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PBL SEM 3 > CASE 10 - temporal lobe, head trauma, anaesthesia etc > Flashcards

CASE 10 - temporal lobe, head trauma, anaesthesia etc Flashcards

1
Q

where is the temporal lobe?

A
  • middle cranial fossa, next to the temporal region/bone
  • lies beneath the lateral fissure
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2
Q

what gyri are located on the lateral surface of the temporal lobe?

A

superior (area 22), middle (area 21) and inferior (area 20) temporal gyri

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3
Q

what gyri are located on the inferior surface of the temporal lobe?

A

inferior temporal gyrus and occipitotemporal (fusiform) gyrus

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4
Q

what sulci does the temporal lobe have on its lateral and inferior surfaces?

A

lateral surface: superior and inferior temporal sulci
inferior surface: collateral sulcus, midfusiform sulcus

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5
Q

what separates the superior and middle temproal gyri?

A

superior temporal sulcus

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6
Q

what separates the middle and inferior temporal gyri?

A

inferior temproal sulcus

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7
Q

where is the primary auditory area (A1)?

A

Brodmann area 41 — superior temporal gyrus

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8
Q

what area is the secondary auditory area (A2) in?

A

Brodmann area 42

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9
Q

where is the auditory association area?

A

brodmann area 22 (lateral to primary auditory area)

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10
Q

where is wernicke’s area?

A

posterior part of brodmann area 22 - superior temporal gyrus of dominant hemisphere

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11
Q

what mark the location of the primary auditory cortex on the superior surface of the superior temporal gyrus?

A

transverse temporal gyri (Heschl’s convolutions)

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12
Q

transverse temproal gyri (of Heschl) = found in the area of the primary auditory cortex buried within the ______ sulcus, occupying Brodmann areas ___ and _____

A
  • lateral sulcus
  • 41 and 42
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13
Q

where does the primary auditory cortex receive auditory information from?

A

medial geniculate nucleus of the thalamus

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14
Q

what is the auditory association area responsible for?

A

interpretation of auditory information and which, in the left hemisphere, constitutes Wernicke’s area (comprehension of the written and spoken language)

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15
Q

what does the temporal lobe work with in the formation of conscious memories?

A

amygdala (medial temproal lobe) and hippocampus (temporal lobe)

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16
Q

blood supply of the temporal lobe?

A

lateral surface supplied mainly by branches of the MCA

inferior surface supplied mainly by branches of PCA

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17
Q

which temporal lobe is typically dominant in most people and is associated with understanding language, learning, memorising, forming speech and remembering verbal information?

A

left

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18
Q

what is the non-dominant temporal lobe commonly associated with?

A

learning and memorising non-visual information (eg. drawings and music), recognising information, and determining facial expressions

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19
Q

how does blood reach the brain?

A
  • anterior circulation = ICA + common carotid
  • posterior circulation = vertebral arteries and subclavian artery
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20
Q

what vessel, if occluded, would affect both Broca’s and Wernicke’s area?

A

middle cerebral artery

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21
Q

what artery supplies blood to the occipital lobe?

A

posterior cerebral

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22
Q

what is the largest branch of the ICA?

A

MCA

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23
Q

what artery runs in midline on ventral surface of pons?

A

basilar artery

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24
Q

The scalp receives a rich arterial supply via the ________ and the _____________ (a branch of the internal carotid).There are three branches of the former involved:
- _________– supplies the frontal and temporal regions
- _________– supplies the area superiorly and posteriorly to the
auricle.
- __________– supplies the back of the scalp
Anteriorly and superiorly, the scalp receives additional supply from two branches of the ____________ – the ________ and _________ arteries. These vessels accompany the ___________ and ____________ nerves respectively.

A

The scalp receives a rich arterial supply via the external carotid artery and the ophthalmic artery (a branch of the internal carotid).There are three branches of the external carotid artery involved:
- Superficial temporal– supplies the frontal and temporal regions
- Posterior auricular– supplies the area superiorly and posteriorly to the auricle.
- Occipital– supplies the back of the scalp
Anteriorly and superiorly, the scalp receives additional supply from two branches of the ophthalmic artery – the supraorbital and supratrochlear arteries. These vessels accompany the supraorbital and supratrochlear nerves respectively.

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25
Q

photoreceptors absorb light using what?

A

11-cis retinaldehyde bound to opsin protein

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26
Q

what keeps opsin in the inactive state?

A

11-cis retinal

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27
Q

what is the G protein in photoreceptors?

A

transducin

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28
Q

what do photoreceptors respond to light with?

A

graded hyperpolarisation

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29
Q

what is the signal photoreceptors transmit in light?

A

reduction in Glu in response to absoprtion of light (lots of Glu released in dark as neurons release Glu when depolarised)

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30
Q

what provide an inhibitory link between bipolar cells and RGCs?

A

amacrine cells

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31
Q

axons from what layer project to the brain?

A

ganglion cell layer

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32
Q

what layer in the retina contains the cell bodies of rod cells?

A

outer nuclear layer

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33
Q

what layer in the retina contains the cell bodies of bipolar cells?

A

inner nuclear layer

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34
Q

what layer contains synapses between bipolar and amacrine cells?

A

inner plexiform layer

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35
Q

what layer contains synapses between photoreceptors (rod cells) and bipolar cells?

A

outer plexiform layer

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36
Q

is onset of anaesthesia faster with inhalation or iv?

A

iv

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37
Q

what is commonly used for induction of general anaesthesia?

A

propofol

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38
Q

when may inhalation be used over iv for induction?

A

where iv access is difficulty to obtain, where difficulty maintaining the airway is anticipated, or due to patient preference (eg. children)

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39
Q

maintenance of general anaesthesia is achieved by allowing the patient to breathe a carefully controlled mixture of what? how can it also be achieved?

A

oxygen, nitrous oxide and volatiles anaesthetic agent (isoflurane)

  • can also be achieved by having a carefully controlled continuous infusion propofol through an intravenous catheter
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40
Q

what is the natural neurotransmitter at the NMJ which causes muscular contraction when it is released from nerve endings ?

A

ACh

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41
Q

muscle relaxants work by preventing…..

A

ACh from attaching to its receptor

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42
Q

since muscle relaxants paralyse the muscles of the larynx, how is the airway protected?

A

endotracheal tube

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43
Q

the effects of muscle relaxants are commonly reversed at the termination of a surgery by what type of drugs?

A

acetylcholinesterase drugs

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44
Q

in terms of airways, what is lost with the loss of consciousness?

A
  • protective airway reflexes (eg. coughing)
  • airway patency
  • regular pattern due to the effect of of anaesthetics, opioids or muscle relaxants
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45
Q

what 2 things are used to reverse any muscle relaxants?

A

neostigmine and glycopyrrolate

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46
Q

what is monitored and assessed in reversal of anaesthesia?

A

oxygenation, pain control, fluid balance, post operative nausea and vomiting (PONV), cardiovascular stability, conscious level, urine output
- late management : wound infection, DVT, chest infection, surgical problems

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47
Q

what are some adverse effects of anaesthesia?

A
  • PONV
  • CV depression
  • arrhythmogenesis
  • hypotension : vasodilation
  • loss of airway tone : airway obstruction
  • malignant hyperthermia (uncontrolled temp —> if untreated, all the ATP stores are burned —> rhabdomyolysis, renal failure and cardiac arrest
  • bronchial muscle relaxation and impaired cough reflex
  • agitation and confusion (esp elderly)
  • nephrotoxicity : RBF, GFR, UOP…. vs fluride induced nephrotoxicity
  • hepatotoxicity : halothane hepatitis
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48
Q
  • an iv anaesthetic for rapid induction = _______
  • an inhalation anaesthetic to maintain anaesthesia during surgery = _______
  • a perioperatie opiod analgesic = _________
  • a muscarinic antagonist to prevent or treat bradycardia or to reduce bronchial and salivary secretions = _______/________
  • anticholinesterase agent to reverse the neuromuscular blockade = ________
A
  • propofol
  • isoflurane
  • fentanyl
  • atropine/glycopyrrolate
  • neostigmine
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49
Q

what are inhalation anaesthetics soluble in?

A

lipid — readily cross alveolar membranes

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50
Q

what are the main factors that determine the speed of induction and recovery? (properties of inhalation anaesthetics)

A

properties of the anaesthetic:

> blood:gas partition coefficient (solubility in blood) = speed of induction/recovery
oil:gas partition coefficient (solubility in fat) = potency

physiological factors:

> alveolar ventilation rate
cardiac output

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51
Q

anaesthetic potency is expressed as the what?

A

minimal alveolar concentration (MAC)

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52
Q

what is the MAC?

A

minimal alveolar conc

= the conc of vapour in the lungs that is needed to prevent movement (motor response) in 50% of patients in response to surgical (pain-incision) stimulus

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53
Q

what does the potency of a drug increase with?

A

increasing lipid solubility

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54
Q

link between lipid solubility and MAC?

A

the higher the lipid solubility, the lower the MAC

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55
Q

why does propofol have rapid recovery with a small hangover effect?

A

very rapidly metabolised to inactive metabolites

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56
Q

MOA of propofol

A

positive modulation of GABA through GABA-A receptor — cause an increased influx of Cl- ions into the post synaptic neuron

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57
Q

where do anaesthetics mainly work?

A

extrasynaptic GABA-A receptors

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58
Q

what type of receptors are GABA-A receptors?

A

ionotropic ligand-gated ion channels

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59
Q

what are common SEs of propofol?

A

SEs are less frequent for propofol than other iv anaesthetic agents. SEs include:
- hypotension and bradycardia
- resp depression
- pain with injection
- involuntary movement and adrenocortical suppression
- nausea and vomiting

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60
Q

what is the msot widely y used inhalation inducing agent and used for maintenance of general anaesthesia?

A

isoflurane

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61
Q

what is isoflurane always administered with?

A

air/pure O2 and nitric oxide

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62
Q

MOA of isoflurane

A

likely binds to GABA, NMDA (glutamates) and glycine receptors. NOT UNDERSTOOD

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63
Q

SEs of isoflurane

A

relatively free from SEs. major ones inc hypotension, coronary vasodilation (exacerbate cardiac ischaemia in patient with coronary disease), resp suppression

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64
Q

name a potent narcotic analgesic

A

fentanyl

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65
Q

MAO of fentanyl

A

strong agonist at the mu opioid receptor. upon binding, GTP —> GDP on the G-proteins which in turn down regulates adenylate cyclase, reducing cAMP concentrations —> reduced Ca++ influx in to cell —> hyperpolarisation of cell and inhibition of nerve activity

When fentanyl binds, downstream signaling leads to the inhibitory effects, such as decreased cAMP production, decreased calcium ion influx, and increased potassium efflux. This inhibits the ascending pathways in the central nervous system to increase pain threshold by changing the perception of pain; this is mediated by decreasing propagation of nociceptive signals, resulting in analgesic effects
adenylate cyclase inhibition —> deceased release of nociceptive substacens such as substance P, GABA, DA etc

66
Q

name a non-depolarising NM blocking agent

A

atracurium

67
Q

describe atracurium

A
  • competitive antagonist at the ACH receptors of the motor endplate
  • cause motor paralysis —> help facilitate endotracheal intubation
68
Q

what are some major SEs of non-depolarising blockers?

A

hypotension, bronchospasm (due to histamine release), wheeze, tachycardia or bradycardia anaphylaxis, incomplete reversal

69
Q

why is the short duration of action of atracurium a clinical advantage?

A

because of decreased CV effects and decreased dependency of good kidney function

70
Q

how is atracurium excreted?

A

esterases and alkaline hydrolysis in plasma

—> Hoffman degradation
—> temperature and pH dependent

71
Q

MOA of suxamethonium (succinylcholine)

A

persistent depolarisation of NMJ by mimicking the effect of ACh without being rapidly hydrolysed by acetylcholinesterase. constant depolarisation leads to desensitisation

72
Q

what is suxamethonium hydrolysed by?

A

plasma cholinesterase (butyryrlcholinesterase)

73
Q

what are some SEs of depolarising NM agents?

A

muscle pain, hyperkalaemia, malignant hyperthermia, anaphylaxis, suxamethonium apnoea, increased intracranial/ocular pressure (due to muscle twitching)

74
Q

what is suxamethonium apnoea?

A

genetic inability to break it down

75
Q

neostigmine MOA

A
  • blocks acetylcholinesterase
  • increases ACh in the NMJ (both nicotinic and muscarinic receptors)
  • increases muscular contraction

—> acts to reverse the effects of non-depolarising muscle relaxants

76
Q

how do atropine and glycopyrrolate work? why are they used?

A
  • they antagonise the muscarinic receptor and thus inhibit cholinergic transmission
  • used to limit the parasympathetic effects caused by neostigmine (prevents neostigmine’ symptoms muscarinic effects such as bradycardia)
77
Q

what are the side effects of anti cholinesterase drugs?

A

autonomic:
- bradycardia
- hypotension
- bronchoconstriction

msucular:
- muscle fasciculations
- twitch tension
- depolarisation block

78
Q

atropine vs glycopyrrolate

A

atropine can cross the BBB but glycopyrrolate cant

79
Q

what else are anticholinesterase drugs used to treat?

A

myasthenia gravis (neostigmine)

80
Q

what are the 2 main forms of cholinesterase?

A
81
Q

describe mannitol

A
  • osmotic diuretic
  • used to treat raised intracranial pressure (eg. cerebral oedema)
82
Q

MOA of mannitol

A
  • pharmalogically inert substances that are filtered in the glomerulus but not reabospred by the nephron
  • cause diuresis because they increase the solute content of the fluid in the proximal and collecting tubules
  • this draws fluid from the body into the proximal tubule, thus decreasing the volume of fluid inside the body
  • results in less water being reabsopred and less sodium
  • decrease in extracellular fluid volume
83
Q

what is NREM 1?

A
  • light sleep
  • lasts 1-5 minutes
  • stage between wakefulness and sleep
84
Q

what are skeletal muscles like in NREM sleep?

A

relax but maintain their tone

85
Q

when in sleep is parasympathetic activity predominant?

A

NREM — promotes gastric motility and a decreased HR and BP

86
Q

what EEG waves and waveforms are present in each of the sleep stages?

A

NREM 1 = 4-7 Hz waves, alpha and theta EEG waveforms
NREM 2 = 10-15 Hz waves, theta EEG waveforms + sleep spindles and K complexes
NREM 3 and 4 = <3.5 Hz waves, delta EEG waveform — “slow wave sleep” — lowest frequency, highest amplitude

awake = beta most common

87
Q

in what type of sleep are BP, metabolism and blood flow to the brain increased?

A

REM sleep

88
Q

when do most dreams occur?

A

REM

89
Q

what act as “REM-on” cells that initiate REM sleep?

A

brainstem cholinergic neurons in the ascending arousal system

90
Q

what are activated in REM sleep, causing skeletal muscles to become flaccid and muscel stretch reflexes to be absent?

A

inhibitory medullary reticulospinal neurons

91
Q

only what muscles remain active in REM sleep?

A

ocular, respiration, and middle ear muscles

92
Q

what act as “REM-off” cells, initiating transition from REM back to non-REM sleep?

A

noradrenergic and serotonergic neurons

93
Q

what type of sleep do you need in order to survive?

A

NREM

94
Q

what type of sleep decreases with age?

A

REM

95
Q

in what sleep is sympathetic activity predominant?

A

REM

96
Q

ASCEDNIG AROUSAL SYSTEM?

A

SEE NOTES

97
Q

describe cytotoxic oedema

A
  • initial mechanism
  • fluid retained in cytoplasm
  • loss of NaK ATPase
  • Glu gated Ca channels open
  • Ca draws water in
    (BBB intact)

cerebral ischaemia - decreased blood flow and glucose supply — exhaustion of energy sources — failure of NaK pump

98
Q

describe vasogenic oedema

A
  • delayed mechanism (48 hours)
  • breakdown of BBB
  • fluid and protein extravasation into parenchyma
  • esp important for patients with stroke or contusions

return of blood flow to these cells after an ischaemic stroke can cause excitotoxicity and oxidative stress — dysfunction of the endothelial cells and BBB disruption

99
Q

what can an ACA occlusion cause?

A

paralysis and sensory loss in contralateral leg and perineum

100
Q

what can a MCA occlusion cause?

A

contralateral paralysis (mostly in lower face and in arm), general somatosensory deficits, speech deficits (aphasia) if dominant hemisphere affected

101
Q

what is the pterion?

A

where these meet:
- parietal bone, squamous part of temporal bone, frontal bone, greater wing of sphenoid

> skull is very thin at this point — structurally weak so more easily broken

102
Q

what does the pterion overlie? clinical significance?

A
  • overlies anterior division of MMA — fracture here can lead to an extradural haematoma
103
Q

describe the typical symptoms of an extradural haematoma?

A

lose consciousness immediately, lucid interval, get drowsier and then lose consciousness again

104
Q

why does the ICP rise rapidly in an extradural haematoma?

A

dura is attached tightly to sutures — blood doesn’t cross so is trapped with no where to go — ICP can rise rapidly

doesnt cross suture lines

105
Q

symptoms of an extradural haemaotma

A
  • headaches, nausea, vomiting, focal neurological symptoms (weakness, numbness, vision and auditory problems). cerebral oedema —> brain herniation —> loss of consciousness, coma, death
106
Q

what is the usual bleeding source i a subdural haematoma?

A

bridging veins (connect superficial veins of skull and dural venous sinuses)

107
Q

what are bridging veins susceptible to and when do they get stretched out?

A
  • bridging veins are vulnerable to rapid acceleration and deceleration — commonly disrupted in car crashes
  • these veins get stretched out in the elderly and in chronic alcohol abus
108
Q

what type of haemotoma can shaking a child cause?

A

subdural

109
Q

what are the typical symptoms of a subdural haematoma?

A

worsening headaches, nausea or vomiting, visual problems, slurred speech, dizziness, unsteady gait, confusion, cognitive impairment, seizures, hemiparesis
- venous therefore haematoma grows slower
- concave crescent shaped CT rhat does cross suture lines

110
Q

why does ICP rise slower in subdural haematoma?

A

cross suture sites — disrupted over larger areas — pressure doesn’t build up as quickly — ICP rises gradually

111
Q

how can density on CT help determine the age of a haematoma?

A
  • acute : hyperdense (white)
  • chronic : hypodense
112
Q

what type of haematoma has a higher morbidity and mortality?

A

subdural — harder to detect in early stages

113
Q

what disease/syndromes can predispose even young people to saccular aneurysms, leading to a subarachnoid haemorrhage?

A

autosomal dominant polycystic kidney disease, marfan syndrome, and ehlers-danlos syndrome

114
Q

what is the first sign of a subarachnoid haemorrhage?

A

‘worst headache of life’ = thunderclap headache

115
Q

symtpoms of subarachnoid haemorrhage

A

headache, nuchal rigidity (neck stiffness), seizures, and due to ICP : vomiting, vision changes and confusion

116
Q

what does a subarachnoid haemorrhage look like on CT?

A

blood in ventricular cisterns, interhemispheric fissures, and within sulci

117
Q

what can cause hydrocephalus and spit-traumatic vasospasm (leading to ischaemia)?

A

subarachnoid haemorrhage, subdural haematoma and cotunison, but not extra dural

118
Q

what causes diffuse axonal injures?

A
  • result from shearing forces on white matter axons in brain, causing the axons to stretch or tear apart
  • can be caused by rapid acceleration or deceleration eg. car crash
119
Q

what do diffuse axonal injures look like on MRI?

A

multiple small, hyperdense punctuate lesions along the gray-white matter junction

120
Q

craniectomy vs craniotomy vs cranioplasty

A

A Craniectomy is similar to a craniotomy as both procedures involve removing a portion of the skull, the difference is that after a craniotomy the bone is replaced and after a craniectomy the bone is not immediately replaced.

cranioplasty : replacing the bone once the swelling is gone. if the bone piece has been preserved then it can be used. if not, options include titanium, acrylic or synthetic bone substitute. modern 3D printing are also used

121
Q

what does fixed dilated pupils indicate?

A
  • transtentorial herniation
  • pressure on brainstem
  • pressure on oculomotor nerve — pupils fixed and dilate, lose pupillary reflex
  • poor prognostic marker
122
Q

descirbe periorbital swelling as a symptom

A
  • raccoon eyes — bilateral eye swelling
  • base of skull fracture
  • often accompanied by battle sign (bleeding behind ear), haemotymoanum, CSF leak
123
Q

what connects broca’s and wernicke’s?

A

arcuate fasciculus

124
Q

describe dysarthria

A
  • difficulty speaking dude to muscle weakness
  • swelling compressing arcuate fasciculus, broca’s
  • damage to cranial nuclei
125
Q

why do you get seizures after a head trauma?

A
  • scarring in brain
  • scars cant transmit electrical signals
  • signals ‘jump over’
  • chemical imbalance
  • too much Glu:GABA
126
Q

what lobe is frequently involved in seizures?

A

temproal

127
Q

what is a seizure?

A

a sudden, uncontrolled electrical disturbance in the brain

128
Q

what things are imbalanced in seizures?

A

excitatory (too much)
- excitatory psotsynaptic potential (EPSP)
- Na+ influx
- Ca++ currents
- paroxysmal depolarisation

inhibitory
- inhibitory postsynaptic potential (IPSP)
- K+ efflux
- Cl- influx
- pumps
- low pH

129
Q

what is esteem support?

A

when other people increase one’s own self-esteem

130
Q

what is informational support?

A

whereby other people are available to offer advice

131
Q

what is companionship?

A

support throguh activities

132
Q

what is instrumental support?

A

involves physical help

133
Q

what are 4 types of social support?

A
  • esteem support
  • informational support
  • companionship
  • instrumental support
134
Q

what does the main effect hypothesis suggest?

A

that social support itself is beneficial and that the absence of social support is itself stressful

135
Q

what does the stress buffering hypothesis suggest?

A

that social support helps individuals to cope with stress

136
Q

what waves are the slowest brain waves?

A

delta

137
Q

what are the most common daytime brain waves, and are dominant in normal wakeful states and when you’re focuses on cognitive tasks?

A

beta

138
Q

what are te fastest brain waves, which process info from various brain regions and are responsibel for conscious perception?

A

gamma

139
Q

what brain waves are in REM sleep?

A

similar to when we are awake — beta

140
Q

BATS DRINK BLOOD (waves)

A

from awake to deep sleep to REM

  • beta = awake
    N1
  • alpha
  • theta
    N2
  • spindles and K complexes

N3
- delta

REM
- beta

141
Q

brain waves during anaesthesia resemble which stage of sleep?

  • N1
  • N2
  • N3
  • REM
  • none of the above
A

none of the above

142
Q

a decrease in which of the following neurotransmitters is most likely to result in post-traumatic epilepsy?

  • serotonin
  • dopamine
  • GABA
  • noradrenaline
  • glutamate
A

GABA

143
Q

which of the following is used to allow intubation during general anaesthesia?

  • neostigmine
  • suxamethonium
  • isoflurane
  • atracurium
  • fentanyl
A

suxamethonium

144
Q

which of the following is NOT assessed by the Glasgow Coma Scale?

  • pupil response to light
  • verbal response to questions
  • eye opening with and without a stimulus
  • motor response to trapezius pinch
  • coherent communication
A

pupil response to light

145
Q

action potentials from the eye are sent down the axons of what tract?

A

retinohypothalamic tract (RHT)

146
Q

where does the AP in the retinohypothalamic tract go?

A
  • to the suprachiasmic nucleus (SCN)
  • releases specific chemicals (usually glutamate) which trigger the SCN
  • the SCN secretes chemicals to stimulate different organs
147
Q

what is the SCN and what does it regulate?

A
  • suprachiasmic nucleus = biological clock
  • regulates sleeping and walking
148
Q

what is stimulated by the SCN? what does it do?

A

the paraventricular nucleus in hypothalamus — sends signals down through the lateral gray column of the spinal cord to the superior cervical ganglion (SCG)

149
Q

where does the superior cervical ganglia send signals to?

A

the pineal gland via post ganglionic motor neurons — these secrete noradrenaline

150
Q

describe the pineal gland

A

made of pinealocytes
- they have specific adrenergic receptors for noradrenaline
- these receptors stimulate every step of the intracellular pathway :

tryptophan —> 5-hydroxytryptamine —> serotonin —> melatonin

151
Q

what sleep stage features hypnogogic hallucinations and hypnic jerks?

A

NREM 1

152
Q

what is created over the course of the day, leading to sleepiness at night?

A

adenosine

153
Q

when do melatonin concentrations peak? when does body temperature reach its lowest?

A

3am

154
Q

what is the name of the area of the frontal lobe that takes up the majority of the lobe and cortex is crucial for the performance of almost all skills requiring intelligence?

A

prefrontal cortex

155
Q

what is the name of the area of the frontal lobe that consciously monitors movement sequences, using sensory feedback and coordinates movement?

A

premotor cortex

156
Q

what kind of fracture is it where the bone is broken but skin is intact?

A

simple/closed

157
Q

what is a compound fracture?

A

involves a break in or loss of skin and splintering of the bone

158
Q

what type of cerebral oedema is this describing : plasma dilution results in an abnormal pressure gradient and movement of water into the brain

A

osmotic

159
Q

describe a tonic-clonic seizure

A

the person loses consciousness, muscles stiffen and jerking movements are seen

160
Q

describe an atonic seizure

A

there is an abrupt loss of muscle tone, also known as a ‘drop attack’

161
Q

which drug acts through the inhibition of ACh on structures with muscarinic ACh receptors?

A

glycopyrrolate

162
Q

which drug may cause a dry mouth, constipation and ear congestion side effects?

A

glycopyrrolate

PBL SEM 3 (49 decks)

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