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Medical Pathophysiology > Week 5- Lecture 1b - Alterations in Central Nervous System Function > Flashcards

Week 5- Lecture 1b - Alterations in Central Nervous System Function Flashcards

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USMLE® Step 1 flashcards
1
Q

What is included in the forebrain

A

telencephalon - cerebral cortex, basal ganglia, hippocampus, amygdala

diencephalon - thalamus, hypothalamus, epithalamus

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2
Q

what is included in the midbrain

A

mesencephalon - tectum, tegmentum

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3
Q

What is included in the hindbrain

A

cerebellum, pons, medulla

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4
Q

4 brain protection

A

bone (skull)
membranes (meninges)
Watery cushion (CSF)
BBB - helps maintain stable environment or the brain - separates neurons from blood borne substances such as hormones and neuro transmitters

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5
Q

CSF composition

A

watery solution formed from blood plasma - less protein and different ion concentrations than plasma

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6
Q

Functions of CSF

A

gives buoyancy to CNS structures

protects CNS from blows and other trauma

nourishes brain and carries chemical signals

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7
Q

What is the choroid plexus

A

hang from the roof of each ventricle

  • clusters of capillaries enclosed by Pia mater and layer of ependymal cells
  • produce CSF at constant rate
  • keep it in motion

ependymal cells

  • use ion pumps to control composition of CSF
  • help cleanse CSF by removing wastes

normal volume of CSF 150ml

  • replaced every 8 hours
  • 500ml formed daily
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8
Q

BBB function

A

helps maintain stable environment for brain and separates neurons from some blood borne substances

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9
Q

BBB composition

A

continuous endothelium of capillary walls

thick basal lamina around capillaries

feet of astrocytes

  • provide signal to endothelium for formation of tight junctions
  • tight junctions complete, forming blood brain barrier
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10
Q

BBB function outlined

A

The blood brain barrier is a selective barrier that allows nutrients to move by facilitated diffusion. As it’s role is to maintain a stable environment for the brain, it denies metabolic wastes, proteins, most drugs, small nonessential amino acids and K+. Alcohol, nicotine and anaesthetics are all substances that are allowed to pass due to their fat solubility

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11
Q

BBB is absent in some areas - why?

A

the blood brain barrier is absent in areas like the hypothalamus and the vomiting centre. This is so hypothalamus can monitor water balance, temperature and metabolic activity of the body. The vomiting centre monitors for poisonous centres

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12
Q

Neuronal injury response is dependant on

A

the specific cell type involved

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13
Q

Support cells injury responses

A

astrogliosis
microgial nodules
ependymal damage which leads to CSF alterations

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14
Q

Injury responses of neuron

A

neuropathy
axonal damage
demyelination

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15
Q

Astrogliosis

A

Astrogliosis is where an astrocyte responds to local injury by the process of proliferation (forms a glial scar)

Contusions, wounds, tumours, abscesses, hemorrhages are all common causes of tissue injury that elicit an astrogliosis response

Unchecked proliferation can lead to neoplastic transformation (glioma - brain cancer)

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16
Q

MOIs of CNS injury

A

Traumatic CNS injury
Ischemic CNS injury
Excitation injury
CNS pressure injury

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17
Q

Microglial

A

Has an immune response, reactive changes include nucleus extension ( rod cells)
Can join to astrocytes to form microglial nodule - brain contains very few lymphocytes - T-Lymphocites do not cross BBB

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18
Q

Ependymal cell damage response

A

CSF production transfer is altered with ependymal cell damage due to infection of ventricles and intraventricular haemorrhaging

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19
Q

Traumatic CNS injury

A

can have impaired neurologic functioning which can either be local or systemic (usually always systemic )

In terms of a local effect, this injury is to neuronal tissue transmitting signals to a specific area

A systemic effects involves injury to a site responsible for integrating transmission of impulses to multiple distant sites (usually CNS)

20
Q

TBI aka concussion

A

MOIs include automobile accidents, falls, sports related injuries and “shaken baby syndrome”

TBIs can lead to changes in physical, intellectual, emotional and social abilities.

Can be categorised as closed head injury and open traumatic injury

21
Q

Closed head injury

A

involves movement of the brain inside of the skull causing the injury

22
Q

Open traumatic injury

A

involves exposure of brain structures such as the meninges and brain tissue

with this comes the risk of infection and also risk of further injury

23
Q

Traumatic brain injuries

A

With traumatic brain injuries comes a lot of complications, these include increased seizure activity, concussion (which has temporary alterations in function -dizzy/unconscious), contusions (which has permanent damage - cortical contusions - may remain conscious
- brainstem contusions - always cause coma / injury to the reticular activiting system (RAAS)

Other complications include hepatomas, oedema, skull fractures, increased ICP, respiratory depression, Brain hernias

24
Q

Diagnosis of TBIs

A

diagnosis tools for traumatic brain injury include
imaging modalities ( CT, MRI)
EEGs for brain activity
Lumbar puncture (spinal tap) : for analysis of CSF and check presence of blood (intracranial haemorrhaging)

25
Q

Treatment for TBIs

A

Treatment for TBI’s is targeted towards the specific injury
surgery can be performed to evacuate haematomas
removal of foreign fragments
Reduce intracranial pressure (ICP)
Pain control
anticonvulsive medication (prevent seizures)
Respiratory support
Antibiotics to prevent infection

26
Q

SCI

A 
most SCI's are among males 
- may be result of 
fractures
-contusions
-compression of the vertebral column 
-trauma to the head or neck

neurologic damage is the result of

  • pulling
  • twisting
  • severing
  • compressing the neural tissue of the spinal cord
27
Q

Different spinal cord injuries

A

lacerations - rip or tear from vertebral fracture, knife or bullet

transection : completely severed, penetrating trauma

incomplete transection

contusion: falls, acceleration/deceleration injury

compression : crushing

distraction : pulling spinal cord apart (top moved while bottom fixed)

28
Q

Clinical manifestations of vertebrae fracture

A

localised pain

29
Q

clinical manifestations of SCI

A

wide range

  • from mild paresthesia (abnormal sensation) to quadriplegia (paralysis of all four extremities)
  • level of SCI and severity contributes to neurologic deficit
30
Q

Diagnosis for a traumatic SCI

A

X-ray for fractures
neuro examination
lumbar puncture
CT, MRI

31
Q

Treatment for traumatic SCI

A

immediate immobilisation to prevent further injury

corticosteroids to lessen inflammation

further treatment : traction , casting, surgery

32
Q

ischaemic central nervous system injury

A

inadequate perfusion to neurologic tissue

  • impaired oxygenation
  • tissue necrosis

cause of ischemia

  1. local ischemia (specific region of the brain
    - occlusion of blood supply by thrombosis in a local vessel
  2. global ischemia (larger areas of CNS affected
    - inadequate blood supply to meet the needs of brain tissue
    - global ischemia

spinal cord ischemia : occlusion of spinal blood vessels

33
Q

6 steps of an ischemic CNS injury

A
  1. impaired blood flow lasting longer than a few minutes
  2. brain tissue infarction occurs
  3. cellular function ceases because of inability to use anaerobic processes or uptake glucose and glycogen
  4. infarction stimulates response to tissue injury that leads to inflammation
  5. inflammatory response leads to oedema development
  6. Oedema leads to increased intracellular pressure (ICP)

cell injury also cause local water, electrolyte imbalances and acidosis

  • calcium, sodium, water build up
  • free radical formation at injury site
  • increased release of excitatory neurotransmitter (glutamate)
34
Q

clinical manifestations of iscaemic CNS injury

A

sensory and motor functions are often affected

If injury in brain : manifestations reflect specific associated functions with motor deficits on contralateral side

loss of consciousness, weakness, difficulty speaking, impaired vision , paresthesia

35
Q

diagnosis for Ischaemic CNS injury

A

CT, MRI, angiography to diagnose ischaemic blockage

PET scan: altered metabolism in surrounding tissue

36
Q

treatment for ischaemic CNS injury

A

manage ICP
restore perfusion
thrombolytic therapy to dissolve clot
anticoagulation therapy to prevent future clot

37
Q

excitation injury

A

pathologic consequences of increased impulse frequency, intensity, cascade of transmission

glutamate is the main excitatory neurotransmitter

  • involved numerous higher order function
  • glutamate binds to its receptor on postsynaptic membrane (many types of receptors)
    • NMDA: N-Methyl-D-aspartate receptor is one subtype with affinity for glutamate

signal transduction initiated

IF : high levels of glutamate binds to NMDA, leads to prolonged action potentials

Prolonged action potentials leads to protein breakdown, formation of free radicals, DNA damage, breakdown of nucleus

38
Q

excitation injury cont’

A

may result from cell inability to meet metabolic demand

  • oxygen needs increase with increased neurologic activity
  • risk of hypoxia increased
  • if ischaemia is present, more glutamate Is released by the cells
  • excitation is intensified by binding to NMDA receptor

tissue sensitive to hypoxia may suffer from permanent damage

  • hippocampus
  • cerebral cortex
39
Q

manifestations of excitation injury

A

reduction in higher order function

cognitive and memory abilities

40
Q

Excitation injury cont’ #2

A

cell death from glutamate may be prevented

  • effects can be blocked
  • excessive level can be removed from synapse

glutamate has wide range of involvement in normal cell functioning
pharmacological blocking is difficult

during periods of deteriorating brain functions excitatory responses may predominate

severe brain injury
difference is based on the injury site
impacted CNS involvement

A . flexor or decorticate posture
- damage to cerebral hemispheres above midbrain

B extensor or decerebrate posture
-damage to midbrain, brainstem

41
Q

CNS pressure injury

A

skull and vertebral column : rigid structure
- restricted expansion

increase in pressure may result in injury : increased intracranial pressure 
cause : 
1. excessive CSF volume 
2. cerebral oedema 
3. Space occupying lesion (tumour)
42
Q

CNS pressure injury

A

excessive CSF volume
increased production

decreased absorption

  • obstruction of the ventricular system
  • obstruction may occur through inflammation, tumour, haemorrhaging or a congenital anomaly

CSF build up in the ventricles leads to dilation of ventricles

43
Q

CNS pressure injury

A

oedema

  • abnormal water accumulation
  • vasogenic oedema : transfer of water and protein from the vascular to interstitial space (following permeability change, pressure change)
  • Cytotoxic oedema : caused by hypoxia secondary to ischaemia - cellular swelling

manifestations

  • altered consciousness
  • intracranial hypertension
  • neurologic deficit
44
Q

CNS tumour can promote pressure injury

A

may obstruct CSF flow
promote brain displacement (brain herniation) to lower pressure area
- stimulation of vomiting centre of medulla : nausea
-personality challenges, memory loss, depression

45
Q

increased ICP

A

common response to pathologic events is increased intracranial pressure

  • leads to blood flow reduction
  • ischemia
  • death of brain cells
  • damage to brain structure
  • functional loss

manifestations of increased ICP

  • headache
  • vomiting
  • papilledema (oedema of optical disk)
  • mental deterioration
46
Q

treatment of ICP

A

excessive CSF : surgical shunting from intraventricular spaces

  • to peritoneum : ventriculoperitoneal shunt
  • to right atrium : ventriculoatrial shunt
    • catheter – left ventricle – internal jugular vein – right atrium

Cerebral oedema

  • osmotic diuretics
  • fluid removal and excretion

Medical Pathophysiology (30 decks)

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