BBEOYS8 Flashcards
A disorder exclusively causing slurred speech would be classified as
Drunk
Dysarthria
Dysphonia
Dysarthrophonia
A disorder exclusively causing slurred speech would be classified as
Drunk
Dysarthria
Dysphonia: voice disorder (voice might be weak / distorted)
Dysarthrophonia: both
PEN-2 & (PEN-1) code for the production of
α-secretase
β-secretase
γ-secretase
δ-secretase
PEN-2 & (PEN-1) code for the production of
α-secretase
β-secretase
γ-secretase
δ-secretase
Focal seizures most commonly start in which lobe
Frontal
Occipital
Temporal
Parietal
.
Focal seizures most commonly start in which lobe
Frontal
Occipital
Temporal
Parietal
.
Pathogenesis of Alzeimers DIsease (AD)
Name the genes [3] and proteins [3] that are critical for early onset AD [3]
Genes for early onset AD (not common). caused by the following genes
* Amyloid precursor protein (APP)
* Presenellin 1 (PSEN1)
* Presenellin (PSEN2)
Which molecule is APOE involved in the metabolism of? [1]
What are the three isoforms of APOE? [3]
Which is the greatest risk for AD and why? [2]
Involved in cholesterol metabolism
APOE2; APOE3 & APOE4
APOE4 has greatest risk factor and decreases clearance of extracellular Aβ.
Which gene encodes tau? [1]
Are mutations to this gene linked to familial AD? [1]
MAPT gene
NOT linked to familial AD; instead to frontotemporal dementia (FTD) and several other Tauopathies.
Treatment strategies in AD
Name the drug class [1] and 3 drug examples you prescribe for mild - moderate AD? [3]
Name the drug class [1] and 3 drug examples you prescribe for severe AD? [1]
Mild-Moderate AD:
* Acetylcholinesterase inhibitors(e.g. donepezil, galantamine and rivastigmine)
Severe AD:
* NMDA receptor antagonists (e.g. memantine)
Presenilin 1 & 2 are responsible for making which secretase? [1]
Presenilin 1 & 2 proteins is one part (subunit) of a complex called gamma- (γ-) secretase.
Describe the inflammatory response caused by familial forms of AD pathogenesis (from early AD genes) [2]
Describe the effect of amyloid plaques within neurons (caused by familial forms of AD pathogenesis) [2]
Inflammatory response:
* Microglial activation - inability to clear AP causes chronic inflammation of microglia
* Astrocytosis (increase in amount) and acute phase protein release
Progressive neuritic injury within amyloid plaques
* Disruption of neuronal metabolism and ionic homeostasis:
* Oxidative Stress
Which posttranslational modification does the microtubule-binding protein, tau undergo which contributes to Alzheimer’s pathology? [1]
Which amino acids can undergo this specific post translational modification? [3]
Hyperphosphorylation.
Tyrosine, serine and threonine.
Define:
Dysarthria [1]
Dysphonia [1]
Dysarthrophonia [1]
What stays the same throughout each of the above? [1]
Dysarthria: disorder affecting articulation (slurred / unclear speech)
Dysphonia voice disorder (voice might be weak / distorted)
Dysarthrophonia: voice and articulation disoder
Language and cognition is normal
What is the name for saying the wrong words? [1]
Paraphasias
What is telegrammatism? [1]
Difficulty forming sentences
TBI injury mechanism:
What are the 3 causes of TBI? [3]
Penetrating injury
* Foreign object (e.g. bullet) enters into brain causing focal damage.
Closed head injury:
* Blow to the head (e.g. road traffic accident).
Blast injury
* Explosion (e.g. bomb) create fast moving pressure wave that passes through the brain and damages axons and vasculature.
Types of traumatic brain injury injury classification
Describe the injury classifications for TBI [2]
Focal injury:
- Coup: at site
- Contrecoup: opposite site
Diffuse injury:
- Diffuse axonal injury
Diagnosis of TBI
Which scale is used to classify TBI? [1]
Which critertia is it based on? [3]
What is the maximum score for each of the criteria? [1]
Glasgow Coma Scale (GCS):
Based on:
- eye opening [/4]
- motor response [/5]
- verbal response [/6]
What are mild, moderate and severe GCSs? [3]
Mild: 14-15
Moderate: 9-13
Severe: less than 8
What can an MRI scan detect that a CT scan cannot? [3]
- diffuse axonal injury ( the shearing (tearing) of the brain’s long connecting nerve fibers (axons) that happens when the brain is injured as it shifts and rotates inside the bony skull)
- non-haemorrhagic contusion
- brainstem injury
1- Pathophysiology of TBI: Increase in intracranial pressure
How do you detect ICP? [1]
ICP bolt
1- Pathophysiology of TBI: Increase in intracranial pressure
Describe the Monro-Kellie Hypothesis [4]
Relationship between the contents of the cranium and intracranial pressure:
- Brain is enclosed in a fixed non-expandable skull.
- Increase in mass (e.g. haematoma) reduces CSF and cerebral blood flow in the brain.
- Decrease in brain blood and CSF causes ischemia and then brain cell death.
- Increase ICP can cause herniation.
4- Pathophysiology of TBI (seizures)
What is a seizure due to? [1]
When can seizures occur post-TBI? :
How long would a early [1] and late [1] post-traumatic seizure be after a TBI?
Seizures are abnormal sudden electrical disturbance in the brain.
Early post-traumatic seizures: A seizure within 1st week of TBI.
Late post-traumatic seizures: A seizure after 1st week of TBI.
5- Acute management of TBI (Mild TBI)
How would you acutely treat mild TBI? [2]
5- Acute management of TBI (Severe TBI)
Which drugs can you use to start seizure prophylaxis? [2]
Which drugs can you use to induce coma? [2]
Start on seizure prophylaxis: phenytoin/levetiracetam
Sedation/Induce coma with propofol or benzodiazepines
5- Acute management of TBI (Mild TBI)
How would you acutely treat moderate TBI?
(Moderate TBI: Experience brain changes and symptoms remains or worsen)
- Transfer to Neurosurgical unit
- Surgical evacuation dependent on size and type of haematoma
- Transfer to intensive care unit (ICU) to allow brain bruising + swelling to reduce by itself.
What size haematoma would be evacuated regardless of GCS? [1]
>30 cm3
5- Acute management of TBI (Severe TBI - ICP)
How could you manage severe ICP:
Acutely [2]
Long term [1]
Short term:
* mannitol
* hypertonic saline
(shift of water from extravascular space to intravascular space across the BBB-controversy which therapy is better.)
Long term:
* extraventricular drain/ external ventricular drain (EVD) or ventriculostomy
Which part of the brain undergoes structural changes during epilepsy? [1]
Which structural changes occur in this area? [4]
Reorganisation of the hippocampal tissue / hippocampal scleoris:
* Atrophy of CA2 and CA3 hippocampal areas
* Different tract orientation
* Compresion of layers
* Loss of neurones
Strucutral changes in epilepsy (I)
What are the consequences of hippocampal sclerosis / degeneration in epilepsy? [1]
Sprouting of axons & neurogenesis- may lead of excess synaptic conduct between neurons
Aberrant circuits may be created within the hippcampus
Overtime, there is transformation within neural networks that promote excitability.
Strucutral changes in epilepsy (II)
Name [1] and explain [2] which cell type, that if lost, can lead to epilepsy
GABAnergic inhibitory chandelier cells:
- Interneuron cells which synapse onto CNS
- Loss of inhibitory cells increases risk of abnormal excitatory activity
Describe the phenomenon / profile of neurones in an epileptic focus [1]
Describe how this occurs [1]
Burst firing: aka paroxysmal depolarising shift phenomenon
- This leads to synchronous, hyperexcitable activity within a neuronal population
- Particularly NDMA glutamate receptor activation
How do astrocyte abnormalities influence the development of epilepsy? [1]
Astrocytes:
- contain EAAT1 and EAAT2 transporters
- EAAT1 and EAAT2 transporters are key in synaptic glutamate uptake
- A deficiency in EAAT1 and EAAT2 transporters leads to a decrease in glutamate reuptake
- This means there is more glutamate in synapse and increases excitability
Which physiological changes occur when the body undergoes EPILEPTOGENESIS to create a Hyperexcitable neuronal network in epilepsy [4]
- Neuroinflammation
- Blood- Brain-Barrier breakdown
- Oxidative stress
- Gliosis
- Network and synaptic changes
Which other major pathways may be disregulated in epilepsy? [2]
The mTOR pathway is a major regulator
of growth and homeostasis
The REST pathway leads to negative regulation
of the expression of many genes in the CNS
