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Flashcards in BRS Histology - Nervous System Deck (15)
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1

Neural crest cells give rise to which of the following?

(A) Dorsal horns of the spinal cord

(B) Adrenal cortex

(C) Sympathetic ganglia

(D) Preganglionic autonomic nerves

(E) Somatic motor neurons

C.

Neural crest cells migrate throughout the body and give rise to ganglia and other struc- tures, including portions of the adrenal medulla, but they do not contribute to the devel- opment of preganglionic autonomic nerves, adrenal cortex, or the dorsal horns of the spinal cord (see Chapter 9 II D).

2

Which one of the following neurotransmit- ters functions to increase cardiac output?

(A) Dopamine

(B) Serotonin

(C) Norepinephrine

(D) Glutamate

(E) GABA

C.

Norepinephrine increases cardiac output, whereas dopamine and

3

Which of the following statements regarding nerve cell membrane potentials is true?

(A) Membrane potentials are maintained at rest by Na+ entering the cell.

(B) Entrance of K+ causes the membrane to return to its resting potential.

(C) Depolarization triggers the opening of voltage-gated K+ channels.

(D) Voltage-gated Na+ channels become activated during the refractory period.

(E) The influx of K+ reverses the resting potential.

 C.

Once the critical threshold is reached, voltage-gated Na

4

Which of the following statements is characteristic of the perineurium?

(A) It is a fascia surrounding many bundles of nerve fibers.

(B) It is the fascia surrounding a single nerve fiber.

(C) It is a thin layer of reticular fibers covering individual nerve fibers.

(D) It is a fascia that excludes macromolecules and forms the external coat of nerves.

(E) It consists in part of epithelioid cells that surround a bundle (fascicle) of nerve fibers.

E.

Each bundle of nerve fibers is surrounded by the perineurium, which consists primarily of several layers of epithelioid cells. Tight junctions between these cells exclude most macromolecules. The external coat of nerves, the epineurium, surrounds many fascicles but does not exclude macromolecules. The layer of reticular fibers that covers individual nerve fibers is the endoneurium; it also does not exclude macromolecules (see Chapter 9 VI A).

5

Acetylcholine is the only neurotransmitter in which of the following regions of the nervous system?

(A) Central nervous system

(B) Presynaptic sensory cortex

(C) Myoneural junctions

(D) Postganglionic sympathetic synapses

(E) Motorcortex

 C.

Acetylcholine is the neurotransmitter for myoneural junctions as well as for preganglionic sympathetic and preganglionic and postganglionic parasympathetic synapses (Table 9.1).

6

Nissl bodies are composed of

(A) synaptic vesicles and acetylcholine.

(B) polyribosomes and rough endoplasmic reticulum.

(C) lipoprotein and melanin.

(D) neurofilaments and microtubules.

(E) smooth endoplasmic reticulum and mitochondria.

B.

Nissl bodies are large, granular basophilic bodies composed of polysomes and rough endoplasmic reticulum. They are found only in neurons (in the soma cytoplasm) (see Chapter 9 III A 3).

7

The axon hillock contains

(A) rough endoplasmic reticulum.

(B) ribosomes.

(C) microtubules.

(D) Golgi complex.

(E) synaptic vesicles.

C

The axon hillock is devoid of large organelles, such as Nissl bodies and Golgi cisternae, but it does contain microtubules arranged in bundles and permits passage of neurofilaments, mitochondria, and vesicles into the axon (see Chapter 9 III A 3 c).

8

Synaptic vesicles possess which of the following characteristics?

(A) Manufacture neurotransmitter

(B) Enter the synaptic cleft

(C) Become in corporated into the presynaptic membrane

(D) Become incorporated into the postsynaptic membrane

(E) Release neurotransmitter via endocytosis

C.

Synaptic vesicles release neurotransmitter into the synaptic cleft by exocytosis. In this process, the vesicle membrane is incorporated into the presynaptic membrane. Although these vesicles contain neurotransmitter, they do not manufacture it (see Chapter 9 IV B 2).

9

A patient with Hirschsprung presents with which of the following symptoms?

(A) Absent cranial vault

(B) Exposed spinal cord

(C) Headache

(D) Large, dilated colon

(E) Absent small intestine

D.

Hirschsprung disease is characterized by a dilated colon caused by the absence of the parasympathetic myenteric ganglia known as Auerbach plexus (see Chapter 9 II D Clinical Considerations).

10

Myelination of peripheral nerves is accomplished by

(A) astrocytes.

(B) oligodendrocytes.

(C) Schwann cells.

(D) neural crest cells.

(E) basket cells.

C.

Schwann cells produce myelin in the peripheral nervous system, whereas oligodendro- cytes produce myelin in the central nervous system. Astrocytes, neural crest cells, and bas- ket cells do not produce myelin (see Chapter 9 V A B).

11

Episodes of demyelination are associated with

(A) meningitis.

(B) Huntington chorea.

(C) spina bifida.

(D) Parkinson disease.

(E) multiple sclerosis

E.

Multiple sclerosis is an immune-mediated disease exhibiting chronic and progressive dysfunction of the nervous system due to demyelination of the CNS and optic nerves, striking the 20- to 40-year age group affecting 1.5 times more women than men. There are random episodes of inflammation, edema, and demyelination of axons followed by peri- ods of remission. Each episode may reduce the vitality of the patient and be sufficient to cause death within months (see Chapter 9 V B Clinical Considerations).

12

Tremors, shuffling gate, and masklike facial expressions are associated with

(A) meningitis.

(B) Huntington chorea.

(C) spina bifida.

(D) Parkinson disease.

(E) multiple sclerosis.

D.

Parkinson disease is a progressive degenerative disease characterized by tremors, mus- cular rigidity, difficulty in initiating movements, slow voluntary shuffling movement, and masklike face. The cause is the loss of dopaminergic neurons from the substantia nigra of the brain. Although the cause of the loss of these cells is unclear, it is known that certain poisons and environmental factors cause Parkinson disease (see Chapter 9 IV A Clinical Considerations).

13

Loss of neurotransmitter GABA is associated with

(A) meningitis.

(B) Huntington chorea.

(C) spina bifida.

(D) Parkinson disease.

 (E) multiple sclerosis

B.

Huntington chorea is a fatal heredity disease that becomes evident during the third and fourth decades of life. It progresses to uncontrolled flicking of joints, motor disfunction, dementia, and death. The cause is apparently the loss of neurons that produce the neuro- transmitter GABA. Dementia symptoms are thought to be related to the loss of cells secret- ing acetylcholine (see Chapter 9 IV A Clinical Considerations).

14

Rapid onset of fever, stiff neck, headache, and an altered state of consciousness are associated with

(A) meningitis.

(B) Huntington chorea.

(C) spina bifida.

(D) Parkinson disease.

(E) multiple sclerosis.

A.

Meningitis results from an inflammation of the meninges caused by viral or bacterial infection in the CSF. Although viral meningitis is not severe, bacterial meningitis is conta- gious and dangerous, leading to hearing loss, learning disability, brain damage, and death if untreated, sometimes within 24 hours. Major symptoms include fever, headache, stiff neck, and alteration of consciousness with rapid onset and progression. Spinal tap and culture of CFS to determine the bacterial species is the only diagnosis. Treatment is by species-specific antibiotic. Bacterial meningitis can be spread by respiratory and throat secretions (i.e., coughing, sneezing, kissing) (see Chapter 9 VI A Clinical Considerations).

15

Deterioration and death of the dopamin- ergic neurons within the substantia nigra of the brain are associated with

(A) meningitis.

(B) Huntington chorea.

(C) spina bifida.

(D) Parkinson disease.

(E) multiple sclerosis.

D.

Parkinson disease is a progressive degenerative disease characterized by tremors, mus- cular rigidity, difficulty in initiating movements, slow voluntary shuffling movement, and masklike face. It is caused by the loss of dopaminergic neurons from the substantia nigra of the brain (see Chapter 9 IV A Clinical Considerations).