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NU 545 Unit 2 Exam | Actual Questions and Answers Latest
Updated (Graded A+)
1. Review the anatomy of the brain. Which portion is responsible for keeping you awake,
controlling thought, speech, emotions and behavior, maintaining balance and posture?
(pg. 448-453 Table 15.1)
Three major structural divisions of the brain are: the forebrain (prosencephalon), the midbrain
(mesencephalon), the hindbrain (rhombencephalon)
Reticular Formation
➔ Collection of nuclei in the brainstem & large network of diffuse nuclei that connect the
brainstem to the cortex & control vital reflexes, such as cardiovascular function &
respiration. essential for maintaining wakefulness & attention, referred to as the
reticular activating system.
Cerebral Hemisphere (part frontal lobe/ prefrontal area)
➔ Responsible for goal oriented behavior, ability to concentrate, short term memory
recall, elaboration of thought & inhibition on the limbic (emotional) areas of the CNS.
The premotor area is involved in programming motor movements.
Broca area (inferior frontal lobe)
➔ Center for speech & language processing. Injury to this area results in difficulty to form
words (expressive aphasia/or dysphasia)
HindBrain (Cerebellum)
➔ Reflexive, involuntary fine tuning of motor control & for maintaining balance &
posture through extensive neural connections w/ the medulla & midbrain.
Hypothalamus
➔ Functions to maintain a constant internal environment, & implement behavioral
patterns. Integrative centers control ANS function, regulate body temperature,
endocrine function, adjust emotional expression. As listed these include, (Pg. 452, See
Box 15.1):
• Visceral & Somatic responses • Hormone synthesis • Fluid Balance
• Affectual responses • Sympathetic & Parasympathetic Activity • Temperature Regulation
• Appetite/Feeding Responses • Sexual Behavior • Physical Expression of Emotions
• Pleasure-Punishment Centers • Level of Arousal or Wakefulness.
2. Know the function of the arachnoid villi. (pg. 459)
The villi function as one-way valves directing CSF outflow into the blood, but
preventing blood flow into the subarachnoid space.
3. Where is the primary defect in Parkinson’s disease and Huntington’s? (pg. 451)
The Basal ganglia. Both are characterized by disruption of the extrapyramidal system
and various involuntary or exaggerated movements.
, 2
4. What is the function of the CSF? Where is it produced? Where is it absorbed? (pg.
458-459)
● Function: prevent the brain from tugging on meninges, nerve roots, & blood
vessels. Exerts pressure within the brain & spinal cord. CSF flow results from
the pressure gradient between the arterial system & the CSF-filled cavities.
● Production: CSF is produced continually but does not accumulate. Instead, it is
reabsorbed into the venous circulation through the arachnoid villi. It is formed
from blood, & after circulating throughout the CNS, it returns to blood.
● Absorption: reabsorbed through a pressure gradient between the arachnoid villi
& the cerebral venous sinuses.
5. Review blood flow to the brain. (pg. 459-460)
The brain derives its arterial supply from two systems: the internal carotid arteries
(anterior circulation) & the vertebral arteries (posterior circulation).
Brain blood flow: The brain receives about 20% of the cardiac output. CO2 serves as a
primary regulator for blood flow within the CNS as it is a potent vasodilator. The brain derives
its arterial supply from two systems: the internal carotid arteries + the vertebral arteries.
• Internal Carotid Arteries:
They supply a proportionally greater amount of blood flow & supply blood to the anterior
portion of the brain. They originate from the common carotid arteries & enter the cranium
through the base of the skull, pass through the cavernous sinus; after giving off some small
branches, they divide into the anterior & middle cerebral arteries.
• Vertebral Arteries:
They supply the posterior portion of the brain. Originate at the branches of the subclavian
arteries & pass through the transverse foramina of the cervical vertebrae & enter the cranium
through the foramen magnum. They join at the junction of the pons & medulla oblongata to form
the basilar artery.
Three major paired arteries perfuse the cerebellum & brainstem: the posterior inferior
cerebella artery, the anterior inferior cerebellar artery, & the superior cerebella arteries.
• Basilar Artery:
Divides at the level of the midbrain to form paired posterior cerebral arteries. Basilar artery gives
arise to small pontine arteries. The large arteries on the surface of the brain & their branches are
, 3
called superficial arteries. The small branches that project into the brain are termed projecting
arteries.
• Circle of Willis:
Provides an alternate route for blood flow when one of the contributing arteries is obstructed.
The circle of willis is formed by the posterior cerebral arteries , posterior communicating
arteries, internal carotid arteries, anterior cerebral arteries, & anterior communicating artery. The
anterior cerebral , middle cerebral, & posterior cerebral arteries leave the arterial circle & extend
to various brain structures.
***Cerebral venous drainage does NOT parallel its arterial blood supply; whereas the
venous drainage of the brainstem & the cerebellum DO parallel the arterial supply of the
structures. The veins drain into the venous plexuses & dural sinus & eventually join the
internal jugular veins at the base of the skull.
6. What is the gate control theory of pain? (pg. 475)
Explains the complexities of pain phenomenon. Pain is modulated by a “gate”in the
cells of the substantia gelatinosa in the spinal cord. Large, myelinated A-delta fibers & small,
unmyelinated C fibers respond to a broad range of painful stimuli, such as mechanical, thermal,
& chemical. Nociceptive transmission INCREASES pain perception. Non-nociceptive
stimulation DECREASES pain perception.
7. Know the type of nerve fibers that transmit pain impulses. (pg. 475)
- The two primary types of nociceptors are A-delta fibers and C-fibers.
❖ A-delta fibers: large-myelinated, rapidly transmit sharp well-localized “fast”
pain sensations. Activation of these = spinal reflex withdrawal of the affected
area from the stimulus before pain sensation is perceived.
Example: intense heat or pinprick to skin.
❖ C-fibers: small-unmyelinated, located in the muscle, tendon, body organs, and
the skin. Slowly transmit dull, aching, or burning sensations. Poorly localized,
often constant.
❖ A-beta fibers: large myelinated fibers that transmit touch and vibration
sensations. They do not normally transmit pain but do play a role in pain
modulation.
8. Where in the CNS does pain perception occur? (pg.476)
- Primarily in the reticular + limbic systems & cerebral cortex.
9. Know different clinical descriptions of pain (acute, chronic, neuropathic); pain
threshold/tolerance. (pg. 481-483, 503, Table 16.3)
[Threshold = the lowest intensity of pain that can be recognized; pg. 476].
, 4
[Tolerance = the greatest intensity of pain that can be recognized; pg. 476].
● Acute: normal protective mechanism, alerts the individual to a condition or experience
that is immediately harmful to the body, mobilizes the individual to take prompt action
to relieve it. (Examples: cutaneous deep somatic, visceral, or referred).
- Can last seconds to days, sometime up to 3 months.
- Begins suddenly, relieved after the chemical mediators
(r/t to inflammation) that stimulate pain receptors are removed.
- Physical manifestations: increased HR, HTN, diaphoresis, dilated pupils.
Anxiety is also common.
→ ‘Somatic’ (skin, joints, muscles); sharp & well-localized (A-delta fiber
transmissions), OR dull, aching, throbbing, & poorly-localized (seen in C-fiber
transmissions).
→ ‘Visceral’ (internal organs, lining of body cavities); transmitted by C-fibers,
poorly-localized, aching, gnawing, throbbing, or intermittently cramping.
Carried by Sympathetic fibers associated w/ N/V, hypotension, & sometimes
shock. Radiates or is referred. Examples: gallstones, pancreatitis, kidney stones,
bowel obstruction, appendicitis, bladder infections.
→ ‘Referred’ (area removed or distant from point of origin); area of referred is
supplied by the same spinal segment as the actual site of pain. Can be acute OR
chronic. Because the skin has more receptors, the painful sensation is
experienced at the referred site INSTEAD of the point of origin.
● Chronic or Persistent: varies w/ the type of injury, is different among age groups, &
produces varietal levels of disability. Changes in PNS & CNS noted.
- Can last more than 3-6 months in adults.
- Lasts well beyond expected normal healing time. Ongoing (ex. low back pain)
or intermittent (ex. migraines).
- Appears to be out of proportion to any observable tissue injury.
- Serves no purpose, poorly understood, causes suffering.
- Behavioral & Psychological changes often emerge → depression, cognitive
deficits, difficulty eating/sleeping, preoccupation w/ pain, avoidance of
pain-provoking stimuli.
● Neurological: chronic pain initiated or caused by a primary lesion or dysfunction in the
somatosensory nervous system. Leads to the long-term changes in pain pathway
structures (neuroplasticity) & abnormal processing of sensory information.
- Amplification of pain w/o stimulation by injury or inflammation.
- Burning, shooting, shock-like, or tingling.
NU 545 Unit 2 Exam | Actual Questions and Answers Latest
Updated (Graded A+)
1. Review the anatomy of the brain. Which portion is responsible for keeping you awake,
controlling thought, speech, emotions and behavior, maintaining balance and posture?
(pg. 448-453 Table 15.1)
Three major structural divisions of the brain are: the forebrain (prosencephalon), the midbrain
(mesencephalon), the hindbrain (rhombencephalon)
Reticular Formation
➔ Collection of nuclei in the brainstem & large network of diffuse nuclei that connect the
brainstem to the cortex & control vital reflexes, such as cardiovascular function &
respiration. essential for maintaining wakefulness & attention, referred to as the
reticular activating system.
Cerebral Hemisphere (part frontal lobe/ prefrontal area)
➔ Responsible for goal oriented behavior, ability to concentrate, short term memory
recall, elaboration of thought & inhibition on the limbic (emotional) areas of the CNS.
The premotor area is involved in programming motor movements.
Broca area (inferior frontal lobe)
➔ Center for speech & language processing. Injury to this area results in difficulty to form
words (expressive aphasia/or dysphasia)
HindBrain (Cerebellum)
➔ Reflexive, involuntary fine tuning of motor control & for maintaining balance &
posture through extensive neural connections w/ the medulla & midbrain.
Hypothalamus
➔ Functions to maintain a constant internal environment, & implement behavioral
patterns. Integrative centers control ANS function, regulate body temperature,
endocrine function, adjust emotional expression. As listed these include, (Pg. 452, See
Box 15.1):
• Visceral & Somatic responses • Hormone synthesis • Fluid Balance
• Affectual responses • Sympathetic & Parasympathetic Activity • Temperature Regulation
• Appetite/Feeding Responses • Sexual Behavior • Physical Expression of Emotions
• Pleasure-Punishment Centers • Level of Arousal or Wakefulness.
2. Know the function of the arachnoid villi. (pg. 459)
The villi function as one-way valves directing CSF outflow into the blood, but
preventing blood flow into the subarachnoid space.
3. Where is the primary defect in Parkinson’s disease and Huntington’s? (pg. 451)
The Basal ganglia. Both are characterized by disruption of the extrapyramidal system
and various involuntary or exaggerated movements.
, 2
4. What is the function of the CSF? Where is it produced? Where is it absorbed? (pg.
458-459)
● Function: prevent the brain from tugging on meninges, nerve roots, & blood
vessels. Exerts pressure within the brain & spinal cord. CSF flow results from
the pressure gradient between the arterial system & the CSF-filled cavities.
● Production: CSF is produced continually but does not accumulate. Instead, it is
reabsorbed into the venous circulation through the arachnoid villi. It is formed
from blood, & after circulating throughout the CNS, it returns to blood.
● Absorption: reabsorbed through a pressure gradient between the arachnoid villi
& the cerebral venous sinuses.
5. Review blood flow to the brain. (pg. 459-460)
The brain derives its arterial supply from two systems: the internal carotid arteries
(anterior circulation) & the vertebral arteries (posterior circulation).
Brain blood flow: The brain receives about 20% of the cardiac output. CO2 serves as a
primary regulator for blood flow within the CNS as it is a potent vasodilator. The brain derives
its arterial supply from two systems: the internal carotid arteries + the vertebral arteries.
• Internal Carotid Arteries:
They supply a proportionally greater amount of blood flow & supply blood to the anterior
portion of the brain. They originate from the common carotid arteries & enter the cranium
through the base of the skull, pass through the cavernous sinus; after giving off some small
branches, they divide into the anterior & middle cerebral arteries.
• Vertebral Arteries:
They supply the posterior portion of the brain. Originate at the branches of the subclavian
arteries & pass through the transverse foramina of the cervical vertebrae & enter the cranium
through the foramen magnum. They join at the junction of the pons & medulla oblongata to form
the basilar artery.
Three major paired arteries perfuse the cerebellum & brainstem: the posterior inferior
cerebella artery, the anterior inferior cerebellar artery, & the superior cerebella arteries.
• Basilar Artery:
Divides at the level of the midbrain to form paired posterior cerebral arteries. Basilar artery gives
arise to small pontine arteries. The large arteries on the surface of the brain & their branches are
, 3
called superficial arteries. The small branches that project into the brain are termed projecting
arteries.
• Circle of Willis:
Provides an alternate route for blood flow when one of the contributing arteries is obstructed.
The circle of willis is formed by the posterior cerebral arteries , posterior communicating
arteries, internal carotid arteries, anterior cerebral arteries, & anterior communicating artery. The
anterior cerebral , middle cerebral, & posterior cerebral arteries leave the arterial circle & extend
to various brain structures.
***Cerebral venous drainage does NOT parallel its arterial blood supply; whereas the
venous drainage of the brainstem & the cerebellum DO parallel the arterial supply of the
structures. The veins drain into the venous plexuses & dural sinus & eventually join the
internal jugular veins at the base of the skull.
6. What is the gate control theory of pain? (pg. 475)
Explains the complexities of pain phenomenon. Pain is modulated by a “gate”in the
cells of the substantia gelatinosa in the spinal cord. Large, myelinated A-delta fibers & small,
unmyelinated C fibers respond to a broad range of painful stimuli, such as mechanical, thermal,
& chemical. Nociceptive transmission INCREASES pain perception. Non-nociceptive
stimulation DECREASES pain perception.
7. Know the type of nerve fibers that transmit pain impulses. (pg. 475)
- The two primary types of nociceptors are A-delta fibers and C-fibers.
❖ A-delta fibers: large-myelinated, rapidly transmit sharp well-localized “fast”
pain sensations. Activation of these = spinal reflex withdrawal of the affected
area from the stimulus before pain sensation is perceived.
Example: intense heat or pinprick to skin.
❖ C-fibers: small-unmyelinated, located in the muscle, tendon, body organs, and
the skin. Slowly transmit dull, aching, or burning sensations. Poorly localized,
often constant.
❖ A-beta fibers: large myelinated fibers that transmit touch and vibration
sensations. They do not normally transmit pain but do play a role in pain
modulation.
8. Where in the CNS does pain perception occur? (pg.476)
- Primarily in the reticular + limbic systems & cerebral cortex.
9. Know different clinical descriptions of pain (acute, chronic, neuropathic); pain
threshold/tolerance. (pg. 481-483, 503, Table 16.3)
[Threshold = the lowest intensity of pain that can be recognized; pg. 476].
, 4
[Tolerance = the greatest intensity of pain that can be recognized; pg. 476].
● Acute: normal protective mechanism, alerts the individual to a condition or experience
that is immediately harmful to the body, mobilizes the individual to take prompt action
to relieve it. (Examples: cutaneous deep somatic, visceral, or referred).
- Can last seconds to days, sometime up to 3 months.
- Begins suddenly, relieved after the chemical mediators
(r/t to inflammation) that stimulate pain receptors are removed.
- Physical manifestations: increased HR, HTN, diaphoresis, dilated pupils.
Anxiety is also common.
→ ‘Somatic’ (skin, joints, muscles); sharp & well-localized (A-delta fiber
transmissions), OR dull, aching, throbbing, & poorly-localized (seen in C-fiber
transmissions).
→ ‘Visceral’ (internal organs, lining of body cavities); transmitted by C-fibers,
poorly-localized, aching, gnawing, throbbing, or intermittently cramping.
Carried by Sympathetic fibers associated w/ N/V, hypotension, & sometimes
shock. Radiates or is referred. Examples: gallstones, pancreatitis, kidney stones,
bowel obstruction, appendicitis, bladder infections.
→ ‘Referred’ (area removed or distant from point of origin); area of referred is
supplied by the same spinal segment as the actual site of pain. Can be acute OR
chronic. Because the skin has more receptors, the painful sensation is
experienced at the referred site INSTEAD of the point of origin.
● Chronic or Persistent: varies w/ the type of injury, is different among age groups, &
produces varietal levels of disability. Changes in PNS & CNS noted.
- Can last more than 3-6 months in adults.
- Lasts well beyond expected normal healing time. Ongoing (ex. low back pain)
or intermittent (ex. migraines).
- Appears to be out of proportion to any observable tissue injury.
- Serves no purpose, poorly understood, causes suffering.
- Behavioral & Psychological changes often emerge → depression, cognitive
deficits, difficulty eating/sleeping, preoccupation w/ pain, avoidance of
pain-provoking stimuli.
● Neurological: chronic pain initiated or caused by a primary lesion or dysfunction in the
somatosensory nervous system. Leads to the long-term changes in pain pathway
structures (neuroplasticity) & abnormal processing of sensory information.
- Amplification of pain w/o stimulation by injury or inflammation.
- Burning, shooting, shock-like, or tingling.
