Vivas Flashcards
Describe hyperalgesia and allodynia and the role they are thought to play in normal nociceptive signalling (p. 252)
Hyperalgesia : is the increase in pain perception which may be caused by a range of effects within the pain pathways and descending pathways but most commonly caused by the inflammatory medicators at the site of injury making the membrane potential closer to the threshold potential. An example of this is post surgery what would normally be considered mild pain to the patient is now considered severe pain due to these imbalances.
Allodynia : this is when something that should not cause pain causes, causes pain. This is due to any abnormalities within the pain pathway and processing but is commonly caused due to central sensitization which is a change to your central nervous system that increases you sensitivity to pain. An example of this is when you touch your arm it should hurt but it really does hurt.
Changing the sensitivity of the neurons through changes in the peripheries, spinal cord and brain restricting the use if the injured limb in order to facilitate healing and prevent re-injury. As the wound heals the mechanisms that led to the injury hyperalgesia and allodynia should be reversed restoring the high-threshold character of the nociceptive neurons. The inability to reverse this process is considered to become neuropathic pain.
Alzheimer’s disease
It is an progressive type of dementia that causes due to its mechanism and onset location memory loss
Alzheimer’s disease can be either sporadic or familial.
Sporadic Alzheimer’s disease can affect adults at any age, but usually occurs after age 65 and is the
most common form of Alzheimer’s disease.
Causes :
• Brain atrophy
• ventricular enlargement
• shrinkage of hippocampus hence we see the symptoms of memory loss as the hippocampus controls this
What are Neurofibrillary tangles :
Mutation of towel gene hence causing them to remodelling and clump together and no structure of microtubules means that the signals cannot get through hence the neurons are not being used then they die and this causes brain atrophy and decrease nerve signalling causes the dementia effects.
Dementia (p. 183)
And what are the 4 main types
Is an umbrella term that describes a collection of symptoms that are caused by disorders affecting the brain. Dementia affects thinking, behaviour and the ability to perform everyday tasks. Brain function is affected enough to interfere with the person’s normal social or working life.
• Alzheimer’s disease
• Vascular dementia
• Lewy body disease
• Frontotemporal dementia
Parkinson’s disease (p. 179)
decreased levels of dopamine being released from the basal ganglia due to it being attacked. This causes muscle tremors as dopamine is the main NT for muscle movement hence when there is no available dopamine then the muscles spasm on their own. The treatment can slow the progression but will not cure
Acute delirium :
an acute change in mental status where the patient is not in touch with reality, has a sudden onset and can be reversed / treated hence how it differs from dementia as this is a progressive onset over years and has no cure.
Acute behavioural disturbance in elderly :
can be caused by infectious agents ranging from minor skin infections to sepsis. This alters their cognition and normal levels, may make them agitate and aggressive but it is due to the underlying medical problems.
Tricyclic antidepressants (lecture/tutorial)
inhibit the reuptake of norepinephrine and serotonin by blocking the transporters responsible for their reabsorption into presynaptic neurons. This results in increased concentrations of these neurotransmitters in the synaptic cleft, enhancing their availability to bind to postsynaptic receptors. Leading to enhanced signalling
Antipsychotics (lecture/tutorial)
Antipsychotics are anti-dopamine
• Decrease the production of dopamine and its ability to be used
• Droperidol :
Benzodiazepines (lecture/tutorial)
benzodiazepines enhance the inhibitory effects of GABA, leading to reduced neuronal excitability.
they increase the frequency of opening of the chloride channel in response to GABA
hyperpolarization and inhibition of neuronal firing
Anticholinergic
is your pharmaceutical overdoses where there is not enough ACh within the synapse / body. This is because the anticholinergic medications bind to the muscarinic receptors no the post synaptic membrane and inhibit ACh form binding. This sends a compensatory response to the body and decreases its ACh synthesis and release therefore reducing ACh.
This also decreases vagal tone therefore patients are at a higher risk of arrhythmias and hyperthermia.
These patients present with hot, dry, flushed skin, and urinary retention.
Activated charcoal for treatment as it has a larger surface area to absorb all the medications.
Cholinergic
Cholinergic is your organophosphate poisoning and therefore there is too much ACh within the synaptic cleft as the AChE (the enzyme the breaks down ACh) is inhibited and therefore ACh cannot be reuptaken into the synapse. The management for these patients would be removing the stimulant or problem and then supporting their ABC’s with special mention for the airway as this can be occluded and therefore leading to aspirations. Also administering atropine in the cases of bradycardia and adenosine in the cases of tachycardia – SLUDGE BBB
Guillain-Barre syndrome (p. 165)
A peripheral nerve disorder by which the immune system wants to fight the body resulting in ascending paralysis beginning at the toes them reaching the brain.
Typically proceeded by an infection with triggers an autoimmune response
Any ages and any gender
Motor neuron disease (p. 191)
Where the immune system attacks the neurons within the brain can be either upper or lower motor neurons or both.
First manifests as:
- Muscle weakness, can vary from person-to-person which areas are week depending on the neurons
- Progressive to point of fatal paralysis
- Average age: 45-60 years
- Prognosis: 1-5 years ( depends on the level of severity )
Unknown causes
Multiple sclerosis (p. 189)
Is a neuromuscular disorder that attacks the glial cells (Schwann cells and oligodendrocytes) / myelin sheaths and therefore disruption in this pathway disrupts the action potential and therefore muscles.
T cells activate macrophages and b cells to attack the myelin sheaths therefore inducing sclerosis of the myelin sheaths and slowing down the propagation of the signal
Optic nerve degeneration hence you can get vertigo and involuntary eye movement and issues with vision as it is a vulnerable nerve because of its size.
Cerebral palsy (p. 167)
– muscle movement, tone and posture
Is a neuromuscular condition that describes a group of permanent disorders of the development of movement and posture causing activity limitations that are attributed to non-progressive disturbances that occur in the developing foetus or infants brain. Due to brain injury and sometimes cerebral hypoxia
The clinical manifestations can present differently as there are variety of different severities due
- Intellectual disability
- Unable to walk
- Unable to talk
- Sleep disturbances
- Speech disturbances
- Salivation issues
- Epilepsy
- Behavioural disorders
Outline the current prehospital research on the management of the traumatic brain injured patient – at the paramedic level (lecture/tutorial)
Diagnosis :
- GCS less than 8
- major changes to systolic BP
- lost ability to cerebral autoregulate - Need to be aware of autoregulation not working hence give fluids to maintain MAP of 90 or a systolic blood pressure of 120
- max scene time of 20 mins
- hyperventilation when there is evidence of cerebral herniation
- do all measure to stop seizures and vomiting
Treat symptomatically :
Bradycardia - atropine
Hypotension - fluids
- 30 degree head tilt
Brain leakage through Forman magnum is really bad hence immediate hospital for ICP release through drilling
Outline the main risk factors for TBI and their implications for the prehospital falls assessment in the elderly (lecture/tutorial)
The main risk factors for a patient are any medication that thins your blood, anticoagulant and antiplatelet medications. These drugs are increasing prevalent within the elderly population and therefore the smallest’s of bleeds can be extremely detrimental for these guys.
And in accordance with the coroners report
1. all patient that are on anticoagulant medication need hospital visit to rule out brain bleeds
2. pre-existing cognitive impairment may have a lot of cerebral shrinkage hence more risk for brain injury and masking brain bleeding symptoms
Describe the signs and symptoms of the potential TBI patient (lecture/tutorial)
The injury = Signs & symptoms
- Mechanism of injury + Patient
- Tissue swelling
- Hypoxia
- Haemorrhage
- Increased intracranial pressure (ICP)
- widening pulse pressure ( an increase difference between systolic and diastolic BP
- pupil changes ( dilated or pin point and no equal and reactive)
- Declining GCS
- raccoon eyes
- chain stokes breathing - irregular respirations
- tachycardia then bradycardia
- irritability
Describe the principle of cerebral autoregulation (lecture/tutorial)
Auto-regulation is the mechanism of maintaining appropriate cerebral perfusion, this occurs through the brains ability to either vasoconstriction if pressure is too high and reduce the amount of blood or vasodilate to increase blood flow and increase glucose and oxygen. The brain can appropriately control this when the mean arterial pressure is within the ranges of 50 - 150 with the optimal number being 90. MAP is a calculation of 1/3 of pulse pressure + diastolic pressure. When MAP is outside these ranges the the brain loses its capacity to autoregulate and therefore too high means max constriction of vessels and too low means max dilation to the point of the vessels collapsing due to the low blood volume.
Cerebral perfusion pressure = MAP - ICP
MAP needs to overcome ICP in order to enter the brain
Explore the relationship of the Monro–Kellie doctrine to traumatic brain injury (p. 206)
This is where there is too much swelling in the brain causing increase ICP which forces the CSF then blood and eventually brain tissue from the brain through the foramen magnum
This can be indicated through a sudden drop in GCS as the brain herniation will disrupt neural tissue at the brain stem
Compare and contrast the pathophysiology of primary and secondary head injury (p. 201)
A primary brain injury is caused directly from the traumatic event itself resulting in tissue damage
The secondary brain injury is caused through intracranial and extracranial causes
- Extracranial causes
- Hypoxia
- Hypoglycaemia
- Intracranial causes :
- Haemorrhage
- Swelling
- Infection
Outline the prehospital management of spinal cord injury, with special attention to the treatment of the shocked patient (lecture/tutorial)
C spine precautions
Treat symptomatically
- bradycardia administer atropine to block ACh at the muscarinic receptors OR cardiac pacing if severe
- hypotension administer IV fluids and potentially adrenaline infusion if severe
- hypoxia administer high flow oxygen 15L with non rebreather and BVM if severe
Describe the use of the Nexus criteria and the Canadian C-Spine rule in the prehospital environment (lecture/tutorial)
It’s a fast tool for either the placing the patient under c spine precautions or if you are able to clear their spine
Both criteria explore all the options that may be present, including
- intoxication
- focal neurological deficits
- distracting injuries
- normal GCS
- c spine tenderness or pain
- above 65 y/o
- dangerous mechanism
- paralysed in peripheries
- MVC above 60mph, rollover / extrication / fall from any motorised vehicles
- fall from elevation 3 feet or 5 stairs
- axial load to head
- bicycle strike or collision
Describe the research on the current use of C-Collars in the prehospital setting (lecture/tutorial)
Immobilisation / neck collar
PRO’s
- Stabilisation for extrication
- Less secondary injury ( which are less prevelant )
CON’s
- Minimal evidence
- Vomit = aspiration
- Pressure sores = infection
- Anxiety
Outline the prehospital diagnosis of a potential spinal cord injury (lecture/tutorial)
You cannot fully diagnose a SCI but can have very high suspicions, this would include ;
- altered sensations on the skin
- determine where they lose sensations to what area of the SC is injured
- assess through all different sensations (light touch, pain, temperature,)
- mechanisms of injury
Examine the common complications associated with spinal cord injury (lecture/tutorial)
Autonomic dysreflexia : Medical emergency!
This may occurs when a patient has a spinal cord injury below T6 and also needs a compensatory mechanism in place due to an infection or something else.
Blocked cathedar : the nerves and neurons below the injury are still functioning but the signals cannot get to the brain. If the cathedar becomes blocked it is sending signals to the brain to compensate but those signals cannot get to the brain hence the continual stretching of the bladder initiates sympathetic stimulation causing blood vessels to constrict and hypertension,
The barroreceptors then detect the increase in blood pressure and compensate to decrease HR hence bradycardia. These signals wont be able to reach below the site of injury hence they will continue to be , Vasoconstricted, pale whereas above the injury site will be vasodilated, flushed.
We can treat this though removal of the stimuli / infection
And decrease the blood pressure to a tolerable range because the blood pressure is really high above the injury this can cause seizures and cerebral haemorrhage therefore reduce blood pressure by GTN but prepare for rebound hypertension and tachycardia
Atropine for bradycardia
Explore the diagnosis and management of spinal cord injury (lecture/tutorial)
Prehospital presentation :
Response - should not be altered with isolated SCI
Airway : may be compromised with injury to C spine
Breathing : may be compromised with injury above C3
Circulation : may be compromised due to vasoconstriction or vasodilation
- flushed above SCI and pale below
- involuntary erection
- weakness
- effected behaviors / awareness
Prehospital Management :
- Continually reassess ABC’s
- immobilise, Collar, VAC mat
- IV access for fluids
- atropine for bradycardia
- adrenaline infusion for hypotension
- oxygen for hypoxia ?
- clinical support
- early notification
- keep then flat and do not move
Cauda equina
Is a spinal cord injury caused by herniated disks, direct trauma or malignancy in which causes the paralysis of the tailbone area, faecal incontinence and sciatic pain.
An injury to the lower back causing lower back pain
Brown Sequard
Injury to one’s side of the spinal cord in which results in same side loss of motor, touch and proprioception and loss of pain and temperature on the other side.
LEFT SIDE TRAUMA :
Pain and temp on right side is lost
Motor, touch and proprioception is lost of left side
Anterior cord
Injury to the anterior aspect of the spinal cord
Caused by ; fractures and dislocations resulting in ischaemia
Loss of motor, touch and pain below the injury
NO LOSS in touch and proprioception
Central cord
Incomplete injury to the spinal cord due to cervical / neck hyperextension
Upper limb motor weakness and loss of light touch, pain, temp, and pressure below the injury
Differentiate between complete and incomplete spinal cord injury (p. 217)
Complete spinal cord injuries occur when there is complete loss of all functions below the injured site. This may or may not be due to the complete cut of the spinal cord.
Incomplete spinal cord injuries are those that still have some function which extends to the S4 and S5 region.
Paraplegic – only the lower two limbs are effected
quadriplegic – partial or total loss of function of all four limbs
Outline the prehospital management of spinal cord injury, with special attention to the treatment of the shocked patient (lecture/tutorial)
The prehospital management for a spinal cord injury involves the recognition of a SCI with special attention to a thorough secondary assessment, looking for any loss in motor function, touch, temperature, pain and proprioception.
From here spinal immobilisation is key, this can be performed through;
- manual stabilisation
- modified towel role
- vac mat
- c collar
With special mention of the shocked patient
- atropine for bradycardia
- adrenaline infusion for hypotension
- ventilation for hypoxia ?
are they hypotensive because they are hypovolemic or do they have a SCI
Loss of ANS and SNS tone
Describe the research on the current use of C-Collars in the prehospital setting (lecture/tutorial)
PRO’s
- Stabilisation
- Less secondary injury
CON’s
- Minimal evidence
- Vomit = aspiration
- Pressure sores = infection
- Anxiety
Outline the prehospital diagnosis of a potential spinal cord injury (lecture/tutorial)
To prehospital diagnose a patient with a SCI the following should be considered ;
- determine what signals are getting through to the peripheries and what are signals are entering the brain
Dermatomes (efferent) myotomes (afferent)
- Canadian c spine rule / precautions
- loss of autonomic nervous system innervation
- loss of sympathetic tone and unopposed parasympathetic tone
Outline the pathophysiology, clinical manifestations, clinical diagnosis and management of Meningitis :
Meningitis a viral or bacterial infection to the Meningie layers of the brain, dura matter, arachnoid matter and pia matter. When these layers becomes infected they become inflamed and hence increase intracranial pressure.
SEPSIS : Bacteria causes the release of endotoxins into the bloodstream
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This causes damage to the capillaries and triggers the clotting cascade hence lots of blood clots in the vessels which is depicted as a rash
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The body will then run out of the clotting factors
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This causes BLEEDING and DIC
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DIC causes limb necrosis and damages capillaries
The clinical manifestations of meningitis are the triad of; neck stiffness, fever and altered mental state. But can also include; headaches, photophobia and non-blanching rash.
Clinical diagnosis for meningitis includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history.
Management of meningitis is early identification, PPE, antibiotics for bacterial and antiviral medications for viral, and monitoring of ABC’s with the anticipate to treat shock as this can progress with cardiac arrythmias, hypotension, vasodilation due to the systemic infection.
Outline the pathophysiology, clinical manifestations, clinical diagnosis and management of
encephalitis :
Is the infection to the grey and white matter of the brain tissue or spinal cord. It can be either viral or bacterial but typically viral is more common as is it smaller hence easier to get to the brain and bacteria is a bigger molecule hence it is harder to get to the brain. This can be caused by herpes, rabies, ebola, ross river, west Nile, covid this viral infection then progress into the brain or spinal cord and hence encephalitis.
Cytotoxic – toxic cells
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WBC fight back – the white blood cells try to fight the cytotoxins
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Inflammation, because the cell are dying and breaking down from the virus
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Cerebral oedema from the cell death
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Death / long term brain damage from all the cell death
Clinical diagnosis for encephalitis includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history.
The clinical manifestations of encephalitis include the triad of CNS infections fever, altered conscious state, neck stiffness, headaches, confusion, seizures, personality changes.
The management includes early identification and notification, sedation for agitated patient and the preparation for seizures.
Outline the pathophysiology, clinical manifestations, clinical diagnosis and management of brain abscesses
Brain Abscess are a bacterial infection caused by the build up of pus and inflamed tissue that builds up due to infections. The pus is a product of bacterial infection and dead white blood cells that have tried to fight the infection. This builds up within the brain and causes large neurological disturbances. This can be caused to a range of bacterial infections dental abscesses, sinus infection ear infections, skull trauma which allows bacteria to enter the brain.
The clinical manifestations of a brain abscess include fever, headache, cannot speak, one sided muscle weakness, vomiting and seizures. Change in personality due to the potential in midline shift of the brain, increased ICP as the abscess is growing in a location where there is no space, so all the signs and symptoms that occur when ICP increases. also Increase ICP when laying flat.
Clinical diagnosis for a brain abscess includes a thorough history and recent infection status and signs and symptoms coherent with the condition as well as vaccination history. The signs and symptoms will have a gradual onset as the abscess needs time to grow hence will not be a sudden onset.
Patient that are higher risk for this infection includes, IV drug users as they use dirty needles potentially with bacteria in then into the veins and those immunocompromised patients.
Management will include early identification and notification, symptomatic management, there is minimal interventions we can do prehospitally but antibiotics is key for treatment.
What is the significance of WBC in CNS infections ?
White blood cells fight infections and therefore are needed to help the immune system to fight meningitis, encephalitis and brain abscesses. WBC are located within the bloodstream and therefore when they are required to fight infections in the CNS they cannot diffuse out of the bloodstream. The capillaries need to vasodilation to increase the permeability of the vessel walls hence WBC can exit. This also causes fluid to follow out of the bloodstream. This then causes ;
Cerebral oedema
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Increased ICP
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Compression
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Herniation
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Death
Outline the pathophysiology, clinical manifestations of the common headache
Paramedics cannot clinically diagnose a common headache or differentiate them from a more serious complication therefore they all need to be treated with high suspicion if they alter from the patients normal perceived headache.
The pathophysiology of a headache can be caused by either a primary source such as
• Dehydration
• Sinus infections
• Alcohol
• Muscle strain
• Anxiety
Or a secondary cause or differential diagnosis
• Subarachnoid haemorrhage
• Cancer
• Space occupying lesion
• Trauma – skull fractures, concussions
• CVA
• Meningitis
• Temporal arteritis
The red flag clinical manifestation of a headache include
• Worst / Different / First headache
• Speed of onset / Progression
• Numbness
• “Thunderclap” headache – comes on in a matter of seconds and is commonly associated with an aura (hallucinations) – subarachnoid haemorrhages
• LOC / Collapse
• Age >50 or <5
• Neuro deficit / weakness, altered sensation, dizziness,
• Persistent / recurrent that are getting worse
Outline the pathophysiology, clinical manifestations of a migraine
A migraine differs from a headache in that they have 4 phases
Their population group is usually boys before puberty, girls after puberty and is thought to be strongly related with hormonal changes (hence decrease with pregnancy, after menopause and boys post puberty)
Phase 1 : Prodromal phase - this is where the patient will feel the migraine coming on and experience a wide presentation including depression or euphoria, heightened sensitivity to smells and sounds, food cravings, muscle aches and GI upsets. This onset my range from days to weeks before the onset of phase 2
Phase 2 : Aura phase – this is the warning sign that the migraine is about to occur and this can present as visual disturbances, sensory issues like numbness and tingling, motor deficits such as loss of proprioception and balances. This typically lasts an hour before the onset of phase 3.
Phase 3 : Pain phase – this is the head pain itself, unilateral head pain on one side and pressure behind the ear, throbbing and intense pain. Can also present with photophobia and phonophobia, neck stiffness, nausea and vomiting and diaphoresis. This phase typically lasts 12 – 24 hours before the onset of phase 4
Phase 4 : Postdromal phase – this is when the pain has ended and the patient is returning to their normal self. This may include depression / euphoria, fatigue, cognitive deficits and confusion, GI symptoms.
The migraine is typically unilateral with a throbbing and pulsating pain, it can be triggered by a range of cause
• Stress / anxiety
• Hormonal changes
• Environmental factors (bring lights, strong smells)
The treatment for migraine differ with each patient therefore whatever worked last time try again and if it didn’t work try something new. There are a range of medication that can help with migraines
• Triptans - serotonin agonist (specific to migraines)
• Topiramate - antiepileptic
• Sodium valproate - antiepileptic
But the most effective treatment for paramedics is to remove the stimuli and reduce light and sounds, NSAID and IV fluids for dehydration and vasodilation to improve perfusion as migraines may decrease blood volume and cause vasoconstriction.
Opioid medication are not to be given to migraine patients as they have been shown to increase the intensity of the migraines. Rather begin with paracetamol and ibuprofen.
Outline the current consensus on the management of patient with a headache or migraine
As prehospital clinicians without access to medical imaging it is difficult to assess the internal working of a patient especially the brain therefore patients that present with abnormal headaches or migraines may have an underlying cause that cannot be determined prehospitally.
If the patient presents with any of the below red flag symptoms they require hospital investigation.
• Worst / Different / First headache
• Speed of onset / different progression
• Numbness
• “Thunderclap” headache – comes on in a matter of seconds and is commonly associated with an aura (hallucinations) that can be indicative of a subarachnoid haemorrhages
• LOC / Collapse
• Age >50 or <5
• Neuro deficit / weakness, altered sensation, dizziness,
• Persistent / recurrent that are getting worse
• Stiff neck, photophobia and vomiting = cerebral bleed or meningitis until proven otherwise
Although headaches may cause an ambulance to ramp for many hours it is better the be safe than to be sorry and leave a patient home with what presents as a typical gradual onset headache that may be a brain abscess.
The only time paramedics can leave a patient with a migraine home are if the cause of the migraine is known to the patient and there is a simple fix ie the patient ran out of migraine medication and is yet to fill their script. ECP may be able to administer medication with the agreement that if the migraine develops that they call an ambulance immediately.
Outline the pathophysiology, clinical manifestations, clinical diagnosis and management of Hydrocephalus
Hydrocephalus is the abnormal build up of CSF within the ventricles of the brain.
There are four different types :
1. communicating hydrocephalus : where the brain has issues with the reabsorption of CFS hence it builds up (subarachnoid haemorrhage)
2. obstructive hydrocephalus : where there is a blockage in the ventricular system preventing CSF to flow freely (tumours)
3. normal pressure hydrocephalus : this is when CS causes ventricle enlargement without increasing ICP and commonly presents with cognitive dysfunction and urinary incontinent.
4. hydrocephalus ex vacuo : is due to brain atrophy causing the ventricles to enlarge and hence increasing the demand for CSF. (Alzheimer’s disease or post stroke)
Signs and symptoms :
Infants –
• Enlarged head : rapidly increase head size or a visibly swollen fontanelle
• Bulging fontanelle : may appear tense or bulging
• Irritability : increased fussiness or crying
• Poor feeding and poor appetite
• Lethargy
• Developmental delays : not hitting correct milestones
Children and adults -
• Headaches : worsen in the morning and after laying down
• Nausea and vomiting :
• Blurred or double vision :
• Balance problems
• Cognitive changes : memory problems, difficulty concentration, changes in personality
Older adults –
• Difficulty walking or feeling unsteady
• Cognitive decline : memory loss, confusion, changes in personality
• Urinary symptoms : increased urgency or incontinence
And in all ages cushing triad – Late stage
- Hypertension : The body attempts to maintain cerebral perfusion despite elevated intracranial pressure.
- Bradycardia : Increased ICP can stimulate the vagus nerve, leading to a reflex bradycardia as a compensatory response.
- Chain stokes respirations : Increased pressure on the brainstem can disrupt normal respiratory control centres.
There’s nothing we can do prehospitally but in hospital they can put shunts in to allow the drainage of CSF into the abdomen
When CFS leaks from the ears and nose this means that their meninges layers have broken
What are the 4 infective microbes and how do how invade a human
Bacteria, virus, parasite, fungi
The microbe needs a temporary place to reside before infecting the patient this may be in waterways or animals. There is then a mode on transmission / how the microbe gets onto out body this can be through the consumption of the animal or water, bites or scratches from the animal, through droplets like sneezing and poor hygiene. The microbe is then on and can enter it through a portal either eyes, nose, ears, mouth, wounds, genitals, skin – some worms can enter the body by burrowing in via the skin. The white blood cells then begin to fight the infection this can either successful or unsuccessful due to autoimmune diseases, elderly or newborns. The microbes then colon on the host which in us and it claims our body as their new home.
What’s the difference between virus and bacteria
Viruses are innate hence they need a host to thrive whereas bacteria their own living organism. Bacteria replicated itself with food and fuel hence keep multiplying whereas viruses have their own DNA and RNA hence they replicate without a biological process. Virus destroy cells by damaging the phospholipid membrane and taking all the cells energy then jumping to the next cell and doing the same, whereas bacteria can kill cells though the release of toxins and invading the host cell.
Outline the APLS algorithm for paediatric seizures
The guidelines address status epilepticus by :
1. vascular access ?
YES – administer IV / IO midazolam 0.15mg / kg (max 10mg)
NO – IM midazolam 0.15mg/kg OR IN / buccal 0.3mg/kg
2. IV / IO administer IV / IO midazolam 0.15mg / kg (max 10mg)
3. Seek ICP help
4. Confirm status epilepticus seizure administer levetiracetam or phenytoin
5. Give the opposite to what was given before either levetiracetam or phenytoin OR phenobarbitone
6. Call for MedStar and RSI (intubation)
The differences between SAAS guidelines and APLS guidelines is that they suggest to administer 0.15mg/kg and SAAS gives 0.1mg/kg.
Discuss the aetiology, pathophysiology and prehospital management of febrile convulsions
The children at risk for febrile convulsions are children ages 6 months to 5 years of age with the main population being 12 – 18 months and more common in females.
The pathophysiology for febrile convulsions are unknown but they were thought to have been from the rapid spike in temperature of above 38 degrees as well as the immature brain unable to thermoregulate as effectively as the adult body therefore are more predisposed to febrile convulsions.
The prehospital treatment for febrile convulsions are to address the root cause of increased temperature therefore removing the peads clothing and applying cool packs on the appropriate areas, arm pits, neck and groin to decrease temperature. Oxygen therapy and glucose for the cerebral hypoxia. And monitor ABCS.
If the seizure has lasted longer than 5 mins or the patient has not returned to their normal GCS during their post ictal phase then administer 0.1mg/kg of midazolam and follow status epilepticus protocols
In regard to paediatric patient assessment, what are the key features of a patient with increased intracranial pressure
The key clinical features of a pead may include but are not limited to
- Vomiting
- Irritability
- Altered consciousness
- Bulging Fontanelle / whole head enlargements
- Sunset pupils / unreactive or not symmetrical pupils
- Cushing triad
o Bradycardia
o Hypertension
o Irregular respirations ( Cheyne Stokes )
Outline the use of the Glasgow Coma Score (GCS) vs. a standard AVPU assessment for paediatric conscious levels
The paediatric GCS scale is a modification from the adults scale with adjustments to the voice aspect, it is altered to
5 : alert and uses words as normal
4 : less words than usual, spontaneous crying
3 : crying to pain
2 : moans to pain and
1 : is no response.
Whereas the AVPU scale is an initial rapid assessment that determines the consciousness of your paediatric patient.
A : Alert
V : Alert to voice
P : Alert to pain
U : unconscious
AVPU is faster but GCS is more through and detailed therefore it is preferred to use AVPU initially then progress to GCS.
Define acute delirium and why would it occur in an elderly patient and the clinical manifestations ?
Acute delirium is an acute change in mental status where the patient is not in touch with reality.
It has a sudden onset and can be reversed / treated hence how it differs from dementia as this is a progressive onset over years and has no cure.
Clinical manifestations :
- not in touch with reality
- acting unusual
- paranoid
- confused
- agitated
Why may this occur :
- infections (UTI) / sepsis
- cerebral hypoxia
- new medications / dosing
- head trauma
- dehydration
Outline the pathophysiology, clinical manifestations and management of Parkinson’s Disease
Pathophysiology : Parkinson’s disease is a result of damage to the cells within the midbrain that synthesise dopamine therefore there is no release in dopamine. As dopamine is essential for motor skill the patient will present with tremors, slowed movements, rigidity.
This can arise form environmental factors or genetic predisposition
There is no cure for Parkinson’s disease but there are treatments that can slow its progression and increase a patients quality of life.
Parkinson’s disease is also linked closely with Lewy body dementia where there is a depletion of dementia as well as some other cognitive dysfunctions.
Define acute behavioural disturbance
Acute behavioural disturbance in elderly can be caused by infectious agents ranging from minor skin infections to sepsis. This alters their cognition and normal levels, may make them agitate and aggressive but it is due to the underlying medical problems.
Describe Dementia
Is an umbrella term that describes a collection of symptoms that are caused by disorders affecting the cognitive function. Dementia affects thinking, behaviour and the ability to perform everyday tasks. Where its progression is severe enough to interfere with the person’s normal social or working life.
The most common types of dementia are
• Alzheimer’s disease
• Vascular dementia
• Lewy body disease
• Frontotemporal dementia
What is the patho behind the formation of amyloid plaque
In a typical brain amyloid prosecutor protein (APP) is broken down into soluble fibres by alpha and gamma secretase but in the presence of beta secretase the APP becomes insoluble and therefore when binding with other insoluble APP clumps creates a beta amyloid plaque. These plaques can continually develop and are typically situated between the neurons and disrupt neuron signalling and can create an inflammatory response damaging surrounding neurons. These beta amyloid plaque can also situate themselves upon the blood vessels within the brain making the vessel wall thinner increasing the risk of intracranial haemorrhage.
Describe the formation of neurofibrillary tangles
neurofibrillary tangles which are subject to the increase in phosphate groups binding to the microtubules changes structure if the tau, therefore inhibiting its binding ability and creating large tangles of tau. The removal of tau from the microtubules means that they can no longer transfer messages which results in disrupt neuronal signalling and can progress to apoptosis of neural cells.
Outline the pathophysiology, clinical manifestations, clinical diagnosis and management of Alzheimers Disease
Alzheimer disease is one of the most prominent types of dementia, it occurs due to the formation of amyloid plaque and neurofibrillary tangles. It can be due to genetic predisposition or sporadic onset.
In conjunction with neurofibrillary tangles and the build up of beta amyloid plaque the brain undergoes atrophy where the cerebral cortex shrinks, the ventricles enlargen and the hippocampus shrinks as well as neuronal cell death due to the healthily neurons losing their ability to function and process information all attributing to the clinical symptoms of
- Memory loss
- Disorientation to time and place
- Changes in mood / behaviour and personality
- Declines in judgement
Describe the physiological complications and management of the overdose patient from
these medications: Tricyclic antidepressants
inhibit the reuptake of norepinephrine and serotonin by blocking the transporters responsible for their reabsorption into presynaptic neurons. This results in increased concentrations of these neurotransmitters in the synaptic cleft, enhancing their availability to bind to postsynaptic receptors. Therefore, enhancing mood and alleviating depressive symptoms. As this medication inhibits the reuptake of serotonin when patients overdose on these medications it causes serotonin syndrome which is when there is too much serotonin in the synapse this causes muscle spasms and hyperreflexia.
As well as this TCAs can block cardiac sodium channels, leading to prolonged depolarization and slowing of cardiac conduction. This can cause arrhythmias, conduction delays (like QRS widening), and potentially lead to ventricular tachycardia or fibrillation.
The management of this anticholinergic overdose includes the administration of Activated Charcoal which will absorb the toxins within the body and prevent them from entering into the bloodstream, but also managing symptoms and preparing for patient deterioration and seizure management.
Therefore the clinical signs and symptoms would correlate with those anticholinergic toxicity which includes
- Dry
- Hot flushed skin
- Urinary retention
- Confusion / delirium
- Tachycardia
- Hypotension
Which leads to
- Hyperthermia
- Seizures
- Dysarrythmias
Describe the physiological complications and management of the overdose patient from
these medications: 1 gen - Antipsychotics
Typical antipsychotic medications are those that are antagonists to the D2 receptor which means that they block the binding of dopamine on three pathways (mesolimbic, nigrostriatal, mesocortical) and therefore the body compensates to this blockage and decreases the amount of dopamine that is synthesised. In relation to psychosis these medication create a more neurochemically balanced environment for the brain therefore decreasing the episodes of psychosis as the brain is more balanced with its neurotransmitters.
These antipsychotics are indicated for patients with schizophrenia and acute psychotic outbursts but can also be used as a second line treatment for nausea and vomiting particularly in chemo patients.
- Haloperidol and droperidol are both very common FGA’s
