhanced communication. Option A is incorrect because chemical synapses, unlike electrical synapses, are unidirectional. Option B is incorrect because neurotransmitters impact communication with multiple neurons, not just a single connected neuron. Option C is incorrect because neurotransmitters cross the synaptic cleft, not gap junctions.

4. A 74-year-old woman states that many of her peers underwent hormone replacement therapy (HRT) in years past. The woman asks the nurse why her primary care provider has not yet proposed this treatment for her. What fact should underlie the nurse's response to the woman?

Correct answer: A

Rationale: The correct answer is A because the main reason HRT is not recommended for all women is due to the increased risks of stroke and breast cancer associated with its use. Hormone replacement therapy (HRT) has been linked to an elevated risk of stroke and breast cancer, which outweigh its potential benefits for many individuals. Choices B, C, and D are incorrect as they do not address the primary concerns regarding HRT use. While HRT can indeed cause mood disturbances and may affect bone health, the significant risks of stroke and breast cancer are the primary reasons why healthcare providers may choose not to recommend HRT for some women.

5. The parents of a 3-year-old boy have brought him to a pediatrician for assessment of the boy's late ambulation and frequent falls. Subsequent muscle biopsy has confirmed a diagnosis of Duchenne muscular dystrophy. Which teaching point should the physician include when explaining the child's diagnosis to his parents?

Correct answer: A

Rationale: The correct teaching point that the physician should include when explaining Duchenne muscular dystrophy to the parents is that 'Your child may develop breathing difficulties as the disease progresses.' Duchenne muscular dystrophy is a progressive condition that affects muscle strength, including respiratory muscles, leading to breathing difficulties as the disease advances. Choice B is incorrect because while physical therapy and exercise can help maintain muscle function and mobility, they do not cure the condition. Choice C is incorrect because Duchenne muscular dystrophy is a genetic disorder with no known cure. Choice D is incorrect as Duchenne muscular dystrophy is primarily characterized by a lack of dystrophin protein due to genetic mutations, not inflammation in the muscles.

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