Pneu2 (31-35)

Front 1

What does the vertebral-basilar system supply?

Back 1

Posterior parts of cerebral hemisphere,cerebellum, brainstem, most of thalamus, spinal cord

Front 2

What does the internal carotid system supply?

Back 2

Rostral 2/3 ofbrain, including most of the basal ganglia & internal capsule

Front 3

What are 5 branches of the vertebral and basilar artery that form posterior circulation?

Back 3

1. Anterior spinal artery
   
2. 3 cerebellar arteries & branches:
   (A) Superior cerebellar artery
   (B) Anterior inferior cerebellar artery
   (C) Posterior inferior cerebellar artery
3. Posterior cerebral artery

Front 4

What 2 types of branches do cerebral arteries have?

Back 4

1. Cortical branches → surface of hemisphere

2. Central / penetrating branches → deeper grey & white matter

Front 5

What areas are supplied by the cortical branches of the posterior cerebral artery?

Back 5

Inferior & medial surfaces of temporal & occipital lobes; extend a little over lateral surface of hemisphere

Front 6

What areas are supplied by the cortical branches of the anterior cerebral artery?

Back 6

Medial surface of frontal & parietal lobes; extend over to margin of lateralsurface

Front 7

What areas are supplied by the cortical branches of the middle cerebral artery?

Back 7

Lateral surface of cerebral hemisphere

Front 8

What areas are supplied by the central branches of the posterior cerebral artery?

Back 8

Thalamus;hypothalamus; lateral & 3rd ventricle(posterior choroidal a.); midbrain

Front 9

What areas are supplied by the central branches of the anterior cerebral artery?

Back 9

Medial striate artery

Head of caudate nucleus & putamen; anterior limb of internal capsule

Front 10

What areas are supplied by the central branches of the middle cerebral artery?

Back 10

Lateral striate artery

Caudate nucleus, putamen & globus pallidus; anterior & posterior limb of internal capsule

Front 11

What are the lenticulostriate arteries?

Back 11

Lateral striate arteries - important ∵ small occlusion leads to large amount of damage (blood supply to internal capsule)

Front 12

What is the venous drainage of the brain?

Back 12

Cerebral veins → dural sinuses → IJV

Front 13

What are the 2 types of cerebral veins? What do they drain?

Back 13

1. Superficial: drains cortex & subcortical white matter
   
2. Deep: drains choroid plexus, basal ganglia, diencephalon, deep white matter → ends in internal cerebral veins & great cerebral vein of Galen to straight sinus
   

Front 14

What is the structure of the ventricular system?

Back 14

• Lined with ependyma
  
• Communicates with subarachnoid space
  
• Filled with CSF secreted by choroid plexus
  

Front 15

What is the volume of CSF in the brain and spine?

Back 15

Total volume ~150 ml

Only ~23 ml in ventricles; rest in subarachnoid space

Front 16

What is the composition of CSF compared to blood plasma?

Back 16

Low in glucose, protein & Ig compared to blood plasma

Only 1-5 cells per microliter, mainly leukocytes

Front 17

What 4 parts constitutes the ventricular system?

Back 17

1. Paired lateral ventricles (anterior, inferior, posterior horns, body)

2. 3rd ventricle (diencephalon)

3. Cerebral aqueduct (midbrain)

4. 4th ventricle (floor: pons & medulla; roof: cerebellum; lateral & median apertures)

Front 18

Where is the caudate nucleus located in relation to the ventricular system? The hippocampus?

Back 18

• Always lateral to lateral ventricle
  
• Inf. horn above hippocampal structure
  

Front 19

What is the direction of flow of CSF?

Back 19

Lateral ventricle → IV foramen → 3rd ventricle → cerebral aqueduct → 4th ventricle → median & lateral apertures

⇒ subarachnoid space → arachnoid granulations → superior sagittal sinus

Front 20

What is an arachnoid cistern?

Back 20

Expanded subarachnoid space - created by separation of arachnoid and pia mater filled with CSF

Front 21

What is the cerebellomedullary cistern?

Back 21

• Located between the cerebellum and the dorsal surface of the medulla oblongata
  
• CSF produced in the fourth ventricle drains into the cisterna magna via the lateral apertures and median aperture
  

Front 22

What is the lumbar cistern?

Back 22

• Enlargement of the subarachnoid space between the conus medullaris of spinal cord (about vertebral level L2) and inferior end of subarachnoid space and dura mater (about vertebral level S2)
  
• Site for lumbar puncture and spinal anesthesia
  

Front 23

What are 3 causes of excessive CSF accumulation?

Back 23

1. ↑ production
2. Interference with circulation
3. Interference with absorption
   

Front 24

What can excessive CSF accumulation lead to?

Back 24

Hydrocephalus, ↑ CSF pressure, dilatation of ventricles, head enlargement, papilledema

Front 25

What are 3 types of bleeding associated with meninges?

Back 25

1. Epidural: from middle meningeal a.

2. Subdural: from torn cerebral vein at its junction with dural sinus

3. Subarachnoid: from a ruptured aneurysm ofartery in subarachnoid space

Front 26

What is spina bifida?

Back 26

Failure of dorsal lamina to form

Front 27

What are 3 types of spina bifida?

Back 27

1. Spina bifida occulta
   
2. Meningocele
   
3. Myelocele: exposure of spinal nerve roots
   

Front 28

What is hydrocephalus?

Back 28

Excess CSF in ventricles

Front 29

What are 6 possible causes of hydrocephalus?

Back 29

1. Aqueductal atresia/stenosis
   
2. Arnold-Chiari malformation (downward displacement of cerebellar tonsils through foramen magnum)
   
3. Periventricular tumors
   
4. Post-intraventricular hemorrhage
   
5. Post-subarachnoid hemorrhage
   
6. Post-meningitis
   

Front 30

What is an important S/Sx of hydrocephalus?

Back 30

Enlarged head ∵ accumulation of CSF fluid + unfused fontanelles

Front 31

What is the cause of cerebral palsy?

Back 31

Brain injury suffered at time of birth → spasticity, dystonia, paresis, ataxia

Front 32

What is Parkinson's disease? What are the S/Sx?

Back 32

Extrapyramidal movement disorder

Clinical triad of tremor, rigidity, bradykinesia

Front 33

What is the cause of PD?

Back 33

Loss of dopaminergic nigrostriatal tract → ↓ inhibition of dopaminergic neurons → ↑ output from globus pallidus & thalamus → ↓ activation of associated motor areas → failure to initiate motor function

Front 34

What are 3 possible causes of PD?

Back 34

1. Oxidative stress & free radicals
   
2. Environmental toxin that selectively destroys dopaminergic neurons via uptake of intermediate chemicals
   
3. Genetics
   

Front 35

What is occurs in multiple sclerosis?

Back 35

Demyelination of CNS

Front 36

What occurs in Guillain-Barre syndrome?

Back 36

Demyelination of PNS

Front 37

What are 4 S/Sx of MS?

Back 37

• Motor weakness
  
• Cerebellar syndrome
  
• Retrobulbar/optic neuritis
  
• Opthalmoplegia
  

Front 38

What are 2 possible causes of MS?

Back 38

• Association with certain HLA types
  
• AI disease ∵ deranged T-lymphocyte functions
  ➤ AI disease ∵ ↑ CSF gamma globulin & oligoclonal band

Front 39

What are the S/Sx of Gullain-Barre syndrome?

Back 39

Acute muscle weakness, parethesia, loss of reflexes

Potentially fatal with respiratory failure

Front 40

What is the function of local anesthetics?

Back 40

• Drugs which blockimpulse conduction in nerve fibres
  
• Drug-induced reversibleblockade of nerve impulses in a restricted regionof the body
  

Front 41

When and why are local anesthetics used?

Back 41

Minor surgery; patient remains awake w/o LOC and protective airway reflexes remain intact

Front 42

What is the MoA of local anesthetics?

Back 42

Block voltage-sensitive Na+ channels to inhibitthe initiation and propagation of action potentials

Front 43

What occurs when there is systemic toxicity to the CNS? To the cardiovascular system?

Back 43

• Excitation → convulsions → coma → respiratory depression

• Vasodilation → depression of myocardium, cardiac slowing → life-threatening hypotension

Front 44

What are 3 unique factors of local anesthetics that allow it to selectively target pain sensations?

Back 44

• Greatest effect on small diameter nerve fibers
  
• Highest affinity for inactivated state of the Na+ channel ⇒ use-dependent quality
  
• Local application to target site

Front 45

What fibers carry pain sensation?

Back 45

Aδ & C fibers ∴ pain sensation disappears first → temperature → touch & deep pressure

Front 46

What systems are affected from most to least?

Back 46

Sympathetic NS > nociception NS > motor NS

Front 47

When are surface/topical anesthetics used?

Back 47

Drugs applied directly to mucus membranes as a solution, spray, jelly, lozenge

Front 48

When is cocaine used medically?

Back 48

Anesthesia for ENT mucosa

• Vasconstriction → ↓ chance of nosebleed

Front 49

What is infiltration anesthesia and when is it used?

Back 49

• Direct injection into tissues to anaesthetise localsensory nerve endings: “local anaesthetic”
  
• For minor surgery
  

Front 50

What is nerve block anesthesia and when is it used?

Back 50

• Drugs injected close to nerve trunk toanaesthetise region of distribution of the nerve
  
• e.g. mandibular nerve block in dentistry
  

Front 51

What is nerve plexus anesthesia?

Back 51

Drugs injected close to nerve plexus toanaesthetise region of distribution of the plexus

Front 52

What is neuro-axial anesthesia and when is it used?

Back 52

• Drugs injected close to the spinal cord toanaesthetise a large region of the body
  
• e.g. spinal anaesthesia, epidural anaesthesia
  

Front 53

What is the difference between spinal and epidural anesthesia?

Back 53

Spinal: faster onset, dense sensory block, more motor block, limited duration (<3hrs)

Epidural: slower onset, less dense sensory block, less motor block, unlimited duration (labor, post-operative analgesia)

Front 54

What is the difference between amounts used in spinal and epidural anesthesia?

Back 54

2ml bupivicaine vs. 20ml bupivicaine

Front 55

What are 3 SE of spinal / epidural anesthesia?

Back 55

• Blocks SNS
  
• Vasodilation → hypotension
  
• Nausea, vomiting, cardiovascular collapse
  

Front 56

What are 3 longer acting local anesthetics?

Back 56

1. Bupivacaine

2. Levo-bupavicaine

3. Ropivacaine

Front 57

What are 2 adjuvants that are used?

Back 57

1. Opioids: to neuroaxial anesthesia, enhance sensory anesthesia, less motor blockade
   
2. Lignocaine w/ adrenaline: vasoconstrictor, ↓ rate of removal of LA from site
   

Front 58

What occurs in local anesthetic toxicity?

Back 58

• Binds to closed Na+ channels of brain & heart → grand mal seizure, refractory ventricular tachyarrhythmias
  
• Blocks mitochondrial transport of fatty acid (heart's preferred fuel during aerobic metabolism)
  

Front 59

What is the stereochemistry of bupivacaine?

Back 59

50/50 mixture of levobupivicaine and dextrobupivicaine (CARDIOTOXIC)

Front 60

What is ropivacaine?

Back 60

• Levo-isomer of propyl homolog of bupivacaine
  
• Less toxic than bupivacaine
  

Front 61

How do mono-isomer anesthetic agents compare?

Back 61

• Safer, less cardiotoxic
  
• Similar potency to bupivacaine
  
• Motor sparing
  

Front 62

How fatal is an overdose of bupivacaine?

Back 62

Almost always fatal

Front 63

How can fat be used for successful resuscitation of LA toxicity?

Back 63

Local anesthetics are lipophilic → drawn into lipid sink

Front 64

What is general anesthesia / what is its function?

Back 64

A drug-induced reversible loss of consciousnessthat permits painless surgery

Front 65

What occurs to the CNS?

Back 65

Dose-related depressant effects

• Sensory impairment
  
• Unconsciousness
  
• Block of somatic responses (paralysis)
  
• Block of autonomic responses
  

Front 66

What are the 4 stages of anesthesia?

Back 66

1. Analgesia
2. Excitement (disinhibition)
3. Surgical anesthesia
4. Medullary paralysis, respiratory arrest, vasomotor collapse (impending death)
   

Front 67

What are 3 commonly used combinations of anesthetics to reduce the amount of general anesthetic drug required?

Back 67

1. IV and inhalation anesthetics → unconsciousness
   
2. Opioid analgesics → suppression of response to noxious stimuli
   
3. Muscle relaxants → specific paralysis if required
   

Front 68

What is the proposed MoA of general anesthetics?

Back 68

Involves effects on synaptic transmission on CNS

Front 69

How is the potency and efficacy of inhalation anesthetics measured?

Back 69

Minimum alveolar concentration (MAC); concentration of inhaled anesthetic measured in end-tidal gas that prevents response to standard painful stimulus in 50% of patients

Smaller MAC → more potent

More lipid-soluble → more potent

Front 70

What are 3 proposed MoA of general anesthetics at the cellular level?

Back 70

1. Enhance tonic inhibition (⊕ GABAA-gated ion channel action)
   
2. ↓ excitation (open K+ channels)
   
3. ⊖ excitatory synaptic transmission (depress transmitter release & inhibit ligand-gated ion channels at NMDA receptors)
   

Front 71

What is the relationship between solubility in the blood of anesthetic and induction?

Back 71

High solubility - slow induction

Low solubility - rapid induction

Front 72

What is the effect of CO on induction of anesthesia?

Back 72

↑ CO → slows the rate of induction ∵ brain blood flow is autoregulated; smaller proportion of total blood gets to the brain

Front 73

What are 3 inhalation anesthetics?

Back 73

1. Halothane: hepatotoxic to staff
   
2. Isoflurane: lower solubility, less SE
   
3. Sevoflurane: low solubility, not pungent
   
4. Nitrous oxide: weak anesthetic, specific analgesic actions, little effect on CNS/respiratory systems, rapid induction, rapid recovery

Front 74

What are 2 uses of intravenous anesthetics?

Back 74

1. Induction of anesthetics: rapid onset (10-30s)
   
2. Maintenance of short-duration anesthetics: usually with propofol
   

Front 75

What are 3 intravenous anesthetics?

Back 75

1. Thiopentone
   
2. Propofol
   
3. Ketamine
   

Front 76

What is the MoA of thiopentone? What are the SEs?

Back 76

• Ultra-short-acting barbiturate (CNS depressant)
  
• Serious risk of hypotension and apnea ∵ direct myocardial depression, ↓ sympathetic output

Front 77

When is propofol used? What are the SEs?

Back 77

• Maintenance of anesthesia; high clearance rate
  
• Serious risk of hypotension & apnea (more vasodilation than thiopentone)
  

Front 78

When is ketamine used? What are the SEs?

Back 78

• Induction of anesthesia in trauma patients ∵ no hypotensive effect
  
• Hallucinations & dysphoria with slow recovery; drug of abuse
  

Front 79

What is the effect of early sensory deprivation on ocular dominance columns in the visual cortex?

Back 79

Changes development - not observed when deprivation is done after critical period (~8 years in humans)

Precise segregation of inputs is achievedthrough a competition between inputs from twoeyes, for limited trophic factors and synapticspace in the target

Front 80

How do the somatotopic maps change?

Back 80

Plastic particularly during development

Change in adults during training processes and pathological conditions (e.g. phantom limb)