SAQs 2014

Question 1

Write brief notes on the physiological changes associated with sleep.

Answer 1

Sleep: A necessary state of rousable unconsciousness which can be reversed by physical stimulus.

Structure:

• Sleep architecture,
• Sleep EEG signature
• Sleep neurochemistry
• Systemic changes

Sleep architecture:

• Cycle
• –NREM stages 1-4 then REM
• Reduced in adults, highest in neonates

Sleep EEG signature:
- Wave types
Beta: 13-30Hz, low amplitude
Alpha: 8-13Hz
Theta 4-8
Delta <4, high amplitude

NREM1: Alpha and theta
NREM2: theta, sleep spindle (high frequency, low amplitude burst), k complex (low frequency, high amplitude pattern)
NREM3+4: Theta and delta waves (all low freq, high amplitude)
REM: Beta waves, similar to awake EEG (i.e. paradoxical)

Resp effects:
NREM:
TV decreased
RR unchanged
Decreased response to PaCO2 and PaO2
Decreased pharyngeal motor tone

REM:

• decreased RR
• Decreased TV
• Very decreased response to hypoxaemia and hypercapnoea
• Muscular atony w/ exception of diaphragm and extraoccular muscles –> pharyngeal obstruction (OSA), no use of intercostals for breathing

Cardio:
- NREM:
dec HR, BP, CO

• REM:
  increased HR, BP, CO

Renal:
- (NREM and REM) decreased rbf, GFR, increased urine concentration and decreased urine output

GIT:
- PSNS tone predominates, Increased GI peristalsis

Endocrine:

• Increased GH
• Cortisol lowest around midnight, increases around 06:00
• Core temperature falls during sleep, thermoregulation ceases during REM sleep

Question 2

Outline the effects of intravenously administering 500 ml of 20% mannitol. Outline the potential problems associated with its use.

Answer 2

Mannitol is the reduction of Mannose, a monosaccharide. A polar molecule (does not cross BBB or cell membrane).
20% mannitol = 200g/L
Hypertonic at 1100mOsm/L

Clinical use:
osmotic diuretic, decrease ICP.
Usual dose 0.5-1g/kg.

Physicochemical:

• Freely filtered at glomerulus, nil absorption
• Doesn’t cross BBB (charged polysaccharide
• 4 x plasma osmolarity

MOA: Increased osmolality of ECF –> Increased osmolality or glomerular filtrate –> increased urine volume.

Effects of 500ml of 20% mannitol (100g of mannitol:

• Increased ECF
• Decreased ICF
• Increased osmolarity

Physiological effects:
CNS:
- Cerebral dehydration, per munro-Kellie doctrine, will decrease ICP

CVS:

• Bi-phasic response
• Expansion of intravascular space will increase HR, BP, blood volume

Resp:
- Due to increased blood volume, may precipitate pulmonary oedema

Renal:
- Freely filtered at glomerulus –. Osmotic diuresis

Question 3

Describe the physiology of the pain pathways and how drugs may modulate the perception of pain

Answer 3

Pain:
- a perceived unpleasant sensory and emotional experience associated with actual or potential tissue damage.

Process:

• Nociceptor
• Primary afferent
• Secondary afferent (different tracts)
• Tertriary afferent
• Descending modulation.
• Drugs that work at each level

Nociceptors:

• Free nerve endings in tissues
• Activated by chemical, mechanical and thermal insults

Primary afferent:
- From periphery, transmitted via Adelta and C fibres dorsal horn.
-Adelta fibres synapse at superficial layers
- c fibres synapse at deeper layers
- Synapse with second order neurons
Drugs:
- Local anaesthetics, inhibit transduction of signal via peripheral nerve
- Paracetamol: Inhibits bradykinin-sensitive nociceptors
-Presynaptic inhibition:

Second order neurons:

• decussate in anterior commissure
• Ascend in spinothalamic tracts

neo-Spinothalamic:
- Deep lamina of dorsal horn –> thalamus –> somatosensory cortext –> Allows for discrimination of pain (location, quality, intensity) and autonomic responses

paleospinalthalamic:
- Dorsal horn –> Brainstem
Drugs:
NMDA antagonists: Ketamine, nitrous, xenon, Mg, tramadol, methadone

Tertiary neurons:

• Thalamus –> primary somatosensory localisation
• Brainstem (paleo) –< thalamus, hypothalamus, amygdala (affective, autonomic)

Drugs:

• Paracetamol (Cox-3 inhibition)
• NMDA antagonist –> thalamocortical dissociation
• GAs inhibit ascending reticular activating system, therefore no perception of pain

Descending modulation:
- Periaquaductal gray –> Dorsal horn, stimulate interneurons which release endogenous opioids, decreasing/inhibiting synapses of first and second order neurons
Drugs:
- Opioids: decrease activity of off cell, decreased inhibiting of on cell.

Question 4

Describe the alterations to the physiology of the nervous system in
the older patient and outline the consequent effects on pain perception

Answer 4

Pain:
- an unpleasant perceived sensory and/or emotional sensation associated with actual or perceived tissue damage.

Three main differences for pain perception in older patients:

1. Changes to CNS
2. Changes to PNS
3. Changes to ANS.

CNS changes:

• Ageing –> Neuronal atrophy (10,000 neurons lost/day from age 20) –> reduction in neuronal mass (approx 10% by age 80) –> cognitive decline and slower reflexes
• –> Compensated through:
• ——> Redundancy (baseline more than required)
• ——> Neuroplasticity (more connections are formed between remaining neurons)
• ——> Neurogenesis (esp hippocampus and basal ganglia

Descending inhibitory pathways are reduced with ageing

Decrease in cerebral blood flow from arteriosclerosis

These CNS changes result in:

• Altered sensory and emotional perception of pain –> Overall increase in pain tolerance
• Potential inability to voice pain despite perceiving pain
• Potential inability to react to pain appropriately (e.g. decreased reflexes, can’t withdraw as fast)

PNS alterations:
- Aging –> neuronal atrophy –> decreased number of both myelinated and unmyelinated axons as well as decreased number of synapses.

Substance P levels decrease witht aging

PNS alterations therefore:
- Slower transduction and transmission of painful stimuli to CNS

ANS alterations:

• Increased circulating NorAd but decreased response to catecholamines –> decreased SNS tone
• —> Less SNS response to painful stimuli (less tachy/hypertension)