Beyond the Brain: Year 2 MCQ Q1-25 Explanations
Summary
E. Urine dip and culture MEQ: Explain what is meant by primary, secondary and tertiary peristalsis in the small bowel (3).
Primary peristalsis occurs when a wave is initiated in the large intestine in a conscious patient. It passes up the GI tract causing a localised reflexive contraction of the small intestine. Secondary peristalsis occurs when the primary wave enters the small intestine which then causes a more widespread segmental contraction. It plays an important part in the propulsion of small intestine content throughout the GI tract. Tertiary peristalsis is a wave of contraction that occurs sporadically over an area of the small intestine. It plays a role in mixing the intestinal contents and allowing for the efficient absorption of nutrients.
Learning objectives
E. Urine dip and culture
- Explain the technique, function and significance of investigations to diagnose acute abdominal pain (3).
- Identify and distinguish between the symptoms of acute appendicitis and other causes of abdominal pain (3).
- List the appropriate investigations for acute appendicitis based on symptoms and signs (3).
- Analyse the differential diagnosis of abdominal pain based on the presentation of the case study (3).
- Critically evaluate the validity of the results of the investigations for diagnosis of acute abdominal pain (3).
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Year 2 Mock MCQ 2440051 B@student.gla.ac.uk01The nephron is the functional unit of the kidney. Electrolytes, glucose and amino acids are reabsorbed along the nephron in an attempt to regulate electrolytes and fluid balance. Where is glucose reabsorbed into the bloodstream? A. Distal convoluted tubule B. Proximal convoluted tubule C. Loop of Henle D. Collecting Duct E. GlomerulusThe nephron is the functional unit of the kidney. Electrolytes, glucose and amino acids are reabsorbed along the nephron in an attempt to regulate electrolytes and fluid balance. Where is glucose reabsorbed into the bloodstream? A. Distal convoluted tubule B. Proximal convoluted tubule C. Loop of Henle Proximal Convoluted Tubules D. Collecting Duct 70% Na+, K+ and Cl- E. Glomerulus 100% Glucose 100% amino acids lucose and the Kidney 1. Na+/K+ ATPase on basolateral surface pumps sodium into the extracellular compartment by active transport 2. This creates an electrochemical gradient between tubular lumen and intracellular compartment 3. Na+ is pulled into the cell (out of the lumen) via several transporters - in this case it is SGLT2 4. On the basal surface, Na+ continues to move through Na+/K+ ATPase to the peritubular capillaries BUT Glucose moves through GLUT2 EQ: Describe the reabsorption of glucose in the idney (3)02You are the medical student on the cardiology ward. A 65 year old man is being started in spironolactone as part of a treatment plan for heart failure. The consultant decides to quiz you on the mechanism of diuretics. Which channel in the kidney is directly affected by aldosterone? A. NKCC2 B. ENaC C. Na+/K+ ATPase D. NCC E. SGLT2You are the medical student on the cardiology ward. A 65 year old man is being started in spironolactone as part of a treatment plan for heart failure. The consultant decides to quiz you on the mechanism of diuretics. Which channel in the kidney is directly affected by aldosterone? A. NKCC2 B. ENaC C. Na+/K+ ATPase D. NCC E. SGLT2RAAS MEQ: Describe the factors that result in the production of renin from the juxtaglomerular apparatus (3). RAAS 1. Blood pressure drops 2. This is sensed by the kidneys due to: a. Reduced renal perfusion (detected by baroreceptors in afferent arteriole) b. Reduced Na+ in DCT (detected by macula densa) c. Sympathetic stimulation of JGA via Beta-1 adrenoreceptors 3. Renin released from JGA 4. Renin cleaves angiotensinogen to angiotensin I 5. ACE converts angiotensin I to angiotensin II 6. Angiotensin II release 7. Electrolyte and water retention 8. Increased blood pressure MEQ: Describe 3 functions of angiotensin II (3). MEQ: Explain how the RAAS system leads to the ngiotensin II release of ADH from the pituitary gland (3). 1. Vasoconstriction of arterioles - increase total peripheral resistance 2. Stimulate “thirst” in hypothalamus leading to ADH secretion from posterior pituitary. ADH increase aquaporins causing water reabsorption and concentrated urine 3. Sympathetic stimulation (increase cardiac output, vasoconstriction and renin release) 4. Renal Effects: a. Efferent>Afferent arteriole constriction b. Contraction of mesangial cells (decreases filtration area i.e. reduces GFR) c. Increases Na+/H+ antiporter and thus increase Na+ reabsorption 5. Stimulates release of aldosterone03A 35 year old woman is brought to A&E. Her blood gases show the following. pH 7.28 (7.35-7.45) CO2 48mmHg (35-45mmHg) HCO3- 22mEq (22-26mEq/L) What is the most likely cause of this ABG? A. Acute asthma exacerbation B. Salicylate overdose C. AKI D. COPD E. Cushing’s SyndromeA 35 year old woman is brought to A&E. Her blood gases show the following. pH 7.28 (7.35-7.45) CO2 48mmHg (35-45mmHg) HCO3- 22mEq (22-26mEq/L) What is the most likely cause of this ABG? A. Acute asthma exacerbation B. Salicylate overdose C. AKI D. COPD E. Cushing’s Syndrome 35 year old woman is brought to A&E. Her blood gases show the following. H 7.28 (7.35-7.45) A note on Asthma: O2 48mmHg (35-45mmHg) CO3- 22mEq (22-26mEq/L) ● Exacerbation usually causes a respiratory alkalosis (blowing off lots of CO2) ● In “life threatening” exacerbation, the patient is hat is the most likely cause of this ABG? tiring and therefore retaining CO2. Additionally, a ‘silent chest’ will be heard as they no longer have the power to ventilate the lungs A. Life threatening asthma exacerbation - respiratory acidosis Salicylate Overdose B. Salicylate overdose - metabolic acidosis ● 99% of the time (at year 2) the answer will be C. AKI - metabolic acidosis “metabolic acidosis” D. COPD ● BUT… as the patient compensates by E. Cushing’s Syndrome - metabolic alkalosis hyperventilating, they may be pushed into respiratory alkalosis ● If it’s been a long time after overdose - they may MEQ: Explain why a patient with asthma might now be in respiratory alkalosis begin in respiratory alkalosis but develop acidosis (2).Metabolic Acidosis Metabolic Alkalosis ● Raised Anion gap ● Vomiting ● DKA ● Loop diuretics ● Lactic acidosis ● Thiazides ● Aspirin overdose ● Conn’s Syndrome - high aldosterone levels ● Renal failure ● Cushing’s Syndrome - high cortisol acts like ● Normal anion gap aldosterone and binds to Mineralocorticoid ● Diarrhoea, ileostomy Receptors ● Addison’s disease ● Renal tubular Acidosis Respiratory Acidosis Respiratory Alkalosis ● Decreased ventilation ● Hyperventilation ● COPD ● Anxiety ● Neuromuscular disorders e.g. GBS ● Pain ● Respiratory depression e.g. opiates ● PE ● Life-threatening asthma exacerbation ● Pneumothorax ○04 A 25 year old man presents to A&E with abdominal pain. The pain is localised in the right lumbar region and radiates to the right iliac fossa. It comes and goes and he rates it 9/10 for pain. He has vomited with the pain twice. What investigations is most likely to make a diagnosis? A. CT - KUB B. Ultrasound C. AXR D. Ureteroscopy E. Urine dip and culture A 25 year old man presents to A&E with abdominal pain. The pain is localised in the right lumbar region and radiates to the right iliac fossa. It comes and goes and he rates it 9/10 for pain. He has vomited with the pain twice. What investigations is most likely to make a diagnosis? A. CT - KUB B. Ultrasound C. AXR D. Ureteroscopy E. Urine dip and culture Kidney Stones Types: ○ Calcium containing (caused by calcium saturation i.e. hypercalcaemia, dehydration) ■ Calcium oxalate ■ Mixed calcium phosphate and oxalate ○ Struvite (produced by bacteria in UTIs, present as staghorn calculus) ○ Urate (Uric acid) stones (uric acid more soluble as high pH therefore acidic urine i.e. in chronic acidosis/gout patients, causes uric acid deposition) ○ Cystine stones (genetic component) Presentation ● Colicky ● Loin to groin pain ● Haematuria ● PMH: recurrent untreatable UTIs, GOUT, Myeloma (or other hypercalcaemia causes), dehydration ○Biochemistry ● Urinalysis + microbiology - infection ● FBC/CRP - infection ● U&Es - assess renal function ● Ca++/urate level - narrow down stone type Imaging: ● Ultrasound (will not see stones BUT can identify hydronephrosis/other structural disease e.g. PCKD) ● Non-contrast CT KUB (stones visible) - for ALL pts with renal colic Treatment ● Watch and wait ± NSAIDs ● Shockwave lithotripsy (lithotripsy extracorporeal) ● Percutaneous Nephrolithotomy (intracorporeal lithotripsy) ● Ureteroscopy (insertion of stent)05A 78 year old man presents to A&E with severe abdominal pain. The pain is in the hypogastric region and does not radiate. On examination, his lower abdomen is dull to percussion and his bladder is grossly distended. What step would you take next for this patient? A. Bladder ultrasound B. Catheterisation C. IM diclofenac D. Abdominal X-Ray E. CT-KUBA 78 year old man presents to A&E with severe abdominal pain. The pain is in the hypogastric region and does not radiate. On examination, his lower abdomen is dull to percussion and his bladder is grossly distended. What step would you take next for this patient? A. Bladder ultrasound B. Catheterisation C. IM diclofenac - pain management for renal colic D. Abdominal X-Ray E. CT-KUB Bladder Outflow Obstruction ● Benign Prostatic Hypertrophy ● Kidney stones in bladder neck ● Bladder cancer ● Urethral stricture i.e. Hx of STI, previous catheterisation ● Pelvic tumours i.e. prostate cervix, rectum Main management -> CATHETERISE (+ record residual volume) then investigate06Eleanor is a 5th year medical student on placement in Addiction Services. Here supervisor ask her about the long-term medical management of alcohol dependency. She remembers that there is a drug that causes unpleasant symptoms when it reacts with alcohol due to accumulation of acetaldehyde. Which drug is she referencing? A. Acamprosate B. Diazepam C. Pabrinex D. Naloxone E. DisulfiramEleanor is a 5th year medical student on placement in Addiction Services. Here supervisor ask her about the long-term medical management of alcohol dependency. She remembers that there is a drug that causes unpleasant symptoms when it reacts with alcohol due to accumulation of acetaldehyde. Which drug is she referencing? A. Acamprosate B. Diazepam C. Pabrinex D. Naloxone E. Disulfiram - used in long term management of alcohol dependency, reacts with ethanol to produce unpleasant “hangover” like symptoms with small volumesLong term medical management of harmful drinking ● Naltrexone: opioid antagonist, blocks pleasurable effects of alcohol, making it easier to stop ● Acamprosate: increases GABA and suppresses serotonin ● Disulfiram: reacts with alcohol to cause aldehyde and ● histamine release causing an unpleasant intoxication ORAL THIAMINE: should always be prescribed in heavy drinkers to prevent Wernicke's Encephalopathy NOTE: IV thiamine in acute setting 07 Another RAAS QIn response the low blood pressure the RAAS system works return normal physiology. In the kidney Aldosterone: A. Increase glucose reabsorption in the proximal tubule B. Enhances the countercurrent multiplier system C. Inhibits Na+/K+ ATPase in the distal tubule D. Increases transport of ENaCs from the cytoplasm to the cell membrane E. Leads to insertion of aquaporin channels into the cell membraneIn response the low blood pressure the RAAS system works return normal physiology. In the kidney Aldosterone: A. Increase glucose reabsorption in the proximal tubule B. Enhances the countercurrent multiplier system C. Inhibits Na+/K+ ATPase in the distal tubule D. Increases transport of ENaCs from the cytoplasm to the cell membrane E. Leads to insertion of aquaporin channels into the cell membrane B Aldosterone 1. Released from adrenal cortex (zona glomerulosa, mineralocorticoid) in response to low blood pressure/RAAS activation and production of angiotensin II 2. Acts on principal cells 3. Increase ENaC expression 4. Increase Na+ reabsorption and thus osmotic water movement (increasing blood volume i.e. BP) 5. HYPERKALAEMIA and HYPONATRAEMIA Think… aldosterone antagonists i.e. spironolactone as a K+ sparing diuretic MEQ: Describe the mechanism of aldosterone in maintaining blood pressure (2).08A 67 year old woman presents to the GP with weakness in her right leg. She noticed she was struggling to get up out of chairs over the last 10 days. You perferom a full neurological examination. You note reduced power in the right leg and hyperreflexia of the lower limbs. What is the spinal root of the knee jerk reflex? A. C5-6 B. C7-8 C. L5-S1 D. L3-4 E. CNVA 67 year old woman presents to the GP with weakness in her right leg. She noticed she was struggling to get up out of chairs over the last 10 days. You perferom a full neurological examination. You note reduced power in the right leg and hyperreflexia of the lower limbs. What is the spinal root of the knee jerk reflex? A. C5-6 B. C7-8 C. L5-S1 D. L3-4 E. CNVReflex Nerve supply Jaw Jerk CN V Biceps jerk C5,6 Supinator jerk C6 Triceps jerk C7 Knee jerk L3,4 Ankle jerk L5,S1 Bulbocavernosus reflex S3,4 Plantar reflex S509In order to confirm brain stem death a series of cranial nerve reflexes must be performed. What is the efferent nerve for the pupillary light reflex? A. CN II B. CN III C. CN IV D. CN V3 E. CN VIIn order to confirm brain stem death a series of cranial nerve reflexes must be performed. What is the efferent nerve for the pupillary light reflex? A. CN II B. CN III C. CN IV D. CN V3 E. CN VI MEQ: Fill in the blanks (5). Reflex Afferent Efferent Pupillary Light Reflex A. CNIII Accomodation CNII B. Vestibulo-ocular CNVIII CN C., IV, VI Jaw Jerk CNV3 D. Gag Reflex E. CNXReflex Afferent Efferent Pupillary Light Reflex CNII CNIII Accomodation CNII CNIII Vestibulo-ocular CNVIII CNIII, IV, VI Jaw Jerk CNV3 CNV3 Gag Reflex CNIX CNX10A 45 year old man is diagnosed with optic neuritis after presenting with right sided eye pain and visual disturbance. When performing an examination of his eyes, what sign would you expect? A. Down and out pupil B. Homonymous hemianopia C. RAPD D. Papilloedema E. Nystagmus A 45 year old man is diagnosed with optic neuritis after presenting with right sided eye pain and visual disturbance. When performing an examination of his eyes, what sign would you expect? A. Down and out pupil - Cranial Nerve III palsy B. Homonymous hemianopia - this pt may have total loss/reduced vision of right eye C. RAPD D. Papilloedema - sign of raised ICP E. Nystagmus11You are in an anatomy lab, looking at a prosection of the brainstem. The Professor asks you to point to the structure which is responsible for relaying sensory and motor information between the spinal cord and the cortex. Which number correlated with this structure? A. 1 B. 2 C. 3 D. 4 E. 5You are in an anatomy lab, looking at a prosection of the brainstem. The Professor asks you to point to the structure which is responsible for relaying sensory and motor information between the spinal cord and the cortex. Which number correlated with this structure? A. 1 B. 2 C. 3 D. 4 E. 5MEQ: Outline the function, origin and exit pathway through the skull of CNIII (3).12A 83 year old woman is brought to the GP by her son who is concerned that here memory i getting worse. She has been misplacing keys, leaving the cooker on on multiple occasions. Last week she was found in the street in her pyjamas at 3pm. What protein is misfolded, causing this presentation? A. Tau protein B. Alpha synuclein C. Prion protein D. Neurofibrillary tangles E. MemantineA 83 year old woman is brought to the GP by her son who is concerned that here memory i getting worse. She has been misplacing keys, leaving the cooker on on multiple occasions. Last week she was found in the street in her pyjamas at 3pm. What protein is misfolded, causing this presentation? A. Tau protein B. Alpha synuclein - PD, LBD C. Prion protein - CJD D. Neurofibrillary tangles - Made up of tau protein E. Memantine - cholinesterase inhibitor used to slow progression of AD Alzheimer’s Disease ● Risk factors: repeated head injury, family history, hypothyroidism ● Neurofibrillary tangles (Tau protein) and amyloid plaques in hippocampus and cerebral cortex (frontal and temporal) ● Presentation ○ Short term memory loss (autobiographical memory often preserved) ○ Dysphasia ○ Dyspraxia ○ Behavioural changes e.g. wandering ○ Psychotic symptoms ○ Apathy ● Clinical features: Progressive decline ● Management (improvement of symptoms) ○ Cholinesterase inhibitions e.g. rivastigmine, donepazil (these are shown to SLOW PROGRESSION) ○ Memantine (NMDA antagonist) V ascular Dementia ● Multiple small infarcts or small vessel disease ● Associated with cardiovascular risk factors ● After a stroke ● Presentation ○ Gait disturbance ○ Personality change ○ Labile mood ○ Urinary symptoms ○ Insight preserved ● Clinical features: stepwise progression, cardiovascular risk factors ● Management: modify cerebrovascular risk factors Dementia with Lewy Bodies ● Lewy bodies in cerebral cortex made of alpha synuclein ● Presentation ○ Fluctuating dementia ○ Delirium ○ Parkinsonism ○ Visual Hallucination ○ Sleep disorders ● Clinical features: progressive disease ● Management: rivastigmine might improve symptoms Frontotemporal Dementia ● Atrophy of frontotemporal lobes, without histology of Alzheimer's Disease ● Presentation - DISHINHIBITION ○ Stereotyped behaviours ○ Personality change ○ Loss of insight ○ Expressive dysphasia ○ Preserved memory ○ Primitive reflexes ● Clinical features: ○ Slow progression ○ Family history ○ Women>men with early onset (<70)13John is on a night out with his friends. He consumes 5 pints of lager over a relatively short period of time. Which of the following is true for Johns metabolism of alcohol at this time? A. Aldehyde dehydrogenase activity is inhibited B. MEOS system is metabolising the excess ethanol C. Catalase was responsible for ethanol metabolism before John’s night out D. Acetate formation proportionally increases with alcohol consumption E. ADH pathway results in formation of catalaseJohn is on a night out with his friends. He consumes 5 pints of lager over a relatively short period of time. Which of the following is true for Johns metabolism of alcohol at this time? A. Aldehyde dehydrogenase activity is inhibited: AD activity will increase with increasing ethanol (to a point). This is the rate limiting step. When excess alcohol is consumed (beyond the capacity of the aldehyde dehydrogenase) acetaldehyde accumulates. B. MEOS system is metabolising the excess ethanol - primary system responsible for dealing with excess C. Catalase was responsible for ethanol metabolism before John’s night out - Catalase is minimally responsible for alcohol excess. ADH pathway will be the main metabolism of ethanol before John started consuming alcohol. D. Amitriptyline formation proportionally decreases with alcohol consumption nonsense E. ADH pathway results in formation of catalase - nonsenseAlcohol Physiology Three mechanisms: 1. ADH 2. MEOS 3. Catalase Don’t complicate it. 1. ADH Disulfuram target ● Most ethanol takes this pathway ● Formation of acetate is rate limiting step ● Excess alcohol -> Acccumulation of acetaldehyde Acetaldehyde causes hangover type symptoms2. MEOS ● Kicks in during periods of EXCESS drinking ● Basically, a different pathway (different enzymes) with the same outcome3. Catalase ● <2% of ethanol goes through this pathway ● ?more of a role in the brain where there is less ADH ● AGAIN… just a different enzyme pathway of the same equation14A woman is brought to A&E by the police after being found unconscious in the street. She is alert on arrival to A&E but has little memory of how she got there. oN Examination she has a general tremor and is sweaty. She complains that she feels like she might vomit. You note on her records she is known to Addiction Services. How many hours ago did this patient stop drinking? A. 2 B. 8 C. 24 D. 48 E. 72A woman is brought to A&E by the police after being found unconscious in the street. She is alert on arrival to A&E but has little memory of how she got there. oN Examination she has a general tremor and is sweaty. She complains that she feels like she might vomit. You note on her records she is known to Addiction Services. How many hours ago did this patient stop drinking? A. 2 B. 8 C. 24 D. 48 E. 72 Alcohol withdrawal A variable presentation. Stages 1. (6-12 hours) Minor withdrawal symptoms e.g. tremor, anxiety, headache, NV, sweating 2. (12-24 hours) Alcoholic hallucinosis 3. (24-48 hours) Alcohol withdrawal seizures - GTC 4. (48-72 hours) Delirium Tremens Treatment aim? STOP DELIRIUM TREMENS15The ICD-11 has several criteria for the diagnosis of ADHD. Which of these is not a feature of diagnosis? A. Pervasive B. Excessive for developmental age C. Apparent after age 18 D. Inattention E. Features of HyperactivityThe ICD-11 has several criteria for the diagnosis of ADHD. Which of these is not a feature of diagnosis? A. Pervasive B. Excessive for developmental age C. Apparent after age 18 - must be apparent after age of 7 D. Inattention E. Features of Hyperactivity16The physiology of the bladder requires a delicate balance of sympathetic, parasympathetic and somatic innervation. Which of the following is true for the control of the bladder? A. Storage phase is controlled by hypogastric nerve B. Detrusor muscle contracts during storage phase C. Pudendal nerve controls the internal urethral sphincter D. Storage phase is controlled by T1 E. Pudendal nerve controls micturition contractionsThe physiology of the bladder requires a delicate balance of sympathetic, parasympathetic and somatic innervation. Which of the following is true for the control of the bladder? A. Storage phase is controlled by hypogastric nerve B. Detrusor muscle contracts during storage phase C. Pudendal nerve controls the internal urethral sphincter D. Storage phase is controlled by T1 E. Pudendal nerve controls micturition contractionsIn bladder physiology… Bladder + internal urethral sphincter = under autonomic control External urethral sphincter = under somatic control Storage phase - SYMPATHETIC 1. Stimulus: afferent sensory fibres (that travel in the hypogastric, pelvic & pudendal nerves) communicate with the cerebral cortex - give information about filling 2. Impulses from cerebral cortex travel to pontine continence centre (coordinates bladder/sphincters) 3. Afferents sent to sympathetic nuclei (T10-L2) 4. Post ganglionic fibres to detrusor muscle and internal urethral sphincter (via hypogastric nerve) 5. The sympathetic innervation causes: a. Detrusor muscle relaxation b. Contraction of internal urethral sphincter NOTE: towards the end of this phase there are micturition contractions starting to occur but not at the threshold frequency and intensity to cause detrusor muscle relaxation.Voiding Phase - PARASYMPATHETIC 1. Voluntary decision to urinate 2. Impulse from pontine micturition centre excite the sacral preganglionic neurons 3. Stimulation of pelvic nerve (S2-4) 4. ACh acts on the bladder and leads to: 5. Detrusor muscle contractions Also… pontine micturition centre inhibits Onuf’s nucleus (suppresses sympathetic outflow). This causes relaxation of the internal urethral sphincter. Voluntary Voiding: voluntary contraction of the external urethral sphincter under the innervation of the pudendal nerve (until a convenient time)17A 68 year old woman presents to A&E with delirium. Her urine dip is normal. Normal breath sounds on auscaltation. ECG shows normal sinus rhythm. Her bloods come back and show hypokalaemia. Which medication is responsible for hypokalemia? A. Eplerenone B. Furosemide C. Bendroflumethiazide D. Spironolactone E. RamiprilA 68 year old woman presents to A&E with delirium. Her urine dip is normal. Normal breath sounds on auscaltation. ECG shows normal sinus rhythm. Her bloods come back and show hypokalaemia. Which medication is responsible for hypokalemia? A. Eplerenone B. Furosemide C. Bendroflumethiazide D. Spironolactone E. Ramipril Diuretics 1. Loop Diuretics e.g. furosemide a. Inhibit NKCC2 in thick ascending limb b. Adverse effects: Hypokalaemia (may be coupled with K+ sparing diuretic) c. Uses: Heart failure, liver failure 2. Thiazide Diuretics e.g. bendroflumethiazide a. Inhibit NaCl in DCT 3. K+ Sparing e.g. a. ENaC inhibitors e.g. amiloride b. Aldosterone antagonists e.g. Spironolactone18The development of the central nervous system is complex. Around week 4 the development of the eyeball begins. What is the origin of the lens of the eye? A. Surface ectoderm B. Diencephalon C. Metencephalon D. Myelencephalon E. MesodermThe development of the central nervous system is complex. Around week 4 the development of the eyeball begins. What is the origin of the lens of the eye? A. Surface ectoderm B. Diencephalon C. Metencephalon D. Myelencephalon E. MesodermAs a reminder from last night… At day 22, shallow grooves appear in the sides of the forebrain (INSIDE THE NEURAL TUBE) Then… Diencephalon neuroectoderm 1. Optic sulcus grows outwards into the mesoderm to form optic vesicle 2. Continues to grow laterally to form optic vesicle (remain connected to forebrain by optic stalk)Lens placode: 1. Optic vesicle meets surface ectoderm and regionally thickening forms the lens placode. 2. Lens placode depresses to form lens pit.● Optic vesicle invaginates and forms a double walled optic cup ● Eventually the lumen (intraretinal space) is lost and the retina forms ● Invagination also happens on the inferior surface to form the choroid fissure ● The hyaloid artery supplies the inner chambers of the eye (passing through the choroid fissures) ● By week 7, the choroid fissure fuses and the mouth of the optic cup forms the pupilBack to the lens… ● Cells of the surface ectoderm elongate to form the lens placode ● Eventually the lens will lose contact with surface ectoderm and lie in the optic cupRetina, Iris & Ciliary Body ● Retina: outer pigmented layer and inner neural layer - division and differentiation of the walls of the optic cup ○ Posterior ⅘ forms rods & cones ○ Anterior ⅕ will form the ciliary body and iris ● Sphincter and dilator pupillae come from loose mesenchyme between optic cup & surface ectoderm Choroid, Sclera & Cornea Loose mesenchyme ● Inner layer differentiates into a layer similar to pia - goes on to form the choroid ● Outer layer forms a layer similar to the dura - goes on to form the sclera ● Layers continuous with the optic nerve ● CORNEA? ○ Anterior mesenchyme forms cornea ○ Vacuolation forms anterior chamber & posterior chamber Vitreous Body The mesenchyme also penetrates the optic cup. Facilitated by choroid fissure. Forms the hyaloid vessels & vascular surface of the retina. Interstitial space of this mesenchyme will fill with the gelatinous vitreous body. Hyaloid vessels disappear in foetal life.19The adolescent brain development is closely linked to the behaviours of this age group. Adolescents classically carry out risky behaviours without consideration of the consequences. Which part of the adolescent brain is responsible for this risk taking behaviour? A. Ventricles B. Temporal lobe C. Limbic System D. Prefrontal cortex E. Mammillary bodiesThe adolescent brain development is closely linked to the behaviours of this age group. Adolescents classically carry out risky behaviours without consideration of the consequences. Which part of the adolescent brain is responsible for this risk taking behaviour? A. Ventricles B. Temporal lobe C. Limbic System D. Prefrontal cortex E. Mammillary bodies Changes of Brain in Adolescence ● Increase in cortical grey matter from back to front ● Limbic system develops before prefrontal cortex ● Prefrontal cortex: proliferation during early adolescence followed by myelination and synaptic pruning Limbic system -> prefrontal cortex means adolescents priorities reward seeking behaviours > executive planning/risk assessment20An 85 year old man is brought to A&E by his daughter. She is concerned that he has dementia. Over the last 72 hours he has been very confused and aggressive. He did sleep at all for the last two nights but has been napping in front of the TV during the day. At the moment her is calm and is wondering what all the fuss is about. What is the most likely diagnosis? A. Alzheimer’s Disease B. Subdural hemorrhage C. Frontotemporal dementia D. Delirium secondary to UTI E. DepressionAn 85 year old man is brought to A&E by his daughter. She is concerned that he has dementia. Over the last 72 hours he has been very confused and aggressive. He did sleep at all for the last two nights but has been napping in front of the TV during the day. At the moment her is calm and is wondering what all the fuss is about. What is the most likely diagnosis? A. Alzheimer’s Disease - history would be more insidious B. Subdural hemorrhage - fluctuating confusion/consciousnes? BUT would be slower onset symptoms C. Frontotemporal dementia - personality change D. Delirium secondary to UTI - classic delirium, flipped sleep-wake cycle, abrupt onset, fluctuating symptoms, Age makes UTI likely E. Depression - anhedonia, low mood and fatigue present on most days for at least 2 weeksDementia vs Delirium21You are 3rd year medical student in Neurosurgery. One of the surgeons asks you to interpret this CT head. What is the likely cause? A. Patient who has fallen with a background of alcohol dependency B. Traumatic head injury C. Elderly patient who has slipped in the shower D. Patient with uncontrolled hypertension E. Patient with a family history of Adult Polycystic Kidney Disease (APKD)You are 3rd year medical student in Neurosurgery. One of the surgeons asks you to interpret this CT head. What is the likely cause? A. Patient who has fallen with a background of alcohol dependency B. Traumatic head injury C. Elderly patient who has slipped in the shower D. Patient with uncontrolled hypertension E. Patient with a family history of Adult Polycystic Kidney Disease (APKD)Type 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 injury22A 58 year old man is due to receive a nephrostomy tube due to severe pain caused by a renal calculus in the renal pelvis. It is causing a significant hydronephrosis. You decide to study the anatomy of the layers of the kidney before watching the procedure. What structure is indicated by the number “4”? A. Renal capsule B. Gerota’s Fascia C. Perirenal fat D. Renal pelvis E. Renal cortexA 58 year old man is due to receive a nephrostomy tube due to severe pain caused by a renal calculus in the renal pelvis. It is causing a significant hydronephrosis. You decide to study the anatomy of the layers of the kidney before watching the procedure. What structure is indicated by the number “4”? A. Renal capsule B. Gerota’s Fascia C. Perirenal fat D. Renal pelvis E. Renal cortex 1. Parenchyma 2. Cortex 3. Medulla 4. Perirenal fat 5. Capsule 6. Ureter 7. Pelvis of kidney 8. Renal vessels 9. Hilum 10. Calyx Coverings of the Kidney 1. Gerota Fascia (Anterior perirenal fascia) 2. Zuckerkandl fascia (posterior perirenal fascia)21A patient presents with acute on chronic right sided loin to groin pain. They have vomited twice. What type of renal stone is visible in this case? A. Cysteine B. Calcium oxalate C. Mixed D. Uric acid E. StruviteA patient presents with acute on chronic right sided loin to groin pain. They have vomited twice. What type of renal stone is visible in this case? A. Cysteine B. Calcium oxalate C. Mixed D. Uric acid E. Struvite Kidney Stones Types: ● Calcium containing (caused by calcium saturation i.e. hypercalcaemia, dehydration) ○ Calcium oxalate ○ Mixed calcium phosphate and oxalate ● Struvite (produced by bacteria in UTIs, present as staghorn calculus) ● Urate (Uric acid) stones (uric acid more soluble as high pH therefore acidic urine i.e. in chronic acidosis/gout patients, causes uric acid deposition) ● Cystine stones (genetic component) Presentation ● Colicky ● Loin to groin pain ● Haematuria ● PMH: recurrent untreatable UTIs, GOUT, Myeloma (or other hypercalcaemia causes), dehydration22In embryology, the nervous system arises from several embryological structures. What is the origin of the melanocytes? A. Neural tube B. Notochord C. Mesoderm D. Neural crest cells E. SomitesIn embryology, the nervous system arises from several embryological structures. What is the origin of the melanocytes? A. Neural tube B. Notochord C. Mesoderm D. Neural crest cells E. Somites23The management of ADHD involves a biopsychosocial approach. Children who are offered medication must be closely monitored. Which of the following side effects is important to monitor in children starting mycophenolate? A. Weight gain B. Vision loss C. Anhedonia D. Growth delay E. Postural hypotensionThe management of ADHD involves a biopsychosocial approach. Children who are offered medication must be closely monitored. Which of the following side effects is important to monitor in children starting mycophenolate? A. Weight gain B. Vision loss C. Anhedonia D. Growth delay E. Postural hypotension24You are a 3rd year medical student sitting their end of year OSCE examination. During an examination of the abdomen you forget to ballot the kidneys. You only remember once the examiner asks you about kidney anatomy. What is the vertebral level of the kidney? A. T8-L4 B. T12-L1 C. T12-L3 D. T11-L3 E. L4-L5You are a 3rd year medical student sitting their end of year OSCE examination. During an examination of the abdomen you forget to ballot the kidneys. You only remember once the examiner asks you about kidney anatomy. What is the vertebral level of the kidney? A. T8-L4 B. T12-L1 C. T12-L3: the kidneys are around 3 vertebrae long, with the right kidney sitting slightly lower due to the presence of the liver D. T11-L3 E. L4-L5 - this is where the lumbar puncture needle should be inserted (spinal cord ends at L1-2)25You are taking a history from a patient during you psychiatry block. The patient is agitated as they believe they are not being treated properly. They describe their bowel is covered in spiders. She was angry at the consultant this morning when it was mentioned that what she is feeling may be a symptom of ongoing psychiatric disease. What is this an example of? A. Illusion B. Hallucination C. Delusion of grandeur D. Pseudohallucination E. Blunted affectYou are taking a history from a patient during you psychiatry block. The patient is agitated as they believe they are not being treated properly. They describe their bowel is covered in spiders. She was angry at the consultant this morning when it was mentioned that what she is feeling may be a symptom of ongoing psychiatric disease. What is this an example of? A. Illusion - a misperception of an external stimuli. If this was the case, the patient would be having bowel symptoms that they think are spiders. B. Hallucination - a misperception in the absence of external stimuli. No pathology for this patient. Not an illusion as there is no external stimulus. C. Delusion of grandeur D. Pseudohallucination - hallucination where the patient has insight. If this was the case pt would not be agitated as they would know that there are no spiders in their bowel E. Blunted affect Definitions in your ILOS 1 Psychosis: an altered relationship with reality Delusion: a false belief held with absolute conviction and out of keeping with the patients culture, social and religious beliefs e.g. partner is cheating on you Hallucination: perception in the absence of a stimulus, perceive objective space with the qualities of normal perceptions e.g. you see a person in an empty room Definitions NOT in your ILOS (but Glasgow exams…) Pseudo-hallucination: usually auditory, true externally sited hallucinations, but with insight into their imaginary nature Illusion: misperceptions of external stimuli, most likely when the general level of sensory stimulation is reduced e.g. someone with dementia interpreting a chair in an empty room as a person Illusion vs hallucination? Illusion has an external stimulus, hallucination does notThank Y ou! Please fill out our feedback form! Make sure to (Emma/Lulu) mentions names