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CBL Year 2 > Collapse > Flashcards

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1
Q

define coma

A

state of unrousable unresponsiveness in which there is no coordinated response to external stimuli or internal need

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2
Q

GCS

A 
glasma coma scale
eye movement (E)=1-4
verbal response (V) = 1-5
motor response (M) =1-6
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3
Q

GCS to classify as a coma

A

3-8

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4
Q

eye movement in GCS

A

spontaneously = 4
to speech = 3
to pain = 2
none = 1

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5
Q

verbal response in GCS

A 
orientated = 5
confused = 4
inappropriate = 3
incomprehensible = 2
none = 1
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6
Q

motor response in GCS

A 
obeys commands = 6 
localises to pain = 5
withdraws from pain = 4
flexion to pain = 3 (decorticate)
extension to pain = 2 (decerebrate)
none = 1
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7
Q

define collapse / blackout

A

transient loss of memory or consciousness with complete recovery

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8
Q

three (branches) most common causes of collapse

A

syncope
neurological
psychogenic

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9
Q

define syncope

A

transient brain hypoxia resulting in loss of consciousness or a near loss of consciousness (presyncope)

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10
Q

define seizure

A

episode of uncontrolled electrical activity of the brain

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11
Q

define psychogenic

A

psychological, no physical/organic cause

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12
Q

5 main branches of syncope (things that cause it)

A 
arrhythmia
structural disorder of the heart
baroreceptor reflex related
posture related (orthostatic)
others
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13
Q

arrhythmia causes of syncope

A

bradycardia or tachycardia

always attach to 12 lead ECG

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14
Q

structural disorders of the heart causes of syncope

A

aortic stenosis
pericardial effusion
hypertrophic cardiomyopathy

found through cvs exam and echocardiogram

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15
Q

baroreceptor reflex related causes of syncope

A

vasovagal
carotid sinus hypersensitivity (rare before 40)
cough or micturition syncope (older men usually during or after urination)

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16
Q

posture related (orthostatic) causes of syncope

A

orthostatic hypertension
autonomic failure (loss of normal innervation of heart and arterioles)
drug induced
volume depletion
postural orthostatic tachycardia syndrome (POTS)

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17
Q

“other” causes of syncope

A

anaemia
aortic dissection
hypoglycaemia
PE

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18
Q

what is postural orthostatic tachycardia syndrome (POTS)

A

occurs in young women

rapid rise in heart rate on standing >130 bpm is diagnostic

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19
Q

start symptoms of vasovagal syncope

A 
feeling hot and lightheaded
nausea 
vomiting
tunnel vision
voices seem distant 
face looks very pale
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20
Q

during symptoms of vasovagal syncope

A 
loss of skeletal muscle tone, goes limp
bradycardia due to increased vagal tone
hypotensive due to vasodilation
may have some jerking movements
(incontinence of urine sometimes)
(tongue biting unusual)
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21
Q

vasovagal syncope symptoms after

A

rapid return of consciousness on <1 min lying flat
may be confused for a minute or two
may feel malaise for a while after (general feeling of discomfort)

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22
Q

what is Wolff Parkinson white syndrome

A

in Wolff-Parkinson-White (WPW) syndrome, an extra signaling pathway between the heart’s upper and lower chambers causes a fast heartbeat (tachycardia). WPW syndrome is a heart condition present at birth (congenital heart defect)

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23
Q

wolff Parkinson white on an ECG

A

The typical ECG finding of WPW is a short PR interval and a “delta wave.“ A delta wave is slurring of the upstroke of the QRS complex.

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24
Q

3 neurological causes of syncope

A

seizure
narcolepsy
vertebrobasilar insufficiency

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25
Q

what is Psychogenic pseudosyncope (PPS)

A

Psychogenic pseudosyncope (PPS) is the appearance of transient loss of consciousness (TLOC) in the absence of true loss of consciousness. Psychiatrically, most cases are classified as conversion disorder, which is hypothesized to represent the physical manifestation of internal stressors

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26
Q

What is non-epileptic attack disorder (NEAD)

A

some people with dissociative disorders also experience physical symptoms such as seizures. These seizures don’t seem to have a physical cause. These are called dissociative seizures or non-epileptic attacks.

> have convulsions of the arms, legs, head or body (on one side or affecting the whole body)
lose control of your bladder
bite your tongue
go blank or stare in an unseeing way
have other symptoms that look like epilepsy.

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27
Q

AVPU

A

alert - patient is awake and responsive
voice - patient responds to voice
pain - patient responds to pain
unconscious

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28
Q

when can action potentials occur

A

only occur when opposite charges exist either side of a membrane

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29
Q

depolarisation is done through which channel

A

voltage gated sodium channels

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30
Q

examples of drugs that bind the Na channel (stop depolarisation of action potentials)

A

local anaesthetics - lidocaine, bupivacaine
antiarrhythmitics - lidocaine
anticonvulsants - carbamazepine
antidepressants - amitriptyline

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31
Q

describe repolarisation

A

inactivation of the sodium channels
activation of the K channels
(k moves out making inside less positive and membrane repolarises)

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32
Q

what is glutamate

A

main CNS excitatory transmitter

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33
Q

what is GABA

A

main CNS inhibitory transmitter

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34
Q

amino acid transmitters

A

glutamate and glycine (abundant in all cells)

GABA (synthesised in the cytoplasm of neurones)

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35
Q

monoamine transmitters

A

acetylcholine, 5-HT, histamine

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36
Q

catecholamine transmitters

A

noradrenaline, dopamine, adrenaline

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37
Q

peptide transmitter

A

substance P

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38
Q

Ionotropic receptor

A 
transmitter (ligand gated) receptor
eg. NMDA subtype of glutamate receptor
nicotinic Ach (NMJ, CNS)
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39
Q

what is NMDA - what are some drug examples that act here

A

is a glutamate receptor and ion channel found in neurons

ketamine (anaesthesia, depression)
memantine (Alzheimers)

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40
Q

GABA (a) receptors (inotropic) are site of action for which drugs

A

benzodiazepines
barbituates
anaesthetic steroids
volatile anaesthetics

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41
Q

loss of ACh cells in Alzheimers disease treated with

A

treatment by cholinesterase inhibitor (rivastigmine, donezepil)

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42
Q

ACh and diseases of neuromuscular junction

A

Myasthenia gravis - usually autoimmune destruction of ACh receptors at NMJ
progressive loss of muscle power eventually leading to paralysis of diaphragm
treatment by cholinesterase inhibitor (neostigmine)

Lambert - Eaton syndrome - autoimmune destruction of calcium channels at the motor nerve endings
is most often seen in people with small cell lung cancer or other cancers, but it can also occur in people without cancer.

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43
Q

toxins that affect NMJ

A

latrotoxin (black widow) - triggers ACh release (muscle spasm)
Crotoxin (rattlesnake) - inhibits ACh release (flaccid paralysis_
Botulinus toxins (bacterial) - inhibits ACh release
Curare (plant poison) - Blocks ACh receptors on skeletal muscle
War gases (eg. sarin)- block AChE - causes ACh buildup , spasm and then paralysis

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44
Q

what does cocaine do to noradrenaline

A

blocks reuptake of noradrenaline

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45
Q

what does Methylphenidate/ritalin do/treat

A

blocks reuptake of noradrenaline

treats ADHD and narcolepsy

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46
Q

myelin producers

A 
oligodendrocytes (CNS)
Schwann cells (PNS)
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47
Q

astrocytes

A

largest glial cell, star shaped

contribute to homeostasis in the neutrophil by metabolising neurotransmitters from the extracellular space

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48
Q

microglia

A

small and mobile

activated during injury or disease to remove debris

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49
Q

ependymal cells

A

type of glial cell
line the ventricles
specialised ones produce CSF in the choroid plexus

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50
Q

3 myelin associated pathologies

A 
multiple sclerosis (autoimmune, plaques on myelin, inflammation)
optic neuritis (frequent symptom of MS, but are other causes)
central pontine myelinosis (consequence in rapid change ins erum vs. CSF electrolyte balance (sudden correction of hyponatreamia))
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51
Q

EEG

A

electro encephalogram

  • simple non invasive technique
  • electrodes attached to head in defined positions
  • voltage changes between pairs of electrodes are measured
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52
Q

electrode placement for EEG (the international 10-20 system_

A

even numbers refer to right hemisphere and odd numbers refer to left hemisphere
z refers to electrode placed on midline
the smaller the numbers the closer to the midline

Also use
F = frontal lobe
T= temporal lobe
P = parietal lobe
O= occipital lobe
C = central point
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53
Q

what does EEG mostly measure

A

the excitation of dendrites of pyramidal neurones (within medulla oblongata)

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54
Q

clinical use of EEG

A

detection of epileptic activity
detection of sleep disorders
brain dysfunction associated with head trauma, brain death, states of altered consciousness
research tool

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55
Q

briefly describe REM phase of sleep

A 
(rapid eye movement)
5-30 min long every 90 mins
cerebral cortex is very active
dreaming
muscular relaxation
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56
Q

EEG is a crude indicator of what

A

the activity of the cerebral cortex

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57
Q

synchronised EEG during sleep

A

large amplitude
slow waves
found during drowsiness and slow wave sleep (SWS)

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58
Q

desynchronised EEG during sleep

A

small amplitude fast waves, found during alert wakefulness and REM sleep

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59
Q

what is insomnia

A

difficulty falling or staying asleep

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60
Q

what is hypersomnia

A

excessive amounts of sleepiness

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61
Q

what is narcolepsy

A

excessive sleepiness and frequent day time sleep attacks

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62
Q

what is sleep apnoea disorder

A

abnormal pauses in breathing or instances of abnormally low breathing during sleep

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63
Q

what is somnambulism

A

sleepwalking

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64
Q

what is nocturnal enuresis

A

bed wetting

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65
Q

what is reticular formation

A

set of interconnected nuclei located throughout the brain stem

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66
Q

functions of local projections of reticular formation

A

chewing, swallowing and vomiting
respiratory activities (coughing, sneezing)
CVS responses

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67
Q

long projection systems ascending to the cortex functions

A

responsible for sleep wake cycle

mediates various levels of alertness and consciousness

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68
Q

long projection systems descending to the spinal cord functions

A

involved in posture and equilibrium as well as ANS activity
involved in sensory pain and motor modulation
receives information from the hypothalamus

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69
Q

what controls levels of consciousness

A

reticular formation

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70
Q

what controls the content of consciousness

A

cerebral cortex

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71
Q

what is brain death equal to

A

reticular formation death - check cranial nerve reflexes and independent respiration

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72
Q

what is epilepsy

A
  • neurological condition characterised by excessive neuronal firing (electrical activity) or either part or the whole brain
  • it is a condition where the person displays recurrent epileptic seizures
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73
Q

define seizure

A

clinical manifestation of synchronisation and excessive firing from a population of cortical neurones

manifestation of sudden excessive electrical activity which disrupts the normal communication between brain cells

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74
Q

define epileptogensis

A

sequence of events that converts a normal neuronal network into a hyperexcitbale circuit which trigger spontaneous seizures

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75
Q

define status epilepticus (SE)

A

neurological and medical emergency characterised by 5 or more minutes of either continuous seizure activity or repetitive seizures with no recovery of consciousness

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76
Q

3 main groups of seizure

A

unknown
focal seizures
generalised seizures

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77
Q

describe what is meany by an unknown seizure

A

insufficient evidence to characterise focal, generalised or both
usually epileptic spasms or other

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78
Q

focal seizure description

A
  • originating within network
  • limited to one hemisphere
  • characterised according to 1 or more features: aura, motor, autonomic
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79
Q

generalised seizure

A

arising within and rapidly engaging bilateral distributed networks

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80
Q

what is an absence

A

seizure

someone stares blankly

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81
Q

what is a myoclonic seizure

A

short jerking movements of parts of the body

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82
Q

what is a Tonic - clonic seizure

A

convulsion, goes stiff, bites tongue, incontinence

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83
Q

tonic seizure

A

goes stiff and falls without convulsion

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84
Q

what is atonic seizure

A

falling limply to the ground

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85
Q

causes of epilepsy

A
  • head injury that causes brain tissue scarring
  • trauma at birth or high temperature
  • excessively rough handling or shaking of an infant
  • certain drugs (large doses), toxic substances (alcohol)
  • stroke or tumour
  • disease which alters balance of blood or its chemical structure
  • disease that damage nerve cells in the brain
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86
Q

suprachiasmatic nuclei

A

The suprachiasmatic nucleus (SCN) is a bilateral structure located in the anterior part of the hypothalamus. It is the central pacemaker of the circadian timing system and regulates most circadian rhythms in the body.

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87
Q

locus coeruleus

A

is the principal site for brain synthesis of norepinephrine (noradrenaline). The locus coeruleus and the areas of the body affected by the norepinephrine it produces are described collectively as the locus coeruleus-noradrenergic system or LC-NA system.

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88
Q

definition of shock

A

acute failure of the CVS to supply sufficient blood to tissues to meet their metabolic demand and maintain life

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89
Q

what is heart rate determined by

A

sympathetic (beta 1 adrenoreceptors) and parasympathetic innervation ( muscarinic receptors)

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90
Q

what is stroke volume determined by

A

contractility
preload
afterload

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91
Q

what is arteriolar tone controlled by

A

circulating hormones (vasopressin, adrenaline, angiotensin II and the sympathetic nervous system)

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92
Q

what is hypovolaemic shock due to

what causes it

A

due to decrease in blood/plasma volume
examples: internal haemorrhage, external haemorrhage, severe burns, Addisons disease, severe dehydration, intestinal obstruction

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93
Q

what is cardiogenic shock

what causes it

A

a sudden severe reduction in cardiac contractility
examples: MI, arrhythmias, valvular regurgitation

essentially its pump failure

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94
Q

what is obstructive shock

what causes it

A

due to mechanical obstruction or impaired cardiac filling
examples: PE, cardiac tamponade

essentially blocked pump or too much external pressure

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95
Q

what is distributive shock

what causes it

A

vascular capacity increases so that even the normal volume of blood can’t fill it
examples: anaphylaxis, sepsis, spinal injury

too much vascular capacity

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96
Q

Hypovolaemic shock what is increased/decreased

blood/plasma volume, JVP, CO, MAP, TPR

A

decrease in blood/plasma volume
decrease in JVP/CVP (Central venous pressure)
decrease in CO
decrease in MAP
Increase in TPR (compensatory response mediated by the baroreceptor reflex)

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97
Q

cardiogenic shock increase/decrease (CVP, Cardiac output, MAP,TPR)

A

increase in central venous pressure
decrease in cardiac output
decrease in MAP
increase in TPR(compensatory response mediated by the baroreceptor reflex))

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98
Q

obstructive shock increase/decrease (CVP, CO, MAP, TPR)

A

increase in central venous pressure
decrease in CO
decrease in MAP
increase in TPR(compensatory response mediated by the baroreceptor reflex)

99
Q

distributive shock increase/decrease (CVP, CO, MAP, TPR)

A

decrease in all

100
Q

symptoms of hypovolaemic shock

A 
anxiety
confusion
muscle weakness 
collapse
and/or thirst
101
Q

signs of hypovolaemic shock

A 
pale/cold skin
increased cap refill time
rapid/weak pulse
tachypnoea
oliguria
102
Q

why do a venous blood gas (VBG) in a patent with suspected hypovolaemic shock

A

to determine severity, predict mortality, and response to treatment

103
Q

does 0-10% blood loss produce shock

A

no

104
Q

does 20-30% blood loss produce shock

A

compensated shock

105
Q

what does >30% blood loss produce

A

decompensated (progressive) shock

106
Q

compensatory mechanisms for hypovolaemic shock

A 
baroreceptor reflex (increase in TPR)
RAAS(withhold ACE inhibitors)
107
Q

positive feedback cycle for hypovolaemic shock

A

shock causes tissue hypoxia
which causes tissue and organ dysfunction \
which causes release of inflammatory mediators
which causes shock

108
Q

decompensated shock

A

failure of vascualture
(decrease in sympathetic output results in profound vasodilation and fall in TPR)
failure of pump
(reduced coronary perfusion leads to decreased myocardial contractility)
failure of microvasculature
(increased capillary permeability with resulting loss of fluid, microthrombosis, and DIC_

109
Q

cellular consequences of hypovolaemic shock

A

reduction in ATP inhibits Na-K-ATPase and cells swell and lose K
lysosomes rupture resulting in cell damage
cells unable to utilise nutrients
ATP degraded to adenosine which leaves cells and is converted to uric acid
multi organ failure

110
Q

universal blood donor

A

O negative

111
Q

why is lactate high in shock

A

Elevated lactate in septic shock is mostly due to stimulation of beta-2 adrenergic receptors. Lactate elevation in sepsis seems to be due to endogenous epinephrine stimulating beta-2 receptors (figure below

112
Q

what is the fluid challenge

A

A fluid challenge is a method of identifying those patients likely to benefit from an increase in intravenous volume in order to guide further volume resuscitation. It is a dynamic test of the circulation.

113
Q

use of inotropes and vasopressors in the management of hypovolaemic shock

A

to create vasoconstriction and increase cardiac contractility

114
Q

relevance of a per rectal examination in a patient who has presented with hypovolaemic shock

A

could be internally bleeding

meleana

115
Q

define stroke

A

an acute focal injury of the CNS due to a vascular cause, including cerebral infarction and intracerebral haemorrhage

116
Q

TIA

A

transient ischaemic attack
ischaemia with symptoms <24hrs
or
without MRI changes of infarction

117
Q

two types of stroke

A 
ischaemic stroke (85%)
haemorrhage stroke (15%)
118
Q

pathophysiology of ischaemic stroke

A

reduced blood flow (usually a blocked artery)
failure of energy production
disruption of homeostasis e.g. ion channels
severity depends on severity of blood flow reduction

119
Q

stroke syndromes

A

total anterior circulation syndrome (TACS)
partial anterior circulation syndrom (PACS)
lacunar syndrome (LACS)
posterior circulation syndrome (POCS)

120
Q

causes of ischaemic stroke

A 
large artery atherosclerosis 
small artery occlusion
cardio-embolism
arterial dissection
other less common causes (anti-phospholipid syndrome, vasculitis)
121
Q

conventional risk factors for small artery occlusion and inherited causes

A

conventional causes: hypertension, diabetes, smoking, hypercholesteramia
inherited causes: collagen type IV mutations, CADASIL

122
Q

cardio-embolic stroke causes

A

AF
MI
patent foramen ovale

123
Q

vertebral dissection causes

A 
neck manipulation (e.g. chiropractor)
martial arts
124
Q

pathophysiology of haemorrhagic stroke

A 
cell death by necrosis
fragile blood vessels by:
-hypertension
-cerebral amyloid angiopathy
-arterio-venous malformation (AVM)
125
Q

what does the stroke unit care do

A

avoid/manage complications
start rehabilitation
identify cause of stroke
initiate secondary prevention

126
Q

ischaemic stroke treatment

A 
reperfusion
maintenance of blood flow:
-hydration
-avoidance of very early mobilisation
surgery for raised ICP
127
Q

haemorrhagic stroke treatment

A

blood pressure control
reversal of anticoagulants
surgery for raised ICP

128
Q

what is a hyper acute stroke patient

A

Patients presenting within 6 hours of stroke onset constitute a category of stroke patient known as the “hyperacute stroke patient.”

129
Q

immediate hyper acute stroke management

A 
Iv thrombolysis
mechanical thrombectomy
soon enough after symptom onset
severe enough to warrant risks of treatment
safe enough to justify treatment
130
Q

what is a thrombectomy

A

Surgical thrombectomy is a type of surgery to remove a blood clot from inside an artery or vein

131
Q

secondary prevention from strokes

A

anti-thrombotic:

  • anti platelets (aspirin +/- clopidogrel)
  • anticoagulants (especially any history of AF or flutter)

blood pressure control

lipid lowering

carotid endarterectomy

132
Q

when considering if collapse is due to bradycardia what do you look at on an ECG

A 
is every QRS preceded by a p wave?
is every P wave followed by a QRS? if not how many P:QRS
is the P to QRS interval the same?
if constant is it normal/prolonged?
if not constant does it follow a pattern
133
Q

what are Stoke Adam Attacks

A

Stokes-Adams attacks refers to syncopal episodes that occur from cardiac arrhythmia, most commonly bradycardia in the form of second degree type II AV block, complete heart block (Lev’s disease) or sick sinus syndrome.

134
Q

heart blocks

A

1st degree - long PR interval
2nd degree - Mobitz type 1 (wenkeback) and mobtiz type 2
3rd degree - complete heart block (AV dissociation)

135
Q

narrow complex tachycardia

A

SVT

supra ventricular tachycardia

136
Q

types of SVT

A 
atrial flutter
atrial fibrillation
atrial tachycardia (ectopic driven)
AV re-enterant tachycardia
AV nodal re-enterant tachycardia
137
Q

AF on an ECG

A

No P waves and an irregular QRS

138
Q

Atrial flutter on an ECG

A

no normal p waves

Saw tooth pattern

139
Q

AVRT (AV re-enterant tachycardia) on an ECG

A 
accessory pathway (delta wave - slurred upstroke of QRS)
short PR interval
140
Q

when considering if collapse is due to tachyarrhythmia what do you look at on an ECG

A

ir regular, irregularly regular, or irregularly irregular?
Are P waves visible?are they preceding/following theQRS?
do the P waves look normal/abnormal?
is the QRS narrow or broad ? is there a delta wave?

141
Q

two types of LV outflow obstruction

A

severe aortic stenosis

hypertrophic (obstructive) cardiomyopathy

142
Q

when to suspect LV outflow obstruction is cause of collapse (but is cardiac cause)

A

no electrical issue on ECG

examination reveals a murmur

143
Q

congenital types of long QT syndrome

A

LQTS type 1 - KCNQ1: swimming, exertion, or emotion

LQTS type 2 - KCNH 2 : auditory stimuli and postpartum

LQTS type 3- SCN5A: events occur during periods of sleep/rest

144
Q

acquired causes of long QT syndrome

A 
drugs:
anti-arrhytmic drugs 
non-sedating anti-histamines
some antimicrobials 
gastric motility drugs
145
Q

what is torsades de pointes

A

is one of several types of life-threatening heart rhythm disturbances. In the case of torsades de pointes (TdP), the heart’s two lower chambers, called the ventricles, beat faster than and out of sync with the upper chambers, called the atria.

146
Q

how to identify torsades de pointes on an ECG

A

It is characterized by rapid, irregular QRS complexes, which appear to be twisting around the electrocardiogram (ECG) baseline.

147
Q

causes of torsades de pointes

A

drug-induced QT prolongation and less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome.

148
Q

how does aortic stenosis cause collapse

A

often occurs upon exertion when systemic vasodilatation in the presence of a fixed forward stroke volume causes the arterial systolic blood pressure to decline. It also may be caused by atrial or ventricular tachyarrhythmias.

149
Q

mortality risk for ruptured AAA

A

65%

150
Q

3 treatment options for ruptured AAA

A

open repair
end-vascular repair (EVAR)
conservative management/palliative

151
Q

open repair for ruptured AAA things to consider

A

major operation
significant blood loss
ICU
10% mortality

152
Q

endo-vascular repair for a ruptured AAA things to consider

A

shorter length of stay
mortality 2%
anatomy may not always be amendable

153
Q

what is the Hardmen Index

A

to assess patients with a ruptured AAA
score >2 = 80% mortality

criteria:
age >76
creatinine >190 micromol/L
haemoglobin <9
myocardial ischaemia on ECG
loss of consciousness
154
Q

anatomy of AAA

A

thin tunica intima lined by epithelium
thick tunica media : elastin and collagen and smooth muscle
tunica adventitia: collagen, vasa vasorum, and lymphatic s

155
Q

pathophysiology of AAA

A
  • increase in collagen to elastin ratio
  • disordered medial elastic fibres and lamellae
  • increase in aortic wall thickness with deposition of collagen and calcification of elastin fibres
  • atherosclerotic changes leading to wall stiffness
156
Q

is intraperitoneal or retroperitoneal more salvageable in a ruptured AAA

A

retroperitoneal is more salvageable

intraperitoneal has a higher mortality rate

157
Q

obvious clinical presentation of someone with a ruptured AAA

A

sudden tearing abdominal/back pain
collapse
clammy/sweaty
shock

158
Q

not obvious clinical presentation of a ruptured AAA

A

constipation
haematuria
haematemesis
nausea and vomiting

159
Q

risk factors for AAA

A 
male sex
hypertension
smoking
diabetes
hypercholesteramia 
FH 
rarer: collagen disorders (Marfan syndrome and Ehlers danlos)
160
Q

type A thoracic aortic aneurysm

A

ascending aorta - needs surgery

161
Q

type B thoracic aortic aneurysm

A

descending aorta - medical management

162
Q

coronary vessel occlusion

A

STEMI

163
Q

common carotid occlusion

A

any type of stroke

164
Q

subclavian occlusion

A

acutely ischaemic upper limb

165
Q

coeliac/mesenteric occlusion

A

ischaemic bowel

166
Q

renal vessel occlusion

A

frank haematuria

167
Q

spinal artery occlusion

A

sudden onset painless paraplegia

168
Q

function of frontal lobe

A

motor control - premotor cortex
problem solving - prefrontal area
speech production - broca area

169
Q

function of temporal lobe

A

auditory process
language comprehension - wernickes area
memory/information retrieval

170
Q

function of parietal lobe

A

touch perception - somatosensory cortex

body orientation and sensory discrimination

171
Q

function of occipital lobe

A

sight (visual cortex)

visual reception and visual interpretation

172
Q

what does a focal onset seizure mean

A

that is starts in one part of the brain and remains there

173
Q

what does a generalised onset seizure mean

A

starts diffusely throughout the whole brain

174
Q

what does focal to bilateral tonic clonic mean

A

starts in one part of the brain then spreads throughout

175
Q

types of generalised seizures

A 
tonic - clonic
tonic
clonic
absence
myoclonic
176
Q

does focal seizures happen with awareness or without

A

can happen either

177
Q

peak incidence of epilepsy

A

childhood (congenital)

elderly - secondary to cerebrovascular and degenerative disease

178
Q

temporal lobe epilepsy causes what types of aura

A

deja vu
abnormal smells
feeling of epigastric rising

179
Q

occipital lobe epilepsy causes what types of aura

A

hallucinations

180
Q

post-ictal phase of epilepsy (typically tonic-clonic)

A 
sleepiness
drowsiness
confusion
tiredness
usually improves in 10 mins to several hours
181
Q

“warning” difference between seizure and syncope

A

seizure: 50% have an aura
syncope: feel faint, lightheaded, blurred/tunnel vision

182
Q

onset difference between seizure and syncope

A

seizure: sudden, any position
syncope: only occurs sitting or standing, avoidable by change in posture

183
Q

feature difference between seizure and syncope

A

seizure: eyes open, rigidity, falls backwards, convulses
syncope: eyes closed, limp, falls forward, minor twitching only (if unable to fall flat)

184
Q

childhood absence epilepsy

A

“day-dreaming”
age 3-12, F>M
remits in teens
treatment: ethosuximide

185
Q

juvenile myoclonic epilepsy

A

early morning myoclonic jerks and tonic clonic seizures
age 10-20 years , lifelong
sodium valproate
may worsen on phenytoin, carbamezapine

186
Q

immediate management of a seizure

A

airway, breathing, circulation
blood glucose immediately
terminate seizure unless resolves by self (IV lorezepam, PR diazepam, buccal midalozam)

187
Q

which neuroimaging is preferred with seizures

A

MRI

188
Q

driving guidance if someone has had one seizure

A

license revoked for a year

6 months if EEG and MRI are normal

189
Q

driving guidance if someone has recurrent seizures

A

license revoked until 1 year seizure free

190
Q

what do anti epileptics act on (AEDs)

A

act on neurone to reduces excitability and raise seizure threshold

  • most reduce sodium channel excitability
  • others prevent synaptic vesicle release or enhance GABA signalling
191
Q

common side effects of anti epileptics (AEDs)

A

act on whole brain
tiredness, mental slowing, mood disturbance
teratogenicity (defects in developing foetus)

192
Q

when would you start anti epileptics (AEDs)

A

2 or more unprovoked seizures or strong likelihood of further seizure

  • brain lesion (acute or chronic)
  • EEG abnormalities
193
Q

choice of AEDs for focal epilepsy

A

carbamezapine
phenytoin
lacosamide

194
Q

choice of AEDs for focal or generalised epilepsy

A

lamotrigine
valproate
topiramate
clobazam

195
Q

choice of AEDs for generalised epilepsy

A

ethosuximide (absences)
clonazepam ( myoclonus)
piracetam (myoclonus)

196
Q

what is diplopia

A

double vision

197
Q

what AEDs can cause a rash

A

carbamezapine
lamotrigine
phenytoin

198
Q

what does SUDEP stand for

A

sudden death in epilepsy

199
Q

what causes sudden death in epilepsy

A

mainly respiratory arrest

200
Q

treatment of status epilepticus

A

immediate IV lorazepam 4mg and repeat 4mg after 10 mins if necessary

201
Q

contraception on anti epileptics

A

combined oral contraceptive on non-enzyme inducing AEDs

POP not recommend

202
Q

safest AEDs for pregnancy

A

lamotrigine
levetricateam
carbamezepan

203
Q

when to consider epilepsy surgery

A

only for focal epilepsy
disabling seizures
recurrent for 2-3 years

204
Q

other treatments for epilepsy

A

vagal nerve stimulator
ketogenic diet (poorly tolerated in adults)
deep brain stimulator
cannabis

205
Q

Jacksonian march

A

A Jacksonian seizure is a type of focal partial seizure, also known as a simple partial seizure. This means the seizure is caused by unusual electrical activity that affects only a small area of the brain. The person maintains awareness during the seizure. Jacksonian seizures are also known as a Jacksonian march.

206
Q

metabolic causes of collapse

A 
hyper/hyponatreamia 
hyper/hypoglycaemia
adrenal insufficiency 
hypo/hypethermia
thyroid dysfunction
207
Q

foreign substances causes of collapse

A

alcohol

drugs - medications and recreational drugs

208
Q

CNS causes of collapse

A

infections
haemorrhage
trauma

209
Q

organ failure causes of collapse

A

respiratory
liver
renal

210
Q

what is it called if you have adrenal insufficiency

A

addisions disease

211
Q

what does the zona glomerulosa produce and what does it do

A 
produce mineralocorticoids (aldosterone)
It's a hormone that plays a big role in keeping your blood pressure in check. Aldosterone balances the levels of sodium and potassium in your body. It signals to your organs, like your colon and kidneys, to put more sodium into your bloodstream or release more potassium into your pee
212
Q

what does the zona fasciculate produce

A

glucocorticoids

213
Q

what do glucocorticoids do

A

increase protein catabolism, hepatic glycogen synthesis , hepatic gluconeogenesis
inhibit ACTH secretion
involved in blood pressure

214
Q

what happens to the U&E during an addisonian crisis

a. Na and K increase
b. Na and K decrease
c. Na increased, K decreased
d. Na decreased, K increased

A

d. Na decreased, K Increased

215
Q

clinical features of Addisons disease

A

aldosterone: Na loss, impaired H and K secretion
hypoglycaemia
postural hypotension: loss of enhanced catecholamine fucntion
loss of appetite stimulation
increased ACTH : hyperpigmentation
decreased adrenal androgens: loss of pubic and axillary hair (women)

216
Q

features of adrenal crisis (addisonian crisis)

A 
dehydration
hypotension
hypoglycaemia
hyponatreamia / hyperkalaemia
may lead to collapse and death
217
Q

testing for adrenal insufficiency

A

plasma cortisol
9am - <100 nmol/L then likely adrenal insufficiency
>500nmol/L then unlikely adrenal insufficiency

218
Q

management of addisonian crisis

A

needs management by endocrinoloigst

replace mineralocorticoids, glucocorticoida

219
Q

in dilution hyponatreamia what is the problem

A

problem with ADH secretion or renal handling of water

220
Q

what does SIADH stand for and what causes it

A 
syndrome of inappropriate ADH secretion
ectopic secretion ofADH - bronchial carcinomas
inappropriate secretion:
-pneumonia
-TB
-PPV
-Head injury
-cerebral tumour
221
Q

management of SIADH

A

fluid restriction

if severe give hypertonic solution (3% saline)

222
Q

what is meant by neurally mediated syncope

A

simple (vasovagal syncope) COMMONENEST

situational syncope: micturition, cough, defecation, pain, swallowing

223
Q

what id meant by cardiac syncope

A

arrhythmias - fast or slow

structural heart disease - LV outflow obstruction (aortic stenosis)

224
Q

red flags of syncope

A 
older age
male sex
abnormal ECG
history of heart problems
abnormal troponin
225
Q

first fit clinic guidelines to refer after seizure

A

above 16
new onset of seizures or blackouts
patient has made full recovery from event
bloods exclude metabolic derangement or infection
imaging excludes space occupying lesion
ECG normal

226
Q

examples of regression to the mean

A

blood pressure
examination performance

In statistics, regression toward the mean is a concept that refers to the fact that if one sample of a random variable is extreme, the next sampling of the same random variable is likely to be closer to its mean.

227
Q

what is meant by term repeatability

A

is how similar to results on the same subjects under the same conditions
e.g. blood sample from X split into two tubes run through the same machine at the same time (test re-test)

228
Q

define reproducibility

A

how similar results are under real world variation

e.g. different observers, machines, etc.

229
Q

define reliability (statistical sense)

A

refers to the magnitude of the measurement error in relation to the variability of the measure in the population

if reliability is high, measurement errors are small in comparison to the true difference between the subjects

230
Q

rank in order the reliability of the following statements:

a. fat consumption as measured in a food frequency questionnaire
b. weight in Kg on an electronic scale
c. random serum cholesterol from the blood
d. central adiposity as measured by weight circumference using a tape measure
e. body fat measured using a CT scan

A

b. weight in Kg on an electronic scale
c. random serum cholesterol from the blood
e. body fat measured using a CT scan
d. central adiposity as measured by weight circumference using a tape measure
a. fat consumption as measured in a food frequency questionnaire

231
Q

what is meant by Korotkoff sounds

A

five sounds which are heard as the pressure in the cuff is released during the measurement of arterial pressure

232
Q

5 Korotkoff sounds

A 
I. Sharp thud (systolic)
II. Loud blowing sound
III. Soft thud
IV. Soft blowing sound
V. Silence (diastolic)
233
Q

when do you use the intra-class correlation coefficient

A

for continuous measurements such as blood pressure, serum cholesterol etc.

234
Q

when do you use the Kappa coefficient (or weighted Kappa)

A

for binary or ordinal categorical variables

235
Q

non-differential misclassification

A

random error

this will attenuate any true association

236
Q

differential misclassification

A

systematic error

this may make an association weaker or stronger depending on the direction of the error

237
Q

what does the Mental capacity act 2005 do

A

governs non-/treatment of adults who lack capacity

238
Q

core principles of the Mental Capacity Act 2005

A
  • presume capacity (over 16) unless contrary is established
  • provide support to enable P to decide if possible
  • make decisions in best interest of incapacitated P
  • respect an unwise decision if P has capacity
  • take the least restrictive option
239
Q

a clinician lead best interests decision is required when

A

1) patient lacks capacity
2) P has not made a valid and applicable advance decision to refuse treatment
3) P has not appointed a health and welfare attorney

240
Q

when determining best interests you should…

A
  • consider whether it is an emergenyc
  • consider whether P may regain capacity
  • consider if it is P’s best interest in the widest sense
  • avoid discrimination
  • encourage P participation
  • not be motivated by a desire to end P’s life
  • find out P’s views
  • consult others
241
Q

who decides best interest

A

health and welfare attorney
courts
doctors

242
Q

who should be consulted when deciding a patients best interest

A 
patient
court appointed deputy
anyone named by patient
those caring for P
independent mental capacity act advocate
243
Q

Tom has been diagnosed in a permanent vegetative state. Tom has no advance decision to refuse treatment and had appointed no health and welfare attorney to make decisions on his behalf. His family and the treating team believe that life sustaining treatment should now be withdrawn. On what legal basis should such a decision be made?

a. any evidence as to Tom’s previous wishes
b. the decision of a court
c. the views of the treating team
d. the wishes of toms family
e. toms best interest

A

e. toms best interest

CBL Year 2 (14 decks)

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