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Patho II > CNS-I > Flashcards

CNS-I Flashcards

1
Q

Astrocytes

A

o Acts as metabolic buffers and detoxifiers within the brain
o Modulate how neurons communicate

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2
Q

Oligodendrocytes

A

o Produce a fatty substance called myelin which is wrapped around axons as layer of insulation (increases conduction)

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3
Q

Ependymal cells

A

o Line the spinal cord and ventricles of the brain

o involved in producing CSF

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4
Q

Microglia

A

o Resident macrophages (involved in neuro-inflammation)

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5
Q

Sensory information enters the CNS through peripheral nerves and is conducted immediately to:

A 
o	The spinal cord at all levels 
o	Medulla, pons and mesencephalon 
o	The cerebellum 
o	The thalamus 
o	Areas of the cerebral cortex
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6
Q

The most important role of the nervous system is to

A

control the various bodily activities

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7
Q

The nervous system controls various bodily activities through three mechanisms

A

o Contraction of skeletal muscles through out the body
o Contraction of smooth muscles in the internal organs
o Secretion of active chemical substances by both exocrine and endocrine glands

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8
Q

Muscle glands are known as the

A

effectors

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9
Q

What sends signals to control the Spinal cord level ?

what responses does the spinal cord level produce?

A

o The upper levels of the nervous system send signals to the control centers of the cord
→ Movement, reflexes -like when you touch a hot stove

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10
Q

Lower Brain or Subcortical Level function??

Its composed of?

A

o Subconscious activities of the body are controlled in the lower areas of the brain
→ The medulla, pons, hypothalamus, thalamus, cerebellum, and basal ganglia

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11
Q

Higher Brain or Cortical Level

A

o Without the cerebral cortex, the functions of the lower brain’s centers are not often accurate
o The cerebral cortex cannot function by itself

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12
Q

Ascending Reticular Activating System (ARAS)

A

o In the brainstem from the medulla to the diencephalon

o Relays innervation from the environment stimuli to the thalamus and then to the cerebral cortex (midbrain?)

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13
Q

Functions of the cerebral cortex

A

o Thinking, learning, and remembering

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14
Q

Functions of the Thalamus

A

o Interprets certain sensory messages such as those of pain, temperature, and pressure

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15
Q

Functions of the Hypothalamus

A

Controls various homeostatic functions – body temp, respiration, and heartbeat

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16
Q

Functions of the Cerebellum

A

Contributes to muscle tone, posture, and balance

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17
Q

Functions of the Brain Stem

A

o Regulates heartbeat and breathing
→ This is why its instant death if your brainstem is injured
o Plays a role in consciousness

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18
Q

CSF production

A

o By the choroid plexus of each ventricle

→ choroid composed of Ependymal cells

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19
Q

CSF functions

A

o Acting as a cushion or “shock absorber”
o Deliver nutrients to the brain and removing waste
o Flow between the cranium and spine, compensate for changes in intracranial blood volume

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20
Q

Blood-brain barrier (BBB):

A

 A series of high-resistance, tight junctions between endothelial cells as well as astrocytes with processes on capillary walls → charged big molecules can’t cross

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21
Q

Blood-CSF barrier:

A

 Formed by tight junctions between choroid epithelial cells

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22
Q

Both the BBB and the blood-CSF barrier

A

o Endothelial cells and astrocytes that make up the BBB and cells forming the blood-CSF barrier can produce cytokines
o Astrocytes can act as antigen-presenting cells that curb the immunologic response to CNS infections

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23
Q

• Wallerian degeneration in PNS (spinal nerves are part of the CNS)

A

o Occurs in the axon distal to the site of a cut
A. Normal nerve innervating skeletal muscle
B. The nerve has been transected and Wallerian degeneration has begun (corresponding atrophy in the muscle)
C. Proximal nerve terminals send sprouts toward the Schwann cells
D. Some of the sprouts make it into tubes and re-innervate the muscle

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24
Q

• Wallerian degeneration in CNS

A

o Damage occurs to Spinal cord axons
o Macrophages (purple) enter to clear the debris and astrocytes begin to enlarge and proliferate
o A glial scar is formed blocking axonal growth

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25
Q

Astrocytes reaction in injury to the glia

A

o Acute cell injury, such as hypoxia, hypoglycemia, and toxic injuries causes cellular swelling

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26
Q

Oilgodendrocytes reaction in injury to the glia

A

o Injury or apoptosis of oligodendrocytes is a feature of acquired demyelinating disorders
 Not producing myelin at all or producing it incorrectly

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27
Q

Intracranial components:

A

o Cerebral parenchyma (80%)
→ Brain tissue
o CSF (10%)
o Blood (10%)

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28
Q

Definition of intracranial pressure?
What is normal?

What is pathologic?

A

o The pressure inside the cranial cavity
o Normally <15mmHg in adults, and
 Pathologic intracranial hypertension (ICH) is ≥ 20mmHG

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29
Q

How does the brain accommodate an increase in ICP?

A

Displacement of CSF into the thecal sac
→ Membrane that covers the cauda equina
o Decrease in the volume of the cerebral venous blood by venoconstriction and extracranial drainage

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30
Q

o The relationship between intracranial volume and pressure is

A

is nonlinear

• As pressure goes up and compensation gets overwhelmed we have much more increase in pressure

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31
Q

o Normal Pressure Hydrocephalus (NPH)

A

o Pathologically enlarged ventricular size (compensation) with normal pressures on lumbar puncture
 Because your ventricles are dilated you have normal pressure
o NPH is a form of communicating hydrocephalus and is different from obstructive or non-communicating hydrocephalus
 Because there is nothing blocking CSF and blood flow
o Shunt placement can decrease CSF accumulation and symptoms resolve

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32
Q

• Pathophysiology: Normal Pressure Hydrocephalus (NPH) is idiopathic, but what are their theories?

A 
o	Idiopathic NPH
	Cerebrovascular disease:
→ HTN, Coronary Artery Disease and Peripheral Arterial Disease 
	Decreased CSF absorption 
→ Leads to accumulated CSF  dilated ventricles 
	Increased central venous pressure
→ Due to lung and heart failure 
	Neurodegenerative disorder 
→ Ex: Alzheimer’s Disease
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33
Q

Secondary NPH can be caused by?

A

 Intraventricular or subarachnoid hemorrhage (either from aneurysm or trauma) and prior acute or ongoing chronic meningitis

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34
Q

What is the Clinical Triad of NPH?

A
  • Wet, Wacky, and Wobbly
    • Gait Difficulty
    o Can’t separate gaits from each-other
•	Cognitive deficits 
o	Psychomotor slowing 
o	Decreased attention and concentration 
o	Impaired executive function 
o	Apathy (lack of interest, enthusiasm, or concern)

• Urinary incontinence

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35
Q

What occurs in the brain that is a direct result of Increased ICP

A

↑ ICP → ↓ blood flows → decreased blood perfusion to the brain → cerebral edema

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36
Q

• Global symptoms of elevated ICP:

A

o Headache
o Decreased consciousness
o Vomiting

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37
Q

• Focal Symptoms of elevated ICP

A

o Herniation

 The displacement of brain tissue through opening in the skull (goes to another location it’s not supposed to be)

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38
Q

Herniation can occur in three three common clinical settings:

A

 Cerebral edema
 Increased CSF volume (hydrocephaluswhen its non-communicating)
 Mass lesions (tumors in the brain)

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39
Q

Tonsillar herniation:

A

• It causes brainstem compression and it compromises vital respiratory and cardiac centers in the medulla (Puts pressure on the brainstem)

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40
Q

Cerebral Blood Flow/Perfusion and Autoregulation

A

o Cerebral blood flow is maintained at a relatively constant level
o Maintenance of cerebral blood flow by autoregulation within a mean arterial pressure range of 60 to 150mmHg

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41
Q

• At about 180 mmHg, autoregulation fails causing:

A

o Cerebral vasodilation and cerebral edema

42
Q

• Cerebral Perfusion Pressure:

A

o Cerebral perfusion pressure (CPP) is a clinical surrogate for cerebral perfusion
o CPP is defined as mean arterial pressure (MAP-blood pressure) minus ICP
o CPP= MAP-ICP

43
Q

• What are the two types of Cerebral Edema and what are they caused by?

A 
o	Vasogenic Edema: irreversible increase in EXTRAcellular fluid (coming from blood vessel)
	Caused by:
•	BBB disruption
•	Increased vascular permeability 
•	No tight junctions

o Cytotoxic edema: potentially reversible increase in intracellular fluid secondary to neuronal, or glial, or endothelial cell membrane injury (blood vessels are fine-swelling happens inside the cell)
 Caused by:
• Hypoxia/ischemia

44
Q

Hypoxic-Ischemic Brain Injury causes?

A

o Cardiac arrest
o Vascular Damage
o Poisoning
o Head trauma

45
Q

Mechanisms of Ischemic Cell Injury and Death

A

• Part of the brain parenchyma (tissue) core undergoes immediate death
• While others may only be partially injured with potential to recover (penumbra-tissues at risk)
o 50 mL/100g/min of cerebral blood flow
 Inhibition of protein synthesis
o 35 mL/100g/min of cerebral blood flow
 Protein synthesis ceases. Glucose utilization transiently increases
o 25 mL/100g/min of cerebral blood flow
 Onset of anaerobic glycolysis. Tissue acidosis
o 17 mL/100g/min of cerebral blood flow
 Neuronal electrical failure
o 11 mL/100g/min of cerebral blood flow
 Membrane failure
o Anything less is cell death

46
Q

Cerebrovascular Disease

A

o Pathophysiological process involving the blood vessels of the brain

47
Q

Cerebrovascular Disease classification

A

o The process may be intrinsic to the vessel
o The process may originate remotely
 Embolism
o The process may result from decreased cerebral blood flow
 ↑ ICP

o The process may result from rupture of a vessel in the subarachnoid space or intracerebral tissue
 Aneurysms

48
Q

Cerebrovascular disease can lead to?

A

• *Can lead to transient ischemic attack (TIA) or Ischemic stroke
o Doesn’t necessarily mean infarction of the brain
• **Can lead to primary hemorrhagic stroke

49
Q

***CHARACTERISTIC OF STROKE SUBTYPES CHART

A

look at powepoint

50
Q

Definition of TIA:

A

o A transient episode of neurologic abnormalities caused by focal brain, spinal cord, or retinal ischemia, without acute infarction
 Could be infarction (less of a chance)

51
Q

• Definition of ischemia stroke:

A

o An infarction of brain, spinal cord, or retinal cell death due to ischemia, based on neuropathologic, neuroimaging, and/or clinical

52
Q

o Embolic TIA

A

o Embolic TIA
 Thrombosis goes to the brain
 *Important to find out origin of emboli (to prevent anymore further event)

53
Q

o Large artery, low-flow TIA:

A

 Often associated with an atherosclerotic lesion

54
Q

o Lacunar or small penetrating vessel TIA caused by stenosis

A

 Lacunar are tiny vessels that are very prone to stenosis so very prone to TIA’s

55
Q

• High risk lesions regarding low-flow or embolic TIA’s:

A

o Atherothrombotic lesions at the origin of the internal carotid artery that are narrowed more than 50%
o Atherothrombotic lesions at the basilar artery
o Emboli to basilar artery
o Dissection lesions at internal carotid artery or as it enters the foramen transversarium

56
Q

• Intraparenchymal brain hemorrhage (IPH)

A

o Develops from tears in the brain tissue and/or vasculature
 Not related to any trauma just issues with the blood vessels inside the brain

57
Q

• Subarachnoid hematoma (SAH):

A

o Non-traumatic causes (could be

o The most common is an aneurysm*** (worst headache of patients life if they survive)

58
Q

Two major causes of Subdural hematoma (SDH):

A

o Two major causes
 Damage to the bridging veins
 Tearing of cortical veins

59
Q

• Epidural Hematoma (EDH) AKA extradural hematoma

A

o A blunt trauma may tear the middle meningeal artery

60
Q

Atraumatic/Spontaneous Intracranial Hemorrhage (ICH)

leads to?

A

leads to ↑ICP

61
Q

Atraumatic/Spontaneous Intracranial Hemorrhage (ICH) etiology?

A

Hypertensive vasculopathy

62
Q

Atraumatic/Spontaneous Intracranial Hemorrhage (ICH) clinical presentations?

A

o Signs and symptoms ICH depend on the location and size of the hemorrhage
o The neurologic symptoms and signs usually increase gradually over minutes or a few hours
o Headache, vomiting, and a decreased level of consciousness

63
Q

Atraumatic/Spontaneous ICH Pathogenesis

3 ways

A

• Cerebral microbleeds:
o HTN→ Necrosis + hyperplasia of blood vessels   permeability
 Microscopic pseudoaneurysm formation with subclinical leaks of blood
• Hemorrhage enlargement:
o Associated with neurologic deterioration and worse outcomes
• Brain Damage

64
Q

Primary Brain Damage after ICH

A

o Parenchymal blood accumulation
 Tissue disruption
 Mechanical damage due to mass effect
 Elevated ICP

→ damaged BBB causes edema

65
Q

Secondary brain damage

A 
o	Thrombin activation 
o	Lysis of RBC’s causes the release of hemoglobin, which is converted to heme and iron 
	By oxidative stress
o	Inflammatory reaction
	Release of proinflammatory mediators
66
Q

Neural Tube Defects (NTD’s)

A 
o	Neural tube defects (NTD’s) are one of the most common congenital anomalies, and are the cause of chronic disability
o	Myelomeningocele (spina bifida) is the most common NTD
	Thicken ectoderm makes neural plate → groove→ tube, BUT if tube doesn’t close → neural tube defect
67
Q

spina bifida aperta?

A

 A cleft in the vertebral column, with a defect in the skin → meninges and spinal cord are exposed aka “open spinal dysraphism” or

68
Q

o Closed Spinal dysraphism aka “occult spinal dysraphism” or spina bifida occulta”

A

is a cleft in the vertebral column, without a skin defect, and neural tissue is not exposed

69
Q

Open and closed spina bifida is caused by?

A

o Multifactorial origin

o Folate deficiency during the first several weeks of gestation

70
Q

Myelomeningocele’s Neurological Abnormalities

A

o Chiari II malformation
→ Downward displacement of the cerebellum and medulla abnormalities in cognitive function
→ This obstructs flow of CSF which leads to Hydrocephalus

o Spinal Cord
→ Typically affect the trunk, legs, bladder, and bowel  complete paralysis and absence of sensation

o Brain stem:
→ Due to the chiari malformation → swallowing difficulties, vocal cord paresis

71
Q

Cerebral Palsy

A

o Permanent non-progressive central motor dysfunction that affect muscle tone, posture, and movement

72
Q

Cerebral Palsy Etiology

A

o Most cases due to prenatal factors, but peri- and postnatal factors or events can also contribute
o Prematurity and low birth

73
Q

Pathogenesis of Cerebral Palsy

A

Pathogenesis of Cerebral Palsy
• Focal white matter injuries are produced at a specific locus in the white matter such as:
→ Periventricular white matter

74
Q

What is Periventricular leukomalacia (PVL)?

Where does it most often occur?

A

o Definition: is the necrosis of the white matter near the lateral ventricles
 Most often occurs in premature infants

75
Q

what causes Periventricular leukomalacia (PVL) ?

A

 Decreased oxygen/blood flow to the periventricular region of the brain
 Damage to the glial cells

76
Q

Three types of brain injuries and their symptoms

A

-In the front lobe: clinically silent
 Not really symptoms
-Severely in the spinal cord: disabling
-In the brainstem: fatal

77
Q

A GCS score: ?

A 
Traumatic Brain Injury (TBI)
•	Definition:
o	A heterogeneous disease 
o	A GCS score: (clinical way of categorizing severity)
	13 to 15  mild traumatic brain injury 
	9 to 12 moderate
	8 or less severe
o	LOWER THE SCORE IS THE WORSE IT IS
78
Q

• Pathophysiology of TBI

-• Primary brain injury ?

A

o Tissue shearing at the interface of grey and white matter known as diffuse axonal injury (DAI) leads to axonal swelling
o Cerebral contusions
o Extra-axial hematomas
 Epidural, subdural, subarachnoid, hemorrhage and intraventricular

79
Q

Secondary Brain Injury causes?

A 
o	Excitotoxicity
o	Electrolyte imbalances
o	Inflammatory responses 
o	Apoptosis 
o	Secondary Ischemia
80
Q

• Acute Mild TBI: Concussion classification?

A

o A Glasgow Coma Scale (GCS) score of 13 to 15, measured at approximately 30 minutes after the injury

81
Q

Acute Mild TBI: Concussion pathophysiology

A

o Mild TBI results from direct external contact forces or from acceleration/deceleration trauma
o The acute clinical symptoms are related to functional rather than structural injury

82
Q

• Clinical Manifestations: of acute mild TBI: concussion

A

o Confusion and amnesia

83
Q

Complicated Concussion: Contusion: defintion

A

o Brain contusions are areas of injury with localized ischemia, edema and mass effect
o Mild TBI can be complicated by ongoing cortical contusions and intracranial hemorrhage
o Brain contusions may delay recovery from a concussion

84
Q

• Chronic Traumatic Encephalopathy (CTE): definitiion

A

Definition
o One of the sequelae of Mild TBI
o A dementing illness that develops after repeated concussions (head trauma)

85
Q

Chronic Traumatic Encephalopathy (CTE): Etiology?

A

o Sports-related concussion (contact sports)

o Combat-related TBI (military)

86
Q

Chronic Traumatic Encephalopathy (CTE): Neuropathy

A

• Neuropathology:
o Tau-immunoreactive degenerative changes that are distinct from Alzheimer’s Disease in their preferred distributive in the superficial cortical layers
→ CTE distribution is different

87
Q

how does Infection damage the central nervous system?

A

• Infection may damage the nervous system:
o Directly through injury of neurons or glia by the infectious agent
o Indirectly through microbial toxins
o The destructive effects of the inflammatory response
o The result of immune-mediated mechanisms

88
Q

Microbes can access the CNS by:

A

o Hematogenous spread (BLOOD VESSELS): most common
o Direct implantation
o Local Extension
o Peripheral Nerves

89
Q

Meningitis

A

inflammatory of the leptomeninges within the subarachnoid space

90
Q

Classification of meningitis:

A

o Acute pyogenic (usually bacterial)
 Harder to treat due to their virulence factors
o Aseptic (usually viral)
o Chronic (usually tuberculous, spirochetal, or cryptococcal)

91
Q

Meningoencephalitis:

A

o Inflammation of the meninges and brain parenchyma

92
Q

Etiology: of meningitis

A

o Mainly in adults: Streptococcus pneumoniae and Neisseria Meningitidis

93
Q

Pathogenesis of Bacterial Meningitis

A

• Colonization (in mucous membrane of meninges): IgA protease inactivates the mucosal antibody (IgA)→ bacterial attachment to host cells
• Invasion: cross the respiratory epithelium and invade the blood
• Intravascular survival: by avoidance of the complement system
• Meningeal Invasion: cross the BBB
o Bacterial pathogens get rid of the tight junctions

94
Q

• Pathophysiology of Meningitis

A

• Inflammation get ride tight junctions in BBB → ↑ BBB permeability → Vasogenic edema (due to failure in autoregulation)→ ↑ICP→ ↓blood perfusion (altered cerebral blood flow) → ischemia → release of ROS species’ → Neuronal damage

95
Q

Aseptic Meningitis (Viral) defintion?

A

o Patients who have clinical and laboratory evidence for meningeal inflammation with negative routine bacterial cultures

96
Q

Etiology of aseptic meningitis

A

o Enteroviruses

97
Q

clinical presentation of aseptic meningitis

A

o Similar presentation to that of bacterial meningitis, but its self-limited
 Goes away by itself, no antibiotics needed

98
Q

Clinical Features and Pathophysiology of each clinical feature of Meningitis

A

• Fever
o Cytokines affect the thermoregulatory neurons of the hypothalamus changing the regulation of body temp

• Headache
o Bacterial exotoxins, cytokines, and ↑ICP stimulate nociceptors in the meninges
 Nociceptors are sensory receptors for painful stimuli

• Stiff Neck
o Flexion of the spine→ stretching of meninges→ leads to pain in neck→ causing limited ROM

• Altered Mental Status
o ↑ ICP → brain herniation → damage to ARAS
 ARAS: system that controls alertness in brain stem

• N/V
o ↑ ICP on the Medulla oblongata
 Vomiting center
 CTZ- chemoreceptors on bottom of 4th ventricle close to BBB

99
Q

when part of the brain parenchyma undergoes immediate death

A

core

100
Q

partially injured parenchyma with potential to recover

A

penumbra

Patho II (12 decks)

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