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HNN Crash Course MCQ Q 1-15 2440051B@student.gla.ac.ukQuestion 01You are the 3rd year medical student in theatre. You notice the Anaesthetist is setting up an infusion of noradrenaline. What is the function of noradrenaline in this patient? A. Elevate blood pressure B. Empty urinary bladder C. Increase lacrimation for eye protection D. Increase digestive tract output E. Reduce heart rateYou are the 3rd year medical student in theatre. You notice the Anaesthetist is setting up an infusion of noradrenaline. What is the function of noradrenaline in this patient? A. Elevate blood pressure B. Empty urinary bladder - parasympathetic C. Increase lacrimation for eye protection - parasympathetic D. Increase digestive tract output - parasympathetic E. Reduce heart rate - parasympathetic Common sense: you don’t want to increase bowel/bladder output if a patient is under a GA! V messyYou are the 3rd year medical student in theatre. You notice the Anaesthetist is setting up an infusion of noradrenaline. What is the function of noradrenaline in this patient? A. Elevate blood pressure B. Empty urinary bladder C. Increase lacrimation for eye protection D. Increase digestive tract output E. Reduce heart rate Be smart - where have you come across NA in basic physiology? AUTONOMIC NERVOUS SYSTEM AutonomicNervous System Sympathetic Parasympathetic Origin Thoracolumbar (T1-L2) Brainstem (CN III, VII, IX, X) & Sacral (S2-4) Location of terminal Paravertebral sympathetic Located near or ganglia ganglion chain embedded in target tissue Preganglionic fibres Short (cholinergic fibres) Long (cholinergic) Post ganglionic fibres Long (adrenergic fibres) Short (cholinergic) Neurotransmitter Noradrenaline (ACh in ACh preganglionic fibres) Divergence vs. Divergence Less divergence convergenceDivergence: ● 1 preganglionic fibres to 20 post-ganglionic fibres (only 1:1-3 in parasympathetic) ● This there is mass sympathetic discharge (NA) to many organs & tissues (Not that important but good demonstration of ‘divergence’, an ILO) What about the adrenals? ● Adrenal medullary cells are basically post-ganglionic fibres. ● Release their own adrenaline Adrenaline vs Noradrenaline ● Adrenaline: a hormone released by adrenal glands ● Noradrenaline: a neurotransmitterHow to remember the origin?? TIP: stop memorising + understand ● Oculomotor (III) - controls sphincter pupillae (constriction) ● Facial (VII) - lacrimal, salivary + mucous membranes ● Glossopharyngeal (IX) - parotid gland ● Vagus (X) - viscera ● S2-4 - organs of pelvic cavity Relate to function? ● Pupillary constriction ● Lots of secretions for digestion e.g. tears, saliva, moist membranes ● Urinary output increased ● Visceral innervation: slows HR, airway constriction, increased digestionQuestion 02 Local anaesthetic lidocaine is a voltage gated Na+ blocker. It prevents propagation of an action potential along the presynaptic neurone. This causes it’s anesthetic effects. Which part of the action potential does this drug target? 5 A. 1 B. 2 C. 3 1 2 D. 4 4 E. 5 3 Local anaesthetic lidocaine is a voltage gated Na+ blocker. It prevents propagation of an action potential along the presynaptic neurone. This causes it’s anesthetic effects. Which part of the action potential does this drug target? 5 A. 1 B. 2 C. 3 1 2 D. 4 4 E. 5 3 Resting Membrane Clinically… some Potential anti-epileptics are NaV RMP (neurone) is -70mV channels blockers. Reduces neuronal excitability in brain, A stimulus must bring membrane potential to reducing chance of seizures threshold potential (-50mV) Depolarisation Hyperpolarization Threshold potential reached. Brief period of hyperpolarization. Opening of Na+ voltage gated channels. Membrane eventually re-stabilises Influx of Na+ ions into cell. itself Intra cellular becomes more +ve Repolarisation Efflux of K+ (lowers electropositivity Overshoot Phase generated by Na+ influx of depolarisation) Na+ channels close suddenly Restoration of RMP (-70mV) K+ channels open.Absolute Refractory Period: a new AP cannot be generated. All Na+ channels are open/opening at maximal speed. Relative Refractory Period: generation of new AP is possible (some Na+ channels are closed and potentially could open). A suprathreshold stimulus required.Question 03You are sitting at home. The doorbell rings and you get up quickly to answer. In the process, you bang your knee hard off a coffee table. You immediately grab hold of your knee firmly. Which axons are you stimulating by placing pressure on the area of pain? A. A-alpha B. A-Beta C. A-Delta D. C fibres E. E-alpha fibresYou are sitting at home. The doorbell rings and you get up quickly to answer. In the process, you bang your knee hard off a coffee table. You immediately grab hold of your knee firmly. Which axons are you stimulating by placing pressure on the area of pain? A. A-alpha B. A-Beta C. A-Delta D. C fibres E. E-alpha fibresSpinothalamic Pathway - Pain/temperature Lateral pathway: pain/temp Anterior pathway: crude touch 1. 1st order neurone (Ab, Ad, C) a. Enter dorsal horn via dorsal root ganglion b. Give of ascending + descending collaterals that travel in Lissauer’s tract c. Synapse with second order neurones rexed laminae of dorsal horn 2. 2nd order neurone a. Decussate at level of entry b. Ascend to the VPL of thalamus 3. 3rd order neuron a. Travel through internal capsule -> corona radiata -> primary sensory cortexDON’T LEARN: ● Lissauer’s Tract (Posterolateral tract) ● In anterior spinal artery stroke - the Lissauer’s Tract + DCML pathways are preservedGate-Control Theory of Pain Gate-Control Theory of Pain Substantia Gelatinosa: contains inhibitory neurones - the “gate” of the spinal cord Two axons from the C fibres + A beta fibres. 1. Nociceptive stimulus fires off the C fibres 2. C fibres inhibit the inhibitory neurone i.e. open the gate whilst simultaneously stimulating the secondary neurone 3. If pressure is applied… A beta fibres excite the inhibitor neurone i.e. close the gateQuestion 04You are examining the lymph nodes of a patient's neck during a gastrointestinal system examination. Your OSCE examiner decides to quiz you on the anatomy of the posterior triangle. Which of the following correctly states the borders of the posterior triangle? A. Anterior border of trapezius, posterior border of sternocleidomastoid, accessory nerve B. Anterior border of trapezius, posterior border sternocleidomastoid, middle ⅓ clavicle C. Inferior border of mandible, common carotid artery, anterior border of sternocleidomastoid D. Inferior border of mandible, midline of neck, anterior border sternocleidomastoid E. Lateral ⅓ clavicle, posterior border sternocleidomastoid, scapular spineYou are examining the lymph nodes of a patient's neck during a gastrointestinal system examination. Your OSCE examiner decides to quiz you on the anatomy of the posterior triangle. Which of the following correctly states the borders of the posterior triangle? A. Anterior border of trapezius, posterior border of sternocleidomastoid, accessory nerve B. Anterior border of trapezius, posterior border sternocleidomastoid, middle ⅓ clavicle C. Inferior border of mandible, common carotid artery, anterior border of sternocleidomastoid D. Inferior border of mandible, midline of neck, anterior border sternocleidomastoid E. Lateral ⅓ clavicle, posterior border sternocleidomastoid, scapular spineAnterior triangle: Posterior triangle: ● Midline of neck ● Anterior border trapezius ● Anterior border ● Posterior border sternocleidomastoid sternocleidomastoid ● Inferior border mandible ● Middle ⅓ clavicleLearn the contents of these borders by scrolling through Anatomy TV.Question 05A 75 year old man presents to A&E. He developed breathlessness over the last 24 hours. On examination notice flushing of his face + shoulders and periorbital swelling. In the last 6 months he has lost 15kg in weight and has been generally more breathless. He insists this is much worse than what he has been experiencing. What is the most likely diagnosis? A. Acoustic neuroma B. Horner’s Syndrome C. Meniere’s Disease D. Pancoast Tumour E. Pulmonary EmbolismA 75 year old man presents to A&E. He developed breathlessness over the last 24 hours. On examination notice flushing of his face + shoulders and periorbital swelling. In the last 6 months he has lost 15kg in weight and has been generally more breathless. He insists this is much worse than what he has been experiencing. What is the most likely diagnosis? A. Acoustic neuroma B. Horner’s Syndrome C. Meniere’s Disease D. Pancoast Tumour E. Pulmonary EmbolismILOS: 1. Identify the boundaries of the root of the neck 2. Describe the main neurovascular components of the root of the neck, including the subclavian vessels, phrenic and vagus nerves, brachial plexus and sympathetic trunk. 3. Explain the clinical features of Horner’s SyndromeSigns of Pancoast Tumour ● Sympathetic Chain: ○ Ipsilateral facial flushing/sweating ○ Horner’s Syndrome: ptosis, miosis and anhidrosis ● Recurrent Laryngeal Nerve: Voice hoarseness ● Brachial Plexus ○ Should/arm pain ○ Wasting of muscles of hand/forearm ● Superior Vena Cava ○ Facial swelling, dyspnoea, flushingNO SYMPATHETIC… pupils constrict, eyes close and stop sweating. You are RESTING because the bear is gone! Summary of Horner’s Syndrome Anhidrosis Miosis Physiology: Ptosis 1. 1st order neurones: originate in hypothalamus, descend through brainstem ipsilateral and terminate at C8-T2 2. 2nd order neurones: exit at T1 and enter Anhidrosis cervical sympathetic chain and ascend to Miosis superior cervical ganglion Ptosis 3. 3rd order neurones: a. Some fibres follow external carotid to sweat glands of face b. Remaining fibres follow internal carotid, though cavernous sinus and Ptosis (sympathetic nerve fibres eventually join CN III, IV, V, VI innervate Muller’s Muscle) Miosis (CN III) SOMETIMES… anhidrosis Summary of Horner’s Syndrome Stroke Ms Physiology: Meningitis Spinal tumour/injury 1. 1st order neurones: originate in hypothalamus, descend through brainstem ipsilateral and terminate at C8-T2 2. 2nd order neurones: exit at T1 and enter cervical sympathetic chain and ascend to superior cervical ganglion 3. 3rd order neurones: a. Some fibres follow external carotid to sweat glands of face b. Remaining fibres follow internal carotid, though cavernous sinus and eventually join CN VI and V1 Summary of Horner’s Syndrome Physiology: 1. 1st order neurones: originate in hypothalamus, descend through brainstem ipsilateral and terminate at C8-T2 2. 2nd order neurones: exit at T1 and enter Pancoast Tumour cervical sympathetic chain and ascend to Iatrogenic e.g. superior cervical ganglion thyroidectomy, CABG 3. 3rd order neurones: a. Some fibres follow external carotid to sweat glands of face b. Remaining fibres follow internal carotid, though cavernous sinus and eventually join CN VI and V1 Summary of Horner’s Syndrome Physiology: 1. 1st order neurones: originate in hypothalamus, descend through brainstem ipsilateral and terminate at C8-T2 2. 2nd order neurones: exit at T1 and enter cervical sympathetic chain and ascend to superior cervical ganglion 3. 3rd order neurones: a. Some fibres follow external carotid to sweat glands of face b. Remaining fibres follow internal carotid, though cavernous sinus and eventually join CN VI and V1 Cavernous sinus thrombosisQuestion 06A 48 year old woman presents with a month long history of worsening ringing in her right ear with hearing loss and difficulty with balance. On examination you note weakness of right frontalis, orbicularis oculi, buccinators and orbicularis oris. There is decreased sensation to pin-prick on the right side of her face. Upper and lower limb neurology intact. Where would her brain lesion be? A. Cavernous Sinus B. Cerebellum C. Primary motor cortex D. Cerebellopontine angle E. Middle earA 48 year old woman presents with a month long history of worsening ringing in her right ear with hearing loss and difficulty with balance. On examination you note weakness of right frontalis, orbicularis oculi, buccinators and orbicularis oris. There is decreased sensation to pin-prick on the right side of her face. Upper and lower limb neurology intact. Where would her brain lesion be? CN VIII - hearing loss & balance CN VII - Weakness of right facial A. Cavernous Sinus muscles B. Cerebellum CN V - reduced sensation on C. Primary motor cortex right side of face D. Cerebellopontine angle E. Middle ear What structure do these CNs have in common?Vestibular Schwannoma vs.Meniere’s Disease Meniere’s Disease: Long term progressive vestibular condition; Accumulation of endolymph in cochlea and vestibular organs (labrinth). Unilateral: ● Vertigo (episodic lasting 20 mins-hours. Not triggered by movement or posture.) ● Hearing loss (sensorineural hearing loss, low frequencies at first) ● Tinnitus (occurs with vertigo initially, then becomes permanent) Others… feeling of aural fullness, unexplained falls, imbalance, spontaneous nystagmus What’s the Difference? MD: starts with episodic Vestibular Schwannoma: symptoms then becomes ● Tumours of schwann cells constant ● Typically found at cerebellopontine angle VS: insidious onset (+ facial ● Unilateral (bilateral in NF2) nerve palsy?) ● Unilateral: ○ Sensorineural hearing loss ○ Tinnitus ○ Continuous vertigo ○ Sensation of aural fullness ○ ?Facial nerve palsyQuestion 07You are shown this prosection of the brain in your anatomy lab. The prof asks you to point to the area of the brain which contains the choroid plexus. Select the number which corresponds to the correct anatomical structure. A. A B. B C. C B D. D C E. E E D AYou are shown this prosection of the brain in your anatomy lab. The prof asks you to point to the area of the brain which contains the choroid plexus. Select the number which corresponds to the correct anatomical structure. A. A B. B C. C B D. D C E. E E D A Don’t get caught out - not just in lateral ventricles CSFProduction& Circulation 1. Produced in choroid plexusoflateral, 3rd & 4th ventricles 2. Flows from lateralto third ventriclethroughinterventricularforamen (ofMunro) 3. Flows from 3rd to 4th via cerebral aqueduct(of Sylvius) 4. Flows into subarachnoid space throughforamina ofLuschkaandforamenof Magendie (connect 4th ventricle tosubarachnoidspace) 5. Absorption into blood occursin superior sagittalsinusthrougharachnoid granulationsBoringCSF stuff to memorise 1. Produced at500mL/day 2. Circulates in subarachnoidspace 3. 140mLin subarachnoidspaceat any time 4. Function? Mechanical andimmunological protection 5. Whydolumbarpunctures? a. Diagnosisbased on biochemistry/microbiology e.g.MS,meningitis b. Measure opening pressuree.g. Idiopathic intracranialHTN c. Antibioticadministration d. Chemotherapyadministration 6. Anatomical landmark for lumbar puncture? a. L4/5 (or L3/4) because… spinal cord endsatL1-2Question 08You are shown this prosection of the brain in your anatomy lab. The prof quizzes you on alcohol and its effects on the brain. If a patient presents with ataxia, nystagmus and confusion alongside a known history of alcohol dependency, which area of the brain is impacted? A. A B. B C. C D. D B E E. E A D CYou are shown this prosection of the brain in your anatomy lab. The prof quizzes you on alcohol and its effects on the brain. If a patient presents with ataxia, nystagmus and confusion alongside a known history of alcohol dependency, which area of the brain is impacted? A. A B. B C. C D. D B E E. E A D CThiamine + Wernicke’s Encephalopathy Thiamine Deficiency causes Wernicke’s Encephalopathy. If left untreated can lead to Korsakoff Syndrome. DON’T LEARN: Thiamine (B1) involved in cerebral metabolism. Deficiency leads Classic Triad of Wernicke’s Encephalopathy: to neuronal cell death in mammillary 1. Eyes: nystagmus, bilateral lateral rectus palsies, conjugate bodies and thalamus. gaze palsies 2. Ataxia: broad based gait, cerebellar signs Exam tip: this is not HNN but is in P&I. 3. Cognitive change: acute stupor + coma, later causes Consider how topics overlap when amnestic syndrome with confabulation studying for exams! WKS - more chronic problem you’re trying to prevent DT - deal with it now, medical emergencyQuestion 09 A 72 year old woman presents to A&E with a 1 hour history of difficulty with her speech. She is able to say some words but cannot speak in fluent sentences. She obeys commands. Which area of the brain is involved in this type of dysphasia? A. Superior Temporal Gyrus B. Posterior Inferior Frontal Gyrus C. Occipital lobe D. Post-central gyrus E. Insular cortex A 72 year old woman presents to A&E with a 1 hour history of difficulty with her speech. She is able to say some words but cannot speak in fluent sentences. She obeys commands. Which area of the brain is involved in this type of dysphasia? A. Superior Temporal Gyrus B. Posterior Inferior Frontal Gyrus C. Occipital lobe D. Post-central gyrus E. Insular cortexWatch videos on YouTube of Broca’s and Wernicke’sQuestion 10 Multiple Sclerosis is a progressive inflammatory demyelinating disorder of the central nervous system. Which cells are damaged in Multiple Sclerosis? A. Astrocytes B. Ependymal cells C. Microglia D. Oligodendrocytes E. Schwann cellsMultiple Sclerosis is a progressive inflammatory demyelinating disorder of the central nervous system. Which cells are damaged in Multiple Sclerosis? A. Astrocytes - form the Blood Brain Barrier B. Ependymal cells - specialised epithelium that lines the ventricles and spinal canal, involved in production of CSF C. Microglia - immune protection of the brain, similarly to macrophages D. Oligodendrocytes - CNS cells that form the myelin sheath around axons E. Schwann cells - myelin sheath forming cells of the peripheral nervous system (affected in peripheral demyelinating disorders e.g. Guillain Barre Syndrome, Charcot Marie ToothQuestion 11The embryological development of the nervous system is delicate process and is a vulnerable aspect of development. Spina bifida is a condition that results from failure of this development. Which aspect of embryological process fails to result in spina bifida? A. Thickening of the ectoderm to form the neural plate B. Closure of the cranial neuropore C. Caudal neuropore fusion at day 27 D. Differentiation of neural crest cells to form melanocytes E. Incomplete migration of myenteric plexusThe embryological development of the nervous system is delicate process and is a vulnerable aspect of development. Spina bifida is a condition that results from failure of this development. Which aspect of embryological process fails to result in spina bifida? A. Thickening of the ectoderm to form the neural plate B. Closure of the cranial neuropore - failure results in anencephaly C. Caudal neuropore fusion at day 27 D. Differentiation of neural crest cells to form melanocytes - failure results in albinism E. Incomplete migration of myenteric plexus - failure results in Hirschsprung's DiseaseQuestion 12You are a 4th year medical student in neurology. You are asked a random embryology question about development of the nervous system. What is the embryological origin of the notochord? A. Ectoderm B. Endoderm C. Mesoderm D. Neural crest cells E. Pharyngeal archesYou are a 4th year medical student in neurology. You are asked a random embryology question about development of the nervous system. What is the embryological origin of the notochord? A. Ectoderm - forms the neural tube B. Endoderm C. Mesoderm - appears in the mesoderm to induce neural plate formation before neurulation can begin D. Neural crest cells - ectodermal origin E. Pharyngeal archesNeurulation - complete by week 4 1. Notochord (the nucleus pulposus of adult life) secretes growth factors i.e. noggin, chordin 2. Differentiation and thickening of ectoderm to form neural plate 3. Neural plate folds to form neural tube a. Hinge points b. Cell wedging c. Extrinsic forces 4. Closure of tube a. Begins in cervical region b. Closure moves cranially & caudaully c. Cranial neuropore (closes by day 25) d. Caudal neuropore (closes by day 27) Somites form, flanking the neural tube. Mesodermal origin. They later form vertebrae, ribs, muscles and skinNeural Crest Cells 1. Neural crest cells arise from the neural folds (that allow neurulation) 2. Undergo epithelial-mesenchymal transition as BMP expression stimulates E-cadherin -> N-cadherin. Mesenchymal cells are highlighly migratory. 3. Neural crest cells migrate to form:Brain Formation 1. Cranial end of neural tube swells (week 5) 2. 3 primary vesicles appear (prosencephalon, mesencephalon and rhombencephalon) 3. 5 secondary vesicles develop (telencephalon, diencephalon, mesencephalon, metencephalon, myelencephalon) NOTE: this a hollow tube (neural tube). The hollow centre will form the ventricles and fill with CSF. The actual brain neurones/glial cells originate from the neuroectoderm. Peripheral nerves/glia are from neural crest cellsSpinal Cord Formation Summary: neural tube made up of neuroepithelium (ectoderm) that differentiates into neuroblasts that divides lots and form 3 layers; ependymal lining, mantle (grey matter), marginal (white matter) 1. Caudal neural tube (after 4th pair of somites) forms spinal cord 2. Neuroepithelium make up the ependymal layer (give rise to all neurons, astroglia and oligodendrocytes. Some cells remain ependymal cells to line the spinal canal) 3. Middle layer forms the grey matter a. Alar plate: dorsal horn b. Basal plate: ventral horn 4. Outer part differentiates into marginal layer (gives rise to white matter as axons from ependymal layer extend out)REMEMBER… Neural tube: forms the central nervous system i.e. brain + spinal cord Neural crest cells: form the peripheral nervous system i.e. cranial nerves(!), peripheral nerves, autonomic nerves, Schwann cells, melanocytes, odontoblasts, meninges, bones and muscles of head Notochord: induces formation of the above and persists into adult life as the nucleus pulposusQuestion 13A 35 year old patient presents to GP with ongoing issues with vertigo. She describes vertigo that lasts around 30 mins at a time. It is associated with ringing and difficult hearing in her right ear. She has a constant feeling like water is in her ear. What structure is causing the sensation of C vertigo in this patient? E A. A A B B. B C. C D D. D E. EA 35 year old patient presents to GP with ongoing issues with vertigo. She describes vertigo that lasts around 30 mins at a time. It is associated with ringing and difficult hearing in her right ear. She has a constant feeling like water is in her ear. What structure is causing the sensation of C vertigo in this patient? E A. A A B B. B C. C D D. D E. EVestibular System: Two sets of end organs: 1. Semicircular canals (rotational movement) 2. Vestibule (utricle, saccule)Vestibular System: ● Semicircular canals contain endolymph ● Head rotates and endolymph flows into expansion of canal (the ampulla) ● In the ampulla: ○ Hair cells (with stereocilia on apical surface) move with the endolymph ○ Neurotransmitter released - tells the brain which plane of movement the head is moving in ● Otolith Organs: ○ Movements, cause movement of otoconia ○ Leads to displacement of the hair cellsQuestion 14A 26 year old male is brought to A&E after receiving a head injury in a rugby game. He was struck on the side of the head by another players shoulder and immediately lost consciousness. He is now alert. He receives a CT head which shows a biconvex hyperdensity. Which artery is most likely to have causes this bleed? A. Middle Cerebral Artery B. Middle meningeal artery C. Temporal artery D. Anterior Cerebral artery E. External carotid arteryA 26 year old male is brought to A&E after receiving a head injury in a rugby game. He was struck on the side of the head by another players shoulder and immediately lost consciousness. He is now alert. He receives a CT head which shows a biconvex hyperdensity. Which artery is most likely to have causes this bleed? A. Middle Cerebral Artery B. Middle meningeal artery C. Temporal artery D. Anterior Cerebral artery E. External carotid arteryType of injury Notes Extradural Bleeding into the space between the dura mater and the skull. (epidural) Often results from acceleration-deceleration trauma or a blow to haematoma the side of the head. The majority of epidural haematomas occur in the temporal region where skull fractures cause a rupture of the middle meningeal artery. Features ● features of raised intracranial pressure ● some patients may exhibit a lucid interval Subdural Bleeding into the outermost meningeal layer. Most commonly occur haematoma around the frontal and parietal lobes. Shearing of bridging veins. Risk factors include old age, alcoholism and anticoagulation. Slower onset of symptoms than a epidural haematoma. There may be fluctuating confusion/consciousness Subarachnoid Classically causes a sudden occipital headache. Usually occurs haemorrhage spontaneously in the context of a ruptured cerebral aneurysm but may be seen in association with other injuries when a patient has sustained a traumatic brain injuryBlow tothe sideofhead? Which artery?Middle meningeal Which bone?Pterion Why?Thin areaof the skull, fractures easily.Middle meningeal a. Resides in the extradural space i.e. between bone and duraFalxcerebri/tentorium cerebelli- Folds of duramater.Containthe duralvenoussinuses.Question15A 65 year old man presents to GP with a 4 month history of worsening tension-like headaches. He has lost 10 kg of weight in that same time period. On neurological examination, he has left arm weakness. On fundoscopy, you suspect raised intracranial pressure. Which of the following is a sign of raised intracranial pressure? A. Focal neurological deficit B. Headache worse when standing up C. Papilloedema D. Slurred speech E. Weight lossA 65 year old man presents to GP with a 4 month history of worsening tension-like headaches. He has lost 10 kg of weight in that same time period. On neurological examination, he has left arm weakness. On fundoscopy, you suspect raised intracranial pressure. Which of the following is a sign of raised intracranial pressure? A. Focal neurological deficit B. Headache worse when standing up C. Papilloedema D. Slurred speech E. Weight lossList the signs and symptoms of List the signs and symptoms of raised intracranial pressure basal skull fracture ● Headache: nocturnal, worse on ● Battle’s Sign coughing, worse lying down ● Racoon eyes ● Reduced GCS ● CSF from nose/ears ● Pupil dilation ● Hemotympanum ● Vomiting ● Papilloedema ● Posturing ● Seizures ● Cushing’s triad (hypertension, bradycardia, irregular respiration)TODO: ● Spend a half a day on Anatomy TV doing all year 2 topics ● Make a list of annoying facts to memorise closer to the time ● High yield ● Attend Year 2 BtB MCQ tomorrow…FeedbackForm Please fill out our feedback form! Make sure to put our names down - Emma/Hassan