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Pathophys Semester II > CNS PT-1 Test II > Flashcards

CNS PT-1 Test II Flashcards

1
Q

What are the Neuroglia?

A

Astrocytes (buffers / detoxifiers)

Oligodendrocytes (Produce Myelin)

Ependymal Cells (Produce CSF)

Microglia (Macrophage)

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2
Q

What are the Major Levels of the CNS & ARAS?

A

Spinal Cord Level

Lower Brain or Subcortical Level (Subconcious level)

  • Medula, Pons, hypothalamus, cerebellum, basal ganglia

Higher Brain or Cortical Level

-Cerebral cortex helps direct Lower Brain level

Ascending Reticular Activating System (ARAS)

  • Brainstem from medulla to diencephalon
  • Relays environmental stimuli to Cerebral Cortex
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3
Q

What is the Role of the Cerebral Cortex?

A

Performs associative activities such as thinking, learning, and remembering.

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4
Q

What is the Role of the Thalamus?

A

Interprets sensory messages such as pain, temp, and pressure.

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5
Q

What is the role of the Hypothalamus?

A

Controls homeostatic functions such as body temp, respiration, and Heartbeat.

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6
Q

What is the role of the Cerebellum?

A

Coordinates muscle tone, posture, and balance.

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7
Q

What is the role of the Brainstem?

A

Regulates Heartbeat and breathing, plays a role in consciousness.

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8
Q

Barrier Systems in the Brain.

A

BBB

A series of high resistance tight junctions between endothelial cells as well as astrocytes with processes on capillary walls

Blood-CSF barrier

Formed by tight junctions between choroid epithelial cells

Both Barriers

Produce cytokines, and Astrocytes can act as APCs

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9
Q

How does Wallerian degeneration work in the PNS?

A

Post nerve transection, nearby peripheral nerve cells will reinnervate the damages nerve / muscle.

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10
Q

How does Wallerian degeneration work in the CNS?

A

Macrophages clear, astrocytes enlarge, proliferate, and a glial scar blocking axonal growth.

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11
Q

Reactions of Glial injury.

A

Astrocytes

Can suffer acute cell injury due to hypoxia/hypoglycemia, and toxic injuries causes cellular swelling.

Oligodendrocytes

Injury or apoptosis of oligodendrocytes is a feature of acquired demyelinating disorders

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12
Q

Intracranial Pressure (ICP)

A

The pressure inside the cranial cavity.

Normal <or></or>

<p>Intercranial Hypertension (ICH) &gt;or = 20 mmHg</p>

<p> </p>

<p>Components</p>

<p>Cerebral parenchyma 80%</p>

<p>CSF 10%</p>

<p>Blood 10%</p>

</or>

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13
Q

How does the brain manage ICP?

A

Displacement of CSF into the thecal sac

Decrease of cerebral Venous volume of the Cerebral Venous blood by Vaso Constriction.

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14
Q

Normal Pressure Hydrocephalus

A

Enlarged ventricular size, but with normal Pressures on Lumbar puncture

Communicating

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15
Q

NPH Idiopathic NPH Pathophysiology

A

Cerebrovascular disease

-HTN, CAD, and PAD

Decreased CSF absorption

Increased Central Venous Pressure

Neurodegenerative disorder

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16
Q

Secondary NPH Pathophysiology

A

Intraventricular or subarachnoid hemorrhage (aneurysm or trauma) and prior acute or ongoing chronic meningitis.

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17
Q

Clinical Triad of NPH

A

Gait Difficulty

Cognitive deficits

Urinary incontinence

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18
Q

Clinical Manifestations of Increased ICP

Global Symptoms

A

Headache

Decreased consciousness

Vomiting

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19
Q

Clinical Manifestations of Increased ICP

Focal Symptoms

A

Herniation

3 Settings

  • Cerebral Edema*
  • Increased CSF volume*
  • Mass/Lesions*

Type

Tonsillar Herniation (brainstem herniation) compromises vital respiratory and cardiac centers in the medulla

20
Q

What is the range of cerebral blood flow regulation?

A

60-150 mmHg

Failure of autoregulation at 180 mmHg

Causes Cerebral edema

21
Q

Cerebral Perfusion Pressure (CPP)

A

Measure for cerebral perfusion

CPP=Mean Arterial Pressure (MAP)-ICP

22
Q

What are the two types of Cerebral Edema?

A

Vasogenic Edema

Irreversible increase in extracellular fluid

Caused by BBB disruption, inc Vascular permiability, no tight junctions

Cytotoxic Edema

Potentially reversable inc in intracellular fluid secondary to neural cell damage

Caused by Hypoxia/ischemia

23
Q

Mechanisms of Ischemic Cell injury and death

A

Part of the brain undergoes immediate death, while others are partially injured and have the potential to recover.

24
Q

Cerebrovascular disease

A

A pathophysiological process involving blood vessels of the brain

Intrinsic to the vessel

Originate Remotely

Decreased blood flow

or

Rupture in the subarachnoid or intracerebral tissue

25
Q

TIA vs Ischemic Stroke

A

Stroke caused by acute infarction with cell death and/or evidence of permanent injury.

TIA transient event caused by ischemia not infarction

26
Q

TIA Mechanisms

A

Embolic

Large artery, low flow

Lacunar or small penetrating vessel TIA, caused by stenosis

27
Q

High risk TIA

A

Atherothrombotic lesions at the origin of the Internal Carotid Artery >50% narrowed

Atherothrombotic lesions at the Basilar artery

Emboli to the Basilar Artery

Dissection lesions at the internal carotid artery or as it enters the foramen transversium

28
Q

Types of Intracerebral Hemorrhage

A

Intraparenchymal Brain Hemorrhage (IPH)

Tears in Brain tissue/vasculature or nontraumatic bleeding

Subarachnoid hematoma (SAH)

nontraumatic Causes

Subdural Hematoma (SDH)

damage to bridging veins or tearing of vortical Veins

Epidural hematoma (EDH)

Blunt trauma may tear the middle meningeal artery

29
Q

Atraumatic/Spontaneous Intracranial Hemorrhage (IGH)

A

Hypertensive Vasculopathy

Symptoms dependent on size and location of bleed, increase gradually over time, headache, vomiting, and decreased level of conciousness.

30
Q

Atraumatic/Spontaneous ICH Pathogenesis

A

Cerebral Microbleeds

Microscopic pseudoaneurysm formation with subclinical leaks of blood

Hemorrhage enlargement

Associated with neurologic deterioration and worse outcomes

Brain Damage

31
Q

Primary Brain Damage Post ICH

A

Primary

Parenchymal blood accumulation

  • Tissue disruption*
  • Mechanical damage*
  • Elevated ICP*
  • Damaged BBB casues Edema*
32
Q

Secondary Brain Damage Post ICH

A

Thrombin activation

Lysis of RBCs causes release of hemoglobin which is converted to Heme and Iron

By Oxidative stress

Inflammatory reaction

Release proinflammatory mediators

33
Q

What is the Etiology of Spinal Dysraphism (Spina Bifida)

A

Multifactoral origin

Folate deficiency during the first several weeks of gestation

34
Q

Myelomeningocelle’s Neurological Abnormalities

A

Chiari II Malformation

Pressure exerted on the Cerebellum and medulla by malformed bone at base of skull

Hydrocephalus

Caused by Chiari II

Spinal Cord

Affect trunk, legs, bladder, and bowell-> complete paralysis and absence of sensation.

Brain Stem

Due to Chiari II -> swallowing difficulties, vocal cord paresis

35
Q

Cerebral Palsy

A

Permanent non-progressive central motor dysfunction, affect Tone, Posture, and movement

36
Q

Etiology and risk factors of CP

A

Multifactorial

Most due to prenatal factors

Prematurity

low birth weight

Periventricular leukomalacia

37
Q

Pathogenesis of Cerebral Palsy

A

Focal white matter injuries produced at specific locus in the white matter such as:

Periventricular white matter

PVL

Necrosis of white matter near the lateral ventricles

usually occurs in premature infants

Etiology

  • Decreased oxygen/blood flow to* periventricular region
  • Damage to glial cells*
38
Q

In TBI what determines the extent of the injury?

A

Location

Bodies ability to repair

Magnitude

Distribution

Affected by shape and force of object impacting, as well as the motion of the head at the moment of injury

39
Q

Primary TBI

A

Tissue shearing at the interface of grey and white matter (diffuse axonial injury (DAI))

Cerebral contusions

Extra-axial hematomas

epidural, subdural, subarachnoid hemorrhage and intraventricular

40
Q

Secondary TBI

A

Excitotoxicity

Electrolyte imbalance

Inflammatory response

Apoptosis

Secondary ischemia

41
Q

Acute mild TBI - Concussion

A

GCS of 13-15

Results from direct external contact forces or from acceleration/deceleration trauma

Symptoms functional rather than structural

Confusion and amnesia common manifestations

42
Q

Chronic Traumatic Encephalopathy (CTE)

A

Dementing illness resulting after repeated minor TBI

Generally Sports and combat-related

Distinct from AD in that there is a preferred distribution in the superficial cortical layers

43
Q

Meningits

A

Inflammation of the leptomeninges within the subarachnoid space.

Acute Pyrogenic (usually bacterial)

Aseptic (Usually Viral)

CHronic (Usually TB, Spirochetal or cryptococcal)

Meningoencephalitis: inflammation of the Meninges and brain Parenchyma

Mainly in adults: Streptococcus pneumoniae and Neisseria meningitidis

44
Q

Pathogenesis of bacterial meningitis

A

Colonization

Invasion

Intravascular Survival

Meningeal Invasion

45
Q

Pathophysiology of Meningitis

A

Cytokine production leading to

Increased BBB permeability

Altered Cerebral blood flow

Increased reactive Oxygen species

46
Q

Aseptic Meningitis

A

PTs who have clinical and laboratory evidence for meningeal inflammation with negative routine bacterial cultures.

Result of Enteroviruses

Similar presentation to bacterial meningitis, but self limiting

Pathophys Semester II (14 decks)

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