Collapse Flashcards
define coma
state of unrousable unresponsiveness in which there is no coordinated response to external stimuli or internal need
GCS
glasma coma scale eye movement (E)=1-4 verbal response (V) = 1-5 motor response (M) =1-6
GCS to classify as a coma
3-8
eye movement in GCS
spontaneously = 4
to speech = 3
to pain = 2
none = 1
verbal response in GCS
orientated = 5 confused = 4 inappropriate = 3 incomprehensible = 2 none = 1
motor response in GCS
obeys commands = 6 localises to pain = 5 withdraws from pain = 4 flexion to pain = 3 (decorticate) extension to pain = 2 (decerebrate) none = 1
define collapse / blackout
transient loss of memory or consciousness with complete recovery
three (branches) most common causes of collapse
syncope
neurological
psychogenic
define syncope
transient brain hypoxia resulting in loss of consciousness or a near loss of consciousness (presyncope)
define seizure
episode of uncontrolled electrical activity of the brain
define psychogenic
psychological, no physical/organic cause
5 main branches of syncope (things that cause it)
arrhythmia structural disorder of the heart baroreceptor reflex related posture related (orthostatic) others
arrhythmia causes of syncope
bradycardia or tachycardia
always attach to 12 lead ECG
structural disorders of the heart causes of syncope
aortic stenosis
pericardial effusion
hypertrophic cardiomyopathy
found through cvs exam and echocardiogram
baroreceptor reflex related causes of syncope
vasovagal
carotid sinus hypersensitivity (rare before 40)
cough or micturition syncope (older men usually during or after urination)
posture related (orthostatic) causes of syncope
orthostatic hypertension
autonomic failure (loss of normal innervation of heart and arterioles)
drug induced
volume depletion
postural orthostatic tachycardia syndrome (POTS)
“other” causes of syncope
anaemia
aortic dissection
hypoglycaemia
PE
what is postural orthostatic tachycardia syndrome (POTS)
occurs in young women
rapid rise in heart rate on standing >130 bpm is diagnostic
start symptoms of vasovagal syncope
feeling hot and lightheaded nausea vomiting tunnel vision voices seem distant face looks very pale
during symptoms of vasovagal syncope
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)
vasovagal syncope symptoms after
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)
what is Wolff Parkinson white syndrome
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)
wolff Parkinson white on an ECG
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.
3 neurological causes of syncope
seizure
narcolepsy
vertebrobasilar insufficiency
what is Psychogenic pseudosyncope (PPS)
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
What is non-epileptic attack disorder (NEAD)
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.
AVPU
alert - patient is awake and responsive
voice - patient responds to voice
pain - patient responds to pain
unconscious
when can action potentials occur
only occur when opposite charges exist either side of a membrane
depolarisation is done through which channel
voltage gated sodium channels
examples of drugs that bind the Na channel (stop depolarisation of action potentials)
local anaesthetics - lidocaine, bupivacaine
antiarrhythmitics - lidocaine
anticonvulsants - carbamazepine
antidepressants - amitriptyline
describe repolarisation
inactivation of the sodium channels
activation of the K channels
(k moves out making inside less positive and membrane repolarises)
what is glutamate
main CNS excitatory transmitter
what is GABA
main CNS inhibitory transmitter
amino acid transmitters
glutamate and glycine (abundant in all cells)
GABA (synthesised in the cytoplasm of neurones)
monoamine transmitters
acetylcholine, 5-HT, histamine
catecholamine transmitters
noradrenaline, dopamine, adrenaline
peptide transmitter
substance P
Ionotropic receptor
transmitter (ligand gated) receptor eg. NMDA subtype of glutamate receptor nicotinic Ach (NMJ, CNS)
what is NMDA - what are some drug examples that act here
is a glutamate receptor and ion channel found in neurons
ketamine (anaesthesia, depression)
memantine (Alzheimers)
GABA (a) receptors (inotropic) are site of action for which drugs
benzodiazepines
barbituates
anaesthetic steroids
volatile anaesthetics
loss of ACh cells in Alzheimers disease treated with
treatment by cholinesterase inhibitor (rivastigmine, donezepil)
ACh and diseases of neuromuscular junction
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.
toxins that affect NMJ
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
what does cocaine do to noradrenaline
blocks reuptake of noradrenaline
what does Methylphenidate/ritalin do/treat
blocks reuptake of noradrenaline
treats ADHD and narcolepsy
myelin producers
oligodendrocytes (CNS) Schwann cells (PNS)
astrocytes
largest glial cell, star shaped
contribute to homeostasis in the neutrophil by metabolising neurotransmitters from the extracellular space
microglia
small and mobile
activated during injury or disease to remove debris
ependymal cells
type of glial cell
line the ventricles
specialised ones produce CSF in the choroid plexus
3 myelin associated pathologies
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))
EEG
electro encephalogram
- simple non invasive technique
- electrodes attached to head in defined positions
- voltage changes between pairs of electrodes are measured
electrode placement for EEG (the international 10-20 system_
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
what does EEG mostly measure
the excitation of dendrites of pyramidal neurones (within medulla oblongata)
clinical use of EEG
detection of epileptic activity
detection of sleep disorders
brain dysfunction associated with head trauma, brain death, states of altered consciousness
research tool
briefly describe REM phase of sleep
(rapid eye movement) 5-30 min long every 90 mins cerebral cortex is very active dreaming muscular relaxation
EEG is a crude indicator of what
the activity of the cerebral cortex
synchronised EEG during sleep
large amplitude
slow waves
found during drowsiness and slow wave sleep (SWS)
desynchronised EEG during sleep
small amplitude fast waves, found during alert wakefulness and REM sleep
what is insomnia
difficulty falling or staying asleep
what is hypersomnia
excessive amounts of sleepiness
what is narcolepsy
excessive sleepiness and frequent day time sleep attacks
what is sleep apnoea disorder
abnormal pauses in breathing or instances of abnormally low breathing during sleep
what is somnambulism
sleepwalking
what is nocturnal enuresis
bed wetting
what is reticular formation
set of interconnected nuclei located throughout the brain stem
functions of local projections of reticular formation
chewing, swallowing and vomiting
respiratory activities (coughing, sneezing)
CVS responses
long projection systems ascending to the cortex functions
responsible for sleep wake cycle
mediates various levels of alertness and consciousness
long projection systems descending to the spinal cord functions
involved in posture and equilibrium as well as ANS activity
involved in sensory pain and motor modulation
receives information from the hypothalamus
what controls levels of consciousness
reticular formation
what controls the content of consciousness
cerebral cortex
what is brain death equal to
reticular formation death - check cranial nerve reflexes and independent respiration
what is epilepsy
- 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
define seizure
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
define epileptogensis
sequence of events that converts a normal neuronal network into a hyperexcitbale circuit which trigger spontaneous seizures
define status epilepticus (SE)
neurological and medical emergency characterised by 5 or more minutes of either continuous seizure activity or repetitive seizures with no recovery of consciousness
3 main groups of seizure
unknown
focal seizures
generalised seizures
describe what is meany by an unknown seizure
insufficient evidence to characterise focal, generalised or both
usually epileptic spasms or other
focal seizure description
- originating within network
- limited to one hemisphere
- characterised according to 1 or more features: aura, motor, autonomic
generalised seizure
arising within and rapidly engaging bilateral distributed networks
what is an absence
seizure
someone stares blankly
what is a myoclonic seizure
short jerking movements of parts of the body
what is a Tonic - clonic seizure
convulsion, goes stiff, bites tongue, incontinence
tonic seizure
goes stiff and falls without convulsion
what is atonic seizure
falling limply to the ground
causes of epilepsy
- 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
suprachiasmatic nuclei
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.
locus coeruleus
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.
definition of shock
acute failure of the CVS to supply sufficient blood to tissues to meet their metabolic demand and maintain life
what is heart rate determined by
sympathetic (beta 1 adrenoreceptors) and parasympathetic innervation ( muscarinic receptors)
what is stroke volume determined by
contractility
preload
afterload
what is arteriolar tone controlled by
circulating hormones (vasopressin, adrenaline, angiotensin II and the sympathetic nervous system)
what is hypovolaemic shock due to
what causes it
due to decrease in blood/plasma volume
examples: internal haemorrhage, external haemorrhage, severe burns, Addisons disease, severe dehydration, intestinal obstruction
what is cardiogenic shock
what causes it
a sudden severe reduction in cardiac contractility
examples: MI, arrhythmias, valvular regurgitation
essentially its pump failure
what is obstructive shock
what causes it
due to mechanical obstruction or impaired cardiac filling
examples: PE, cardiac tamponade
essentially blocked pump or too much external pressure
what is distributive shock
what causes it
vascular capacity increases so that even the normal volume of blood can’t fill it
examples: anaphylaxis, sepsis, spinal injury
too much vascular capacity
Hypovolaemic shock what is increased/decreased
blood/plasma volume, JVP, CO, MAP, TPR
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)
cardiogenic shock increase/decrease (CVP, Cardiac output, MAP,TPR)
increase in central venous pressure
decrease in cardiac output
decrease in MAP
increase in TPR(compensatory response mediated by the baroreceptor reflex))
obstructive shock increase/decrease (CVP, CO, MAP, TPR)
increase in central venous pressure
decrease in CO
decrease in MAP
increase in TPR(compensatory response mediated by the baroreceptor reflex)
distributive shock increase/decrease (CVP, CO, MAP, TPR)
decrease in all
symptoms of hypovolaemic shock
anxiety confusion muscle weakness collapse and/or thirst
signs of hypovolaemic shock
pale/cold skin increased cap refill time rapid/weak pulse tachypnoea oliguria
why do a venous blood gas (VBG) in a patent with suspected hypovolaemic shock
to determine severity, predict mortality, and response to treatment
does 0-10% blood loss produce shock
no
does 20-30% blood loss produce shock
compensated shock
what does >30% blood loss produce
decompensated (progressive) shock
compensatory mechanisms for hypovolaemic shock
baroreceptor reflex (increase in TPR) RAAS(withhold ACE inhibitors)
positive feedback cycle for hypovolaemic shock
shock causes tissue hypoxia
which causes tissue and organ dysfunction \
which causes release of inflammatory mediators
which causes shock
decompensated shock
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_
cellular consequences of hypovolaemic shock
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
universal blood donor
O negative
why is lactate high in shock
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
what is the fluid challenge
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.
use of inotropes and vasopressors in the management of hypovolaemic shock
to create vasoconstriction and increase cardiac contractility
relevance of a per rectal examination in a patient who has presented with hypovolaemic shock
could be internally bleeding
meleana
define stroke
an acute focal injury of the CNS due to a vascular cause, including cerebral infarction and intracerebral haemorrhage
TIA
transient ischaemic attack
ischaemia with symptoms <24hrs
or
without MRI changes of infarction
two types of stroke
ischaemic stroke (85%) haemorrhage stroke (15%)
pathophysiology of ischaemic stroke
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
stroke syndromes
total anterior circulation syndrome (TACS)
partial anterior circulation syndrom (PACS)
lacunar syndrome (LACS)
posterior circulation syndrome (POCS)
causes of ischaemic stroke
large artery atherosclerosis small artery occlusion cardio-embolism arterial dissection other less common causes (anti-phospholipid syndrome, vasculitis)
conventional risk factors for small artery occlusion and inherited causes
conventional causes: hypertension, diabetes, smoking, hypercholesteramia
inherited causes: collagen type IV mutations, CADASIL
cardio-embolic stroke causes
AF
MI
patent foramen ovale
vertebral dissection causes
neck manipulation (e.g. chiropractor) martial arts
pathophysiology of haemorrhagic stroke
cell death by necrosis fragile blood vessels by: -hypertension -cerebral amyloid angiopathy -arterio-venous malformation (AVM)
what does the stroke unit care do
avoid/manage complications
start rehabilitation
identify cause of stroke
initiate secondary prevention
ischaemic stroke treatment
reperfusion maintenance of blood flow: -hydration -avoidance of very early mobilisation surgery for raised ICP
haemorrhagic stroke treatment
blood pressure control
reversal of anticoagulants
surgery for raised ICP
what is a hyper acute stroke patient
Patients presenting within 6 hours of stroke onset constitute a category of stroke patient known as the “hyperacute stroke patient.”
immediate hyper acute stroke management
Iv thrombolysis mechanical thrombectomy soon enough after symptom onset severe enough to warrant risks of treatment safe enough to justify treatment
what is a thrombectomy
Surgical thrombectomy is a type of surgery to remove a blood clot from inside an artery or vein
secondary prevention from strokes
anti-thrombotic:
- anti platelets (aspirin +/- clopidogrel)
- anticoagulants (especially any history of AF or flutter)
blood pressure control
lipid lowering
carotid endarterectomy
when considering if collapse is due to bradycardia what do you look at on an ECG
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
what are Stoke Adam Attacks
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.
heart blocks
1st degree - long PR interval
2nd degree - Mobitz type 1 (wenkeback) and mobtiz type 2
3rd degree - complete heart block (AV dissociation)
narrow complex tachycardia
SVT
supra ventricular tachycardia
types of SVT
atrial flutter atrial fibrillation atrial tachycardia (ectopic driven) AV re-enterant tachycardia AV nodal re-enterant tachycardia
AF on an ECG
No P waves and an irregular QRS
Atrial flutter on an ECG
no normal p waves
Saw tooth pattern
AVRT (AV re-enterant tachycardia) on an ECG
accessory pathway (delta wave - slurred upstroke of QRS) short PR interval
when considering if collapse is due to tachyarrhythmia what do you look at on an ECG
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?
two types of LV outflow obstruction
severe aortic stenosis
hypertrophic (obstructive) cardiomyopathy
when to suspect LV outflow obstruction is cause of collapse (but is cardiac cause)
no electrical issue on ECG
examination reveals a murmur
congenital types of long QT syndrome
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
acquired causes of long QT syndrome
drugs: anti-arrhytmic drugs non-sedating anti-histamines some antimicrobials gastric motility drugs
what is torsades de pointes
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.
how to identify torsades de pointes on an ECG
It is characterized by rapid, irregular QRS complexes, which appear to be twisting around the electrocardiogram (ECG) baseline.
causes of torsades de pointes
drug-induced QT prolongation and less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome.
how does aortic stenosis cause collapse
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.
mortality risk for ruptured AAA
65%
3 treatment options for ruptured AAA
open repair
end-vascular repair (EVAR)
conservative management/palliative
open repair for ruptured AAA things to consider
major operation
significant blood loss
ICU
10% mortality
endo-vascular repair for a ruptured AAA things to consider
shorter length of stay
mortality 2%
anatomy may not always be amendable
what is the Hardmen Index
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
anatomy of AAA
thin tunica intima lined by epithelium
thick tunica media : elastin and collagen and smooth muscle
tunica adventitia: collagen, vasa vasorum, and lymphatic s
pathophysiology of AAA
- 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
is intraperitoneal or retroperitoneal more salvageable in a ruptured AAA
retroperitoneal is more salvageable
intraperitoneal has a higher mortality rate
obvious clinical presentation of someone with a ruptured AAA
sudden tearing abdominal/back pain
collapse
clammy/sweaty
shock
not obvious clinical presentation of a ruptured AAA
constipation
haematuria
haematemesis
nausea and vomiting
risk factors for AAA
male sex hypertension smoking diabetes hypercholesteramia FH rarer: collagen disorders (Marfan syndrome and Ehlers danlos)
type A thoracic aortic aneurysm
ascending aorta - needs surgery
type B thoracic aortic aneurysm
descending aorta - medical management
coronary vessel occlusion
STEMI
common carotid occlusion
any type of stroke
subclavian occlusion
acutely ischaemic upper limb
coeliac/mesenteric occlusion
ischaemic bowel
renal vessel occlusion
frank haematuria
spinal artery occlusion
sudden onset painless paraplegia
function of frontal lobe
motor control - premotor cortex
problem solving - prefrontal area
speech production - broca area
function of temporal lobe
auditory process
language comprehension - wernickes area
memory/information retrieval
function of parietal lobe
touch perception - somatosensory cortex
body orientation and sensory discrimination
function of occipital lobe
sight (visual cortex)
visual reception and visual interpretation
what does a focal onset seizure mean
that is starts in one part of the brain and remains there
what does a generalised onset seizure mean
starts diffusely throughout the whole brain
what does focal to bilateral tonic clonic mean
starts in one part of the brain then spreads throughout
types of generalised seizures
tonic - clonic tonic clonic absence myoclonic
does focal seizures happen with awareness or without
can happen either
peak incidence of epilepsy
childhood (congenital)
elderly - secondary to cerebrovascular and degenerative disease
temporal lobe epilepsy causes what types of aura
deja vu
abnormal smells
feeling of epigastric rising
occipital lobe epilepsy causes what types of aura
hallucinations
post-ictal phase of epilepsy (typically tonic-clonic)
sleepiness drowsiness confusion tiredness usually improves in 10 mins to several hours
“warning” difference between seizure and syncope
seizure: 50% have an aura
syncope: feel faint, lightheaded, blurred/tunnel vision
onset difference between seizure and syncope
seizure: sudden, any position
syncope: only occurs sitting or standing, avoidable by change in posture
feature difference between seizure and syncope
seizure: eyes open, rigidity, falls backwards, convulses
syncope: eyes closed, limp, falls forward, minor twitching only (if unable to fall flat)
childhood absence epilepsy
“day-dreaming”
age 3-12, F>M
remits in teens
treatment: ethosuximide
juvenile myoclonic epilepsy
early morning myoclonic jerks and tonic clonic seizures
age 10-20 years , lifelong
sodium valproate
may worsen on phenytoin, carbamezapine
immediate management of a seizure
airway, breathing, circulation
blood glucose immediately
terminate seizure unless resolves by self (IV lorezepam, PR diazepam, buccal midalozam)
which neuroimaging is preferred with seizures
MRI
driving guidance if someone has had one seizure
license revoked for a year
6 months if EEG and MRI are normal
driving guidance if someone has recurrent seizures
license revoked until 1 year seizure free
what do anti epileptics act on (AEDs)
act on neurone to reduces excitability and raise seizure threshold
- most reduce sodium channel excitability
- others prevent synaptic vesicle release or enhance GABA signalling
common side effects of anti epileptics (AEDs)
act on whole brain
tiredness, mental slowing, mood disturbance
teratogenicity (defects in developing foetus)
when would you start anti epileptics (AEDs)
2 or more unprovoked seizures or strong likelihood of further seizure
- brain lesion (acute or chronic)
- EEG abnormalities
choice of AEDs for focal epilepsy
carbamezapine
phenytoin
lacosamide
choice of AEDs for focal or generalised epilepsy
lamotrigine
valproate
topiramate
clobazam
choice of AEDs for generalised epilepsy
ethosuximide (absences)
clonazepam ( myoclonus)
piracetam (myoclonus)
what is diplopia
double vision
what AEDs can cause a rash
carbamezapine
lamotrigine
phenytoin
what does SUDEP stand for
sudden death in epilepsy
what causes sudden death in epilepsy
mainly respiratory arrest
treatment of status epilepticus
immediate IV lorazepam 4mg and repeat 4mg after 10 mins if necessary
contraception on anti epileptics
combined oral contraceptive on non-enzyme inducing AEDs
POP not recommend
safest AEDs for pregnancy
lamotrigine
levetricateam
carbamezepan
when to consider epilepsy surgery
only for focal epilepsy
disabling seizures
recurrent for 2-3 years
other treatments for epilepsy
vagal nerve stimulator
ketogenic diet (poorly tolerated in adults)
deep brain stimulator
cannabis
Jacksonian march
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.
metabolic causes of collapse
hyper/hyponatreamia hyper/hypoglycaemia adrenal insufficiency hypo/hypethermia thyroid dysfunction
foreign substances causes of collapse
alcohol
drugs - medications and recreational drugs
CNS causes of collapse
infections
haemorrhage
trauma
organ failure causes of collapse
respiratory
liver
renal
what is it called if you have adrenal insufficiency
addisions disease
what does the zona glomerulosa produce and what does it do
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
what does the zona fasciculate produce
glucocorticoids
what do glucocorticoids do
increase protein catabolism, hepatic glycogen synthesis , hepatic gluconeogenesis
inhibit ACTH secretion
involved in blood pressure
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
d. Na decreased, K Increased
clinical features of Addisons disease
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)
features of adrenal crisis (addisonian crisis)
dehydration hypotension hypoglycaemia hyponatreamia / hyperkalaemia may lead to collapse and death
testing for adrenal insufficiency
plasma cortisol
9am - <100 nmol/L then likely adrenal insufficiency
>500nmol/L then unlikely adrenal insufficiency
management of addisonian crisis
needs management by endocrinoloigst
replace mineralocorticoids, glucocorticoida
in dilution hyponatreamia what is the problem
problem with ADH secretion or renal handling of water
what does SIADH stand for and what causes it
syndrome of inappropriate ADH secretion ectopic secretion ofADH - bronchial carcinomas inappropriate secretion: -pneumonia -TB -PPV -Head injury -cerebral tumour
management of SIADH
fluid restriction
if severe give hypertonic solution (3% saline)
what is meant by neurally mediated syncope
simple (vasovagal syncope) COMMONENEST
situational syncope: micturition, cough, defecation, pain, swallowing
what id meant by cardiac syncope
arrhythmias - fast or slow
structural heart disease - LV outflow obstruction (aortic stenosis)
red flags of syncope
older age male sex abnormal ECG history of heart problems abnormal troponin
first fit clinic guidelines to refer after seizure
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
examples of regression to the mean
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.
what is meant by term repeatability
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)
define reproducibility
how similar results are under real world variation
e.g. different observers, machines, etc.
define reliability (statistical sense)
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
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
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
what is meant by Korotkoff sounds
five sounds which are heard as the pressure in the cuff is released during the measurement of arterial pressure
5 Korotkoff sounds
I. Sharp thud (systolic) II. Loud blowing sound III. Soft thud IV. Soft blowing sound V. Silence (diastolic)
when do you use the intra-class correlation coefficient
for continuous measurements such as blood pressure, serum cholesterol etc.
when do you use the Kappa coefficient (or weighted Kappa)
for binary or ordinal categorical variables
non-differential misclassification
random error
this will attenuate any true association
differential misclassification
systematic error
this may make an association weaker or stronger depending on the direction of the error
what does the Mental capacity act 2005 do
governs non-/treatment of adults who lack capacity
core principles of the Mental Capacity Act 2005
- 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
a clinician lead best interests decision is required when
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
when determining best interests you should…
- 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
who decides best interest
health and welfare attorney
courts
doctors
who should be consulted when deciding a patients best interest
patient court appointed deputy anyone named by patient those caring for P independent mental capacity act advocate
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
e. toms best interest
