Session 5 Neurology .uk



EMQ Revision Notes (Sessions 5-8)These notes have been made from the learning slides of the previous 2-3 years of EMQ sessions. There may be some repetition of material and this document is not exhaustive. 2008 team; Retesh Bajaj, Maresa Brake, Raekha Kumar2009 team; Retesh Bajaj, Maresa Brake, Raekha Kumar, Jayna Patel, James Masters 2011 team; Amar Shah, Navdeep Singh Alg, Upama Banerjee, Daniel Halperin; Marta Mlynarczyk, James Renshaw2012 team: Amar Shah, Navdeep Singh Alg, Upama Banerjee, Daniel Halperin, Marta Mlynarczyk, Chris Hogan, Hannah Barrett, Anand Ramesh 2013 team: Hannah Barrett, Anand Ramesh, Hannah Brooks, Majd Al-Harasees, Frances Conti-Ramsden, James GilbertCompiled by Hannah Brooks, Majd Al-Harasees, Frances Conti-Ramsden and James GilbertMedical Education Revision notes (session 5- 8)Session 5 NeurologyHeadacheMigraineEpidemiology: F>M, adolescence, 70% FH, rare for onset > 50 .Presentation: Headache typically unilateral, throbbing, associated nausea, vomiting, photophobia, phonophobia. Can be associated with certain foods eg. Wine, chocolate as precipitants.Aura: 15-30 mins, followed by headache within 1h. Can be any modality.Visual: distortions, shimmering lines, scotoma, hemianopia. MOST COMMON.Somatosensory: paraesthesiaeMotor: dysarthria, ataxia, hemiparesisSpeech: dysphasiaDDx: TIA Ix: nil Management: pain relief, prophylaxis (severe)Cluster headaches – daily clusters for 4-6 wks then nothing for monthsM>>>F (middle aged men)Intense pain at night – getting out of bed and walking relievesLacrimation,ptosis during attackBIH (benign intracranial hypertension) – middle-aged, large womenPapilloedema, blurred visionHigh intracranial pressure: Headaches (dull pain all over) worse on cough, stooping strainingWorse in the morning, and lying downAssociated signs: Papilloedema, fits, vomiting, drowsiness, behavioural changes, false localising signs (CN VI palsy)Space occupying lesions: present with raised ICP as above. + Focal neurological signs: Suggestive of mass e.g. tumour, abscess. Meningitis and SAH (sub-arachnoid haemorrhage)Both cause meningism (neck stiffness, photophobia and headache)SAH – more sudden, ‘worse headache ever’Associated with PCKD – Berry aneurysms in the Circle of WillisMeningitis – look for fever and rashes; Kernigs signTension headache – stress, ‘tight band’Trigeminal neuralgia – pain on TOUCHING the faceDivision of the trigeminal nerveCf. temporal arteritis/giant cell arteritis – ‘tender’ to touch...Epidemiology: rare, typically > 50, 2:1 F:MPresentation: Unilateral/bilateral FRONTAL headache with scalp tendernessReproduced by pressing on temples, may feel thickened pulseless temporal arteriesJaw claudication (pain on chewing), amaurosis fugaxAssociated: polymyalgia rheumatica (painful shoulders)Ix: temporal artery biopsy, high ESRTx: STEROIDS urgently (empirical high dose prednisolone) without awaiting results of biopsy, as untreated risk of BLINDNESS. 3000 people/yr are blinded by temporal arteritis. SinusitisFeverNasal obstruction/ purulent nasal dischargeLoss of smellAggrevated by bending overSubdural HaematomaPresentation: Insidious; over days/weeks, no symptoms/worsening confusion as venous pressure builds slowly. Is a slow bleed (cf. extradural). Typically fluctuating loss of consciousness, confusion, ataxia.Typical groups:Alcoholics: as fall overElderly: brain atrophies, pulls on venous sinuses which are then more likely to tearAetiology: Can occur after minor head trauma! So there may be no history of head trauma.Ix: URGENT CT head, see crescent shaped bleed.Management: May need neurosurgical decompression.Extradural Haemorrhage. A Neurosurgical emergency.Presentation: High impact trauma e.g. cricket ball, RTA. Often impact at pterion, MMA (middle meningeal artery) sheared. Typically short history; blackout on impact, then lucid interval, followed by rapidly declining neurological status (to unconscious/dead)Increasing pressure: risk of brain herniationIx: URGENT CT head, see lens shape bleed (see below).Management: neurosurgical evacuationMeningitis – see belowNeuro-muscular DisordersMG (Myasthenia Gravis)Young women with muscle weaknessAntibody to ACh receptor on post-synaptic membraneProgressive weakness, difficulty swallowing, eye involvement (bilateral ptosis)Edrophonium testEMG – decreased muscle action after continuous stimulationLEMS (Lambert-Eaton myasthenic Syndrome) hyporeflexia, autonomic disturbancePre-synaptic membrane antibody to Ca2+ receptorAssociated with small cell lung CaNO EYE INVOLVEMENT Increased muscle action after continuous stimulationMyotonic dystrophySleepy, balding, diabetic men with cataractsDistal muscle weakness and wastingFamily history (with genetic anticipation)MND (Motor Neurone disease) – UMN and LMN signsEyes unaffected, tongue fasciculationUMN signs in lower limbsLMN signs in upper limbsNO SENSORY LOSSPost- infectious Neurological syndromesGuillian-Barre – Campylobacter infectionAscending paralysis 2-3 wks after infection‘walking on air’Miller-Fischer - triad of:Ophthalmoplegia AtaxiaAreflexia MeningitisDiseaseCSF PressureGlucoseProteinCellsBacterialRaisedDOWNUPUP – NEUTROPHILSTBMay be normalDOWNUPUP – LYMPHOCYTESViralNormalNORMALNORMAL LYMPHOCYTESInfective organisms: (that cause meningitis)Meningococcus – Gram negative (diplococcus) sepsis, purpuric rash etcStrep pneumoniae – alcoholic, elderly, skull fractureHiB (Haemophilius Influenza)M TbListeria – pregnant, alcoholic, immunocompromised (Cryptococcus) - HIV TreatmentTB – 12 monthsMeningococcus – ceftriaxone+ Dexamethasone in children w/S.pneumoniaeMultiple SclerosisOptic neuritis/ visual disturbance Weakness/ numbness/ tremor/ bowel or bladder disturbance. Increased CSF protein, oligoclonal IgG bands on electrophoresis.F>MRelapsing remittingEye signs – early...Optic neuritisTransient blindnessBlurred visionMRI – demyelination Oligoclonal bands in CSF (antibodies)Lhermitte’s sign and Uthoff’s phenomenon Dizziness and vertigoRamsay Hunt syndrome - Ramsay Hunt syndrome is a herpes zoster infection of the geniculate ganglion. O/E – paralysis of facial muscles on affected side, herpetic eruption on ear canal, tinnitus, hearing loss vertigo. Aciclovir is the treatment of choice. Menière’s disease triad – vertigo, tinnitus and deafness. Aetiology unknown (accumulation of endolymph). Patient generally 40-60, ? of cases are bilateral. Causes intermittent rotational vertigo lasting a few hours with distorted hearing. Vertigo can be disabling – so patient may vomit or call an ambulance. Benign paroxysmal positional vertigo - BPPV occurs due to otolith stimulation of the auditory canal for several seconds after head movement. Patients have short episodes of vertigo triggered by head movement, often rolling over in bed. Diagnosis confirmed by Hallpike test and treated with Epley manoeuvre. Without Epley resolution usually occurs within weeks.Lateral medullary syndrome - Eponymously known as Wallenberg’s syndrome. Posterior inferior cerebellar artery occlusion Ipsilateral signs;- Decreased pain and temperature sensation of face- Vocal fold paralysis- Horner’s syndrome- Cerebellar signsContralateral signs;-decreased pain and temperature sensation of the bodyVestibular neuronitis/ Labyrinthitis - most common cause of vertigo, may be viral in origin. In an EMQ the person will have had a previous viral infection, probably the flu. Causes ‘explosive’ severe vertigo, vomiting and ataxia. No tinnitus or deafness. Symptoms settle over a few days but manage with antiemetics for patient comfort. Some patients go on to develop BPPVStrokeOver 24 hours!Haemorrhagic (15%) vs ischaemic (85%)NEED CT head to rule out haemorrhagic 300 mg aspirin chewed – 1st line treatment + heparinHaemorrhagic… neurosurgical referralCollapseEither Cardiovascular or Neurological!Risk factors (age, PMH)Neurological: (causes)Meningitis:Pyrexia – infection!Meningeal irritation – neurological symptomsPurpuric rash in meningococcal septicaemiaiv benzylpenicillinNormal Pressure Hydrocephalus:Triad of: cognitive impairment, gait dyspraxia (falls), urinary incontinenceSubcortical dementiaSubarachnoid haemorrhage:Sudden onset, occipital headacheSyb-hyloid haemorrhageFH of Polycystic Kindey DiseasePostural Hypotension:DM – Autonomic NeuropathyAntihypertensive medicationAlcohol Induced Cerebellar Syndrome:Signs of Chronic Liver DiseaseDANISH (signs of a cereballar problem:Dysdiadochokinesia; Ataxia; Nystagmus; Intention tremor; Slurred Speech/dysarthria; HyporeflexiaSeizures: (causes)Hyponatraemia (Esp if serum Na+ <115 mmol/L)Presentation (related cerebral oedema): N&V, confusion, lethargy, agitation, headache, seizuresAetiology: SIADHIatrogenic. Culprits: in the elderly: Bendroflumethiazide, thiazide and loop diuretics, ARBs, ACEi, SSRIs, PPIs and mnay many more…Management hyponatraemia:Dependent on cause, fluid restriction may be enough, or cautious replacement 0.9% saline (beware CPM – central pontine myelinolysis)Emergency (seizures): Consider hypertonic saline, aim for gradual increase 125 mmol/L, care CPM. NEVER correct Na >15mmol/L per day chronic, or >1mmol/L per hour acuteHypocalcaemiaPresentation: Chvostek’s sign: twitching of facial muscles induced by gently tapping cheekTrousseau’s sign: tetanic spasm in fingers and hand after inflating cuff for several minutes when taking BP. Due to hypocalcaemia -> hyperexcitability of nervesOthers: confusion, cramps, perioral numbness/paraesthesia, laryngospasm, seizures. Causes: Transient post-thyroidectomy hypocalcaemia (?cause)Inadvertent parathyroidectomy at thyroidectomy (LT)HypoparathyroidismVit D deficiencyRespiratory alkalosis (Hyperventialtion ->, alkalinsation increases Ca-binding capacity of pp, reduces ionized Ca2+)Management: Mild: oral Ca, severe 10 mL 10% calcium gluconate IV.Delirium TremensMust assume as a possibility in all patients within the first 4 days of admission with new onset seizures.= severe alcohol withdrawal, complicated by delirium, sudden and severe mental or NS changes. Most often within 96 h of last drinkMental function: agitation, confusion, hallucinations, illusions (Lilliputian, formication), clouding consciousness, mood changesNS function: Tremor: coarse, irregular, Autonomic overactivity: Raised HR, RR, BP, sweating, dilated pupils, Seizures: most common 12-48 h after last drink.Management: Fluid and electrolyte replacement, parenteral thiamine, asses/tx for infection and sedation with BZD regime e.g. chloridazepoxide.Hypomagnaesaemia S/e of frusemide Decompensated hepatic failureHepatic encephalopathyHypoglycaemiaGliclazideOral hypoglycaemicsulfonylureaEpilepsy= tendency to recurrent unprovoked seizures.ClassificationPartial/focal:Simple: awareness unimpaired, focal symptoms, no post plex: impaired awareness, often post-ictal.2* generalisation: 2/3rds of partial, spread -> general.Generalised: unconscious, therefore incontinence, tongue biting. - Tonic: ridigity- Clonic: rhythmical muscle jerksManagementType of Epilepsy1st line TxFocal/Partial seizuresCarbamazepine or LamotrigineGeneralised tonic clonic (GTC) Sodium valproate (note teratogenecity) or LamotrigineAbsence seizuresEthosuximide or sodium valproateMyoclonicSodium valproate Tonic/Atonic seizuresSodium valproateSo if in doubt, sodium valproate is a good guess, apart from females of reproductive age, as due to teratogenicity of valproate, lamotrigine is a better choice.Status epilepticus= >30 mins seizure, or without full conscious recovery between several seizures)—Management:—Airway: open and maintain airway—Breathing: 100% 02 + suction as required—Circulation: IV access and take bloods (routine, toxicology, blood glucose, anticonvulsant levels)—Anti-convulsants: —Community/No IV access: Buccal midazolam/rectal diazepam in community or no IV access—Hospital: IV lorazepam bolus. —Administer max 2 doses of 1st line Tx (inc pre-hospital tx). —If seizures continue administer IV phenytoin infusion.—If still refractory, call for senior anaesthetic help.Dementia (causes)Vascular dementia:Previously ‘multi-infarct disease’ – due to recurrent cerebral infarctsStep-wise loss of cognitive functionFrontal lobe dementia:Early personality changes with relative sparing of intellectAlzheimer’s Disease: - The commonest of all dementiasInsidious deterioration of cognitive function, associated with dyspraxia, visuospatial and speech problemsInitial phases with short-term memory lossFolstein test:Cognitive test, tests short-term memory, long-term memory and cognitive skills (e.g. concentration)Out of 30, 23-26 mild impairment, 16-22 moderate to severe impairment, ≤15 severe impairmentHypothyroidism:Reversibe cognitive impairment providing no other underlying dementia Alcoholic dementiaLong-term excessive drinkingSymptoms similar to Alzheimer’sDepressive pseudo-dementia Alcohol related:Wernicke’s encephalopathy – nystagmus/ opthalmoplegia/ ataxia. Thiamine def.Reversible….Untreated -? Korakoffs- Korsakoff’s syndrome – gross defect in memory of recent events. Confabulation.IrreversibleUnilateral facial palsyAcoustic neuroma – benign/ hearing deficit/ 5/6/7 can be affectedRamsay Hunt – form of herpes zoster of the geniculate ganglion. LMN facial palsy, with herpetic vesicles in the EAM / soft palate. DeafnessGait disturbancesAntalgic gait: associated with osteoarthritisCerebellar ataxia: signs of chronic liver disease and cerebellar disease evidenced by dysdiadochokinesia and past pointing, pts classically have a wide-based ataxic gaitFestinating gait: pt has parkinsonism, most likely due to idiopathic PD, no arm swing, characterized by a flexed trunk with the legs flexed stiffly at the knees and hips. The trunk is the part of the body below the head, not including the arms and legs. People with festinating gait take short steps, which eventually become faster. The steps become faster because the person is trying to catch up with him/herself, since is/her center of gravity (the part where the entire weight of the body is concentrated) has been altered.Hemiparetic/ circumducting gait: pt with hemiplegiaHysterical gait: foot dragged or pushed ahead, pt with hysterical neurosis i.e. somatoform disorder Scissoring gait: most common in pts with spastic cerebal palsy, Legs flexed slightly at the hips and knees, giving the appearance of crouching, with the knees and thighs hitting or crossing in a scissors-like movement. Often mixed with or accompanied by spastic gait, a stiff, foot-dragging walk caused by one-sided, long-term muscle contraction.Sensory ataxia: pt has developed a high stepping gait consistent with sensory ataxia due to peripheral sensory neuropathy, pt described as anaemic which suggests possible B12 deficiencyTrendelenburg gait: due to severe osteorarthritis around the hipsWaddling gait: pt has been on long term steroids, which has caused secondary Cushing’s and proximal myopathy as evidencedby the weakness of the upper limbs in abduction and being unable to stand from a sitting position, proximal myopathy produces a “waddling” gaitSpecific nerve lesions – Limb;Ulnar nerve lesions = wasting of hypothenar eminence, sensory loss over medial one and a half fingers, claw hand deformity, can test for weakness in abductor digiti minimi.Median nerve lesions = wasting of thenar eminence, sensory loss on lateral palmar surface of three and a half digits, test for weakness in abductor pollicis brevis, affected in carpal tunnel syndrome.Radial nerve lesion = paralysis in extensors of the wrist causing wrist drop, sensory loss on dorsal surface of most of the first three digits.Tibial nerve lesions = inability to invert foot or stand on tiptoes, sensory loss over the sole of the footCommon peroneal nerve lesions = Weakness in dorsiflexion and eversion of foot, sensory loss over dorsum of the foot.Optic;Superior quadrantopia = temporal lobe lesionInferior quadrantopia = parietal lobe lesionHomonomous hemianopia = optic radiation, visual cortex injuryCentral scotoma = macula (degeneration or oedema)Bitemporal hemianopia = chiasma lesionsCerebral venous thrombosisPreggers, thrombophiliacs…Presents as raised ICPCushing’s reflex!SACDBilateral, absent ankle jerks, spastic paraparesis, peripheral neuropathySE Asian womenFolate – will worsen it!!Rx - B12 Miscellaneous conditions with neurological symptomsSyringomyelia - Due to a fluid filled cavity (syrinx) in spinal cord. Compression of the ord results in loss of pain and temperature first as compresses the decussating spinothalamic fibres anteriorly in the ventral horns. Often ‘cape distribution’. Wasting/weakness due to involvement of cervical anterior horn cells. Patient may have Charcot’s joints and horners syndrome. Can be associated to an Arnold-Chiari malformationVon Hippel Lindau – Von Hippel Lindau is an AD defect on chromosome 3. Syndrome characterised by retinal and intracranial haemangiomas and haemangioblastomas, renal cysts, renal cell adenocarcinoma, pancreatic tumours and phaeochromocytomas. Presenting complaint for one of the tumours e.g. phaeochromocytoma (neuro link is that patient will present claiming they have frequent panic attacks – EMQs stems sometimes have tenuous connections)but PMH of other tumoursNeurofibromatosis is an AD disorder characterised by the development of multiple neurofibromas from the sheaths of central and peripheral nerves. There are 2 types;Type 1 = ‘peripheral form’ (70% of cases), patient has multiple cutaneous neurofibromas, café-au-lait patches, axillary/inguinal freckling and hamartomas on the iris (Lisch nodules). Also known as von Recklinghausen’s diseaseType 2 = ‘central form’, few or no cutaneous lesions but development of bilateral neural tumours.Brown-Séquard syndrome = unilateral transection (/Hemisection) of the spinal cord. Ipsilateral loss of motor function with impaired proprioception and vibration sense. Contralateral loss of pain and temperature sensation. -657225370205Glasgow Coma Scale (GCS)EO – Eye opening: 1-4BMR – Best motor response: 1-6BVR – Best eye opening response: 1-5MINIUMUM SCORE: 3Head InjuryGCS 8: EO: 2, BMR: 4 normal flexion (withdraws from pain), BVR: 2 incomprehensible sounds – GCS 8: Severe head injuryExtradural haematoma: classically a lucid interval before a rapid decline, GCS 12GCS 11: EO to pain: 2, BMR: 5 localises pain, BVR: 4 confused speech; moderate head injury (GCS 9-13)Basal skull fracture: Evidenced by characteristic signs: “panda or racoon eyes”, subconjunctival haemorrhage, otorrhoea from eyes, not emergency, but should be admittedSubdural haematoma: Due to rupture of bridging vein, GCS 5, death imminent withoutintervention, long-term prognosis poorSession 6 – Renal medicine and urologyHaematuriaHx: Timing is importantBleeding at the start – think urethral/ prostate causeBleeding at the end – think more bladder causeIf painful as well – think infection!Painless – think cancer!Causes:Bladder cancer:Presentation bladder cancer: M:F 4:1, peak 60-70.Painless haematuria (bladder cancer until proven otherwise, can be intermittent), Recurrent UTIs, Voiding irritabilityTwo types:Transitional cell carcinoma – 90% - common in westSquamous cell carcinoma – 7% - associated with shistosomiasis Risk factorsTCC: 90% transitional cell carcinoma (cells line kidney -> urethra). Smoking, aromatic amines (rubber), alanine dyes, dry cleaning, pesticides. Cyclophosphamide, pelvic irradiationSCC: 10%. From chronic inflammation/irritation.Developed: Stones, infection, LT catheters, Developing: Shistosomiasis (fluke worm – trematode), inflammatory reaction to eggs PyelonephritisAscending UTI that has reached the pyelum (pelvis) of the kidneyIn this case will get the UTI symptoms – haematuria, painful micturition;Then if have loin pain, fevers/rigors, confusion – think of pyelonephritis Common cause is a renal stone!Others:SexPregnancyFemaleDiabetesIncomplete bladder emptyingRenal TumoursRenal Cell carcinoma/Grawitz Tumour. 90% renal tumoursPresents most commonly in 5th decade of life. Arise from proximal tubular epithelium and may be solitary, multiple and occasionally bilateralPresentation: TRIAD: Haematuria; loin pain and loin mass. Can get general malaise; fever; wt lossPolycythaemia; hypertension; hypercalcaemia Cannon ball mets!- RFs: Smoking, obesity. Also see in von Hippel-Lindau. Wilms tumour – Commonest intra-abdo tumour <10, peak 2-4y. Presents large flank mass + haematuria (less common). - Nephroblastoma – an anablastic tumour, (mesoderm: kidney, fat, bone), rapidly growing tumour, often metastasises to lungs.CystitisUTI – but in this case, no fever/rigorsJust local symptomsTherefore think of cystitis in this instance.Most common cause is E coliOthers include:Proteus Mirabilis, strep faecalis Treat with a 3-5 day course of oral amoxicillin, nitrofurantoin or trimethoprim ShistosomiasisFluke worm (trematode)Disease is caused by inflammatory response to eggs or adult wormsThe earliest symptom is painless terminal haematuria (for haematobium)As bladder inflammation progresses – increased urinary frequency and groin painStrong association with chronic shistosomiasis and squamous cell carcinoma of the bladder.More on UTI;E coli commonestproteus (can cause urate stones)Trimethoprim, nitrofurantoin Dipstick – nitrites and leucocytesMCS of MSU – if no bacteria but positive white cells – sterile pyuria - TBGlomerulonephritisInflammation of the glomeruliCan present in different ways; Nephrotic syndrome, Nephritic syndrome and Acute/chronic renal failure Nephrotic SyndromeMassive proteinuria Hypoalbuminemia EdemaHyperlipidemia/hyperlipiduriaE.g. Minimal change GN, Membranous GN‘Non proliferative’ Nephritic SyndromeHematuriaOliguriaUremia HypertensionE.g. IgA nephropathy, Post-streptococal. ‘Proliferative’ Minimal Change GlomerulonephritisSigns and symptoms all point to nephrOtic syndrome. Think loss of prOtein.The most common cause of nephrotic syndrome in children is minimal change GNOn renal biopsy the histological appearance is normal, hence ‘minimal change’ Membranous GlomerulonephritisAgain nephrOtic syndromeBUT this is an adult….most common cause of nephrotic syndrome in adults is membranous GNMainly idiopathic, but can be induced by a number of disease processes; SLEHBVDrugsOther causes of Nephrotic SyndromeMinimal change GN…childrenMembranous GN…adultsDiabetic nephropathyAmyloidosis Henoch-Schonlein Purpura Triad of purpura, arthritis and abdo pain in childrenRash is found on legs and buttocks.IgA Nephropathy – Berger’s diseaseThis is nephritic syndrome Upper respiratory tract infection IgA deposition in kidney30% develop CRF 1-2 days after infection, generalised fluCfPost-streptococcal glomerulonephritisUsually seen 1-2 weeks after an infection caused by a group A β-haemolytic streptococcus e.g. tonsilitis or cellulitis Nephritic syndrome and ‘pepsi urine’ Investigations reveal an elevated anti-steptolysin O titres.Goodpasture’s SyndromeAuto-antibodies formed against glomerular basement membrane, (anti glomerular basement membrane antibody).Renal failure, pulmonary haemorrhage and haemoptysis.Rapidly progressive glomerulonephritisWegner’s granulomatosis and polyarteritis (ANCA antibody) Renal failureComplications of Renal FailureRenal failure can arise from numerous causesThe effect of Renal failure is extensive and can manifest in a variety of ways Need to understand complication and appropriate treatment Anaemia…’Lethargic…pale conjunctivae’‘ejection systolic murmur’ = murmur created by high output state…no valve pathology Reduced secretion of erythropoietin by kidneysRecognise treatment… Iron stores are normal so not corrected by iron supplementation Primarily treat root of problem – give IV EPORenal osteodystrophy…bone disease due to renal failure.High phosphate due to reduced excretion Renal Disease – leads to – Reduced Vit D – leads to – Osteomalacia (hypocalcaemia)Recognise treatment…Alfacalcidol is a form of Vit DHigh BPRenal disease causes high BP and uncontrolled high BP can induce renal diseaseRecognise treatment…Renal artery stenosis is contraindication of ACE inhibitor. So give alternative…CCBUraemic encephalopathy …high levels of urea are entering the brain.Definitive treatment is dialysis Uremia…build up of ureaLethargy, irritability Pruritus, hiccups, flapping tremorPericarditis Skin colour…yellow/pale tinge GIAnorexia, nausea and vomiting Neurological Motor, sensory and autonomic neuropathyHyperkalaemia: tented T waves, absent P waves, wide QRS complexes on ECG. Some causes of Urinary tract obstructionBenign Prostatic Hypertrophy (BPH)Epidemiology: 70% of men have benign hyperplasia by the age of 70Aetiology: The inner portion of the prostate gland (transition zone) hypertrophies during late adult life. As it grows it compresses the outer layers in a false capsule and therefore bulges centrally into the urethraSo majority of symptoms – mechanical obstruction to the act of micturition Presentation: Irritative (muscular instability of bladder): Nocturia, frequencyObstructive; Hesitancy; poor flow; intermittent flow; terminal dribbling, strangury, overflow incontinence, bladder stones, UTIs.Can get haematuria at the end of micturition.Prostate CancerAetiology: Begins in its outer part and so NO false capsule and so can easily spread in the floor of the pelvis. Are adenocarcinomas, 80% arise from peripheral zone. Epidemiology: >50Commonly quite advanced before symtpoms Presentation: Commonest symptoms – prostatism (poor stream, urgency, frequency). Also can present with weight loss + bone pain + raised AlkP (metastasis).Rectal exam - prostate is asymmetrically enlarged or distorted, irregular texture ‘craggy’, nodular, loss of midline sulcus. Diagnosis: Transrectal USS and biopsy. Then staging: TNM and Gleason grading.PSA –(NR < 4ng/ml) A PSA alone does NOT give enough information to distinguish between benign and cancer.N in 30% of cancers, elevated in BPH so cannot distinguish benign and malignant disease. But once cancer is diagnosed, it is a very good marker of disease progression/recurrence following treatment.Renal Stones – can cause urinary obstruction amongst other things (like haematuria)Presentation: Loin-groin, colicky pain, N&V, sweaty, pale, cannot lie still (v. peritonism). Macro/micro haematuria. Aetiology: form in collecting ducts of kidney, when high concentration of solutes in urine, especially dehydrationPredisposing factors to stone formation;Increased urinary concentrationInadequate volumeIncreased excretion of calcium (hypercalciuria): Familial tendency, hyperparathyroidism, renal tubular acidosis.Increased uric acidStagnant urineDrugs (loop diuretics, antacids…)UTI – generally produces phosphate stones. Can get a large stag-horn calculus deposited within a pyonephros (infection of renal collecting system)Ix: CTKUB: Gold standard, most appropriate to gain diagnosis. Replaced IVU. Adv: No contrast, safe iodine allergy. ALL stones radio-opaque – pick up 99%. May see ureter dilatation or hydronephrosis.Disadv: Radiation, expenseIVU: plain abdo film, then iodine contrast, serial xrays. 90% stones radio-opaque. Initial: Urine dipstick +MCS, U&E, then KUB XrayManagement: Conservative: If <.5cm, in lower ureter. Give analgesia, lots fluids, medical expulsive therapy (Tamsulosin a-blocker) sieve urine. To relieve obstruction: Can cause hydronephrosis, renal failure.Nephrostomy or JJ stentSurgical (Usually if >1cm): Kidney/upper ureteric: ESWL (<2cm), Percutaneous nephrolithotomyBladder/lower ureter: Flexible ureteroscopy and LithoclastStone typesContentFrequencyXrayNotesCalcium75-85%RadiopaqueCalcium oxalate/calcium phosphate. Increased conditions cause hypercalcaemiaMagnesium ammonium phosphate (Struvite)15%RadiopaqueInfection urease +ve: Proteus, Staph, Klebsiella. Can form staghorn calculiUric acid5%RadiolucentHyperuricaemia e.g. gout, leukaemia (metabolism)Cystine1%Radiopque2* cystinuriaMultiple myeloma can cause renal problems – like obstructionMultiple myeloma is a malignant disorder of B cells characterized by abnormal plasma cells in the bone marrow compartment.It is characterised by lytic lesions!!Also have bence-jones proteins (light chains) which can obstruct tubules.MM can also cause renal failure for other reasons.High calcium is typical (due to lytic lesions)High ESRNeurogenic BladderRefers to a dysfunction of the bladder due to a disease of the CNS such as stroke, tumours and cord compressionOr due to peripheral system damage due to direct invasion of the nerves or damage to the sacral plexusIN this patient bony metastasis has caused spinal cord compressionUrinary Incontinence – some causesSpinal Cord CompressionBreast cancer? Metastasis? spread to vertebra? Spinal cord compression Look out for ‘sensory level’ Paralysis of the limbs‘automatic bladder’Categorised as ‘overflow incontinence.’ Nerve supply to bladder is interrupted? urine builds up? urine leaves at certain pressureNeurogenic bladder – AutonomicTransection of spinal cord Bladder automatically empties Neurogenic Bladder – AtonicLesions to the sensory nerves(DM) Bladder fills, but no micturation reflex and dribbling Normal Pressure HydrocephalusClassical triad of confusion, incontinence and gait dyspraxia in an elderly patients BPH – can also cause incontinenceEnlarged prostate blocks outflow of urine? bladder is never fully empty? frequently need to urinate but outflow is obstructed so poor stream.‘Overflow incontinence’ Alpha blockers such as terazosin relax smooth muscle at neck of bladder so aid voiding. Prostate cancer can also lead to overflow incontinence, so also look for weight lossUTIVery very commonElderly womenFrequency, urgency and feverCan also present insidiously, NO URINARY SYMPTOMS….sepsis UTI is an example of urge incontinenceStress IncontinenceLeak of urine when intra-abdominal pressure rises.Event in the past has weakened the pelvic musclesChild birthPelvic surgerySummary of IncontinenceOverflow – BPH and Spinal Cord CompressionUrge – Often Idiopathic in Women. Treat with anticholinergicsStress – Increase in abdominal pressure. Treat with pelvic floor exercises/bladder retrainingFunctional – dementia, poor mobilityPolycystic kidney disease—ADPKD = 1/1000. Adults. Mutation in PKD1 or PKD2. Bilateral ballotable masses +/- abdo pain + haematuria, infections, calculi, progressive renal failure. Associated risk berry aneurysms -> SAH. —ARPKD = RARE (1/40,000). Infancy. Mutation PKHD1 gene. Causes CKD, HTn, hepatic fibrosis.Scrotal Swellings4 questions Can you get above the swellingCan you identify the testis and epididymis Is the swelling translucentIs the swelling painful Swellings NOT confined to the scrotumHernia – you CANNOT get above it! – Infantile hydrocele – extends from testis to the internal inguinal ring BUT does NOT pass into peritoneal cavityIt is TRANSLUCENTNo cough impulse; not reduble Testis not palpable Swellings CONFINED TO THE SCROTUMTestis and Epididymus NOT definableOpaque and NON-tenderChronic haematocele – collection of blood within the tunica vaginalis Gumma (rare) – congenital syphilisTumour:Seminoma – carcinoma of seminiferous tubulesTeratoma – malignant germ cell tumourHeavy testis – almost diagnostic!TenderTorsionSevere Epididymo-orchitis Acute haematoceleTranslucentvaginal hydroceleTestis and epididymis DEFINABLE:Opaque and NON tender:TumourTuberculous epidiymis – rare now in the UK. May be systemic symptoms of Tb. Vas deferens is often irregular and swollen and feels like a string of beads (rare physical sign but diagnostic)Tender:Acute epididymo-orchitis Translucent:Cyst of epididymis – usually contains clear fluidThe swelling is separate from the testis (cf to hydrocele) More Information on some conditionsIndirect inguinal hernia – may be aware of the lump, and may be able to reduce it. impossible to get above the swelling. May become painful and irreducibleHydrocele – Painless scrotal swelling. Over 50 years. Unilateral. Fluctuant, transilluminates and dull to precussion. Testis cannot be palpated separately. Impossible to get above the swelling.= An abnormal quantity of fluid in the tunica vaginalis (so testis impalable)Primary (idiopathic) – occurs in men over the age of 40 and develops slowly, ? due to excessive fluid production/poor absorption.Secondary: 2* to Infection, Trauma, Malignancy .These will appear rapidly and will usually be associated with other symptoms.World wide, Filariasis (parasitic infection Wuchereria bancrofti)Infantile: If processus vaginalis remains patent, peritoneal fluid can fill the sac, causing a communicating hydrocele (if bowel -> infantile hernia). CANNOT get above these.Ix: You can drain the fluid – straw coloured with flecks of cholesterol Tx: Only if symptomatic, surgical Lord’s repair or JAboulay’s repair.Epididmal cyst – Painless, smooth, well circumscribed along any part of epididymis. Slowly enlarge over yrs. Can be bilateral. Feels lobulated. Above and behind the testis, so the testis can be palpated separately. Fluctuant. Don’t always transilluminate.= A simple fluid cyst.Ix: USS to confirm.Tx: Benign, so only if symptomatic. Do cystectomy/spermatoclectomy.Epididymo-orchitis – Pain, swelling, unilateral. Malaise, fever. Accompanied with UTI with dysuria and frequency. Scrotal skin is hot, red, oedematous, tender. Acute infections usually arise in the vas deferens, spreading first to the epididymis and then the testisOccasionally blood borne (Mumps – most common. Usually follows a week after parotid gland enlargement)Ascending infection is usually a consequence of preceding UTI or prostatitis from an STDCommon in young/middle aged menDD – torsionMay be a history of urethral dischargeManagement: Young (<35), and sexually active: Chlamydia, gonorrhoea, other STIs.. Cover with: Doxycycline (Chlamydia), 3rd G Cephalosporin: Ceftriaxone (Gonorrhoea)Older (>35), especially with BPH: Enteric organisms e.g. E. coli. Cover with: Ciprofloxacin (E.coli, Klebsiella)Mumps orchitis: 1/5 males get orchitis with mumps. Testicular swelling usually 4-8d after parotitis. Acute onset testicular swelling, erythema, tenderness. —Cf bacterial infection; usually orchitis + epididymitis.- Management: No anti-virals for mumps, so symptomatic relief; bed rest, analgesia, fluids, scrotal elevation, cold compress etc.Testicular torsion – Surgical emergency!= testicle twists, compromising blood supply in spermatic cord -> ischaemia -> infarction.Epidemiology: 2 peaks - Neonates, adolescents (peak 10-14). Presentation: Initially poorly localised abdominal pain (T10), then acute pain, swelling of testicle, N&V. Possible Hx exercise. Diagnosis clinical. O/E: Testis horizontal/retracted/higher. Red, hot, tender, swelling confined to sctroum. Negative Prehn’s sign; pain not relieved by elevation. Absence cremasteric reflex.Aetiology: Neonates: extravaginal torsion. Adolescents: Intravaginal torsion = Testicle rotates freely on spermatic cord within tunica vaginalis. In mature, tunica vaginalis is attached securely to posterior lateral aspect of testicle, and within it, spermatic cord not very mobile. Some variability in extent to which tunica covers testis, Usually congenital abnormality implicated (Bellclapper deformity). Adults: May be associated with testicular malignancy (increased size testicle).Management: URGENT surgical exploration, have 4-6h to save the testicle.The appendix testis/hyatid morgagni = vestigial remnant of Mullerian duct, present on the upper pole of testis. Rarely undergoes torsion, causing acute unilateral testicular pain, 1/3 have ‘blue dot’ on scrotum. Can mimic testicular torsion, but does not lead to impairment of testicular function.Varicocele – ‘= abnormal dilatation & tortuosity of pampiniform venous plexus in scrotumEpidemiology: 15-20% all males, 40%infertile males.Presentation: Dragging/aching pain, heaviness, atrophy. More common L. O/E: visible or palpable enlarged veins, particularly standing. Classically ‘bag of worms’ in EMQs (cf to tuberculous epididymis where the vas deferens feels like a string of beads!)Ix: USSAetiology: Valvular incompetence: Valves of veins within spermatic cord incompetent. 98% LCompression of venous drainage: Pelvic/abdominal malignancy e.g. RCC, concern if new onset >40, nutcracker syndromeManagement: Varicocelectomy my improve plications:? Arterial blood supply/ ? Thermoregulation -> infertility. Commonest cause poor sperm production and decreased semen qualityAcute HaematoceleA haematocele is a collection of blood within the tunica vaginalis Acute haematocele is a common accompaniment of scrota trauma.The testis cannot be felt!Also does not transilluminate!It will be very tense and tender Ix: Both clinically and sonographically difficult to distinguish from a neoplasm. So surgical exploration may be warranted.Tuberculous EpididymisCondition is now uncommon in the UKInfection develops slowly without causing severe or acute pain or tendernessPresentation: May be systematic signs of TBEpidiymus is hard and can be 2-3 times its normal sizeThen vas deferens is often irregular and swollen and feels like a string of beads – physical sign is rare but diagnostic Management: Anti-TB meds (Rifampicin, isoniazid, pyrazinamide).Testicaular cancerTeratoma are germ cell tumours which usually occur in 20-30Seminoma (30-40)Both present as a swelling or lump in the testis which is palpable as a hard, irregular massAlpha fetoprotein is raised in teratoma BUT not in seminoma Beta HCG can be high in bothTx: Seminoma; ORchidectomy.% AgesOriginBloodsFeaturesSeminoma40>30Germ cell, Epithelium seminiferous tubulesB-hCG (AlkP) Low grade tumour, homogenous USSTeratoma1020-30Germ cellB-hCG, a-FPMore aggressive, hetergenous USS-Non germ cell (5%): Leydig cell & Sertoli cell tumours: Rare, can produce steroid hormones.-Lymphomas: Can occur in 50-60s, most common testicular cancer of older menSession 7 – Infectious disease and eponymous syndromesRespiratory Infections:Pneumonia:Streptococcus pnneumonia – rust coloured sputum, rapid onset of fever with SOB and cough, - lobar consolidation.Strep pneuomniae: most common form of pneumonia, precedes hx of viral infection, cough productive with rusty coloured sputum, consolidation – AMOXICILLIN (sensitivity: erythromycin)Staphylococcal/klebsiella – cavitating lungsMycoplasma pneumonia Younger pts. Flu like symptoms (malaise , headache) precedes chest symptoms-> Dry cough, SOB, (NON specific)CXR: – bilateral patchy consolidationIx: Do serology to confirm diagnosisExtra-pulmonary featuresCold agglutinins (IgM to RBCs, activate below body temperature): Can cause AIHAErythema multiforme (blistering targetoid) or Stevens-Johnson’s (AKA EM Major: mucous membrane/genital/conjunctival involvement, systemic upset, fever).Hepatitis -> derranged LFTsPericarditis/myocarditisMeningoencephalitisGuillain-Barre syndromeTx: MACROLIDE e.g. ClarithromycinStaph aureus: previous H Influenzae infection, then deteriorates, circular opacities, Gram +ve cocci and clustersLegionella pneumonia – dry cough, dyspnoea, diarrhoea and confusionplumber, recently on holiday in a hotel, shower and cooling systems contaminated, usually middle-aged, smokers, multilobar shadowing Pseudomonas aeruginosa – intensive care, - cystic fibrosis / bronchiectasisPneumocystis carinii – HIV, bilateral hilar shadowingChlamydia psittaci – BIRDS!Other respiratory infectionsStreptococcus PyogenesScarlet feverTonsillitisErythematous rash (trunk)Sore coated tongue (strawberry tongue)Desquamation of the skin of the palms and soles Burkholderia CapaciaPneumonias in immunocompromised or those with underlying lung disease (CF)Staph AureusPost viral-infectionCavities on CXR Bordetella PurtussisWhooping cough (100 days’ cough)Starts with cold-like symptoms1-12 days later develops paroxysmal violent cough with ‘whoop’ noiseCoughing spells may lead to vomitting and LOCIn UK: vaccination programme CytomegalovirusImmunocompromised patients develop infection, which can be life threatening. Commonly:AIDSPost-transplant (BMT, solid organ)Infections:CMV pneumoniaCMV retinitisCMV gastroenteritisCMV oesophagitis Diarrhoea:Staphylococcus Aureus (G+ve bacteria)prominent vomiting and watery diarrhoea in hours (through an enterotoxin)Self-limitingCryptosporidum pavum (protozoan)Severy watery diarrhoea in immunocomrpomisedLook for oocytes in the stoolBacilus Cereus (G+ve bacteria)Spores germinate in reheated fried rice (Chinese take-away)Self-limiting watery diarrhoeaGiardia Lamblia (protozoan) Trophozoite ‘pear shaped’ with ‘owl-eye nucleus’, attaches to the duodeumCauses malabsorption of fat and proteinFoul smelling, non-bloody, explosive diarrhoea, abdo cramps, flatulencem no fever, pale fatty stoolsVibrio cholerae (G-ve)Toxin mediated diarrhoea (doesn’t invade the epithelium)Massive diarrhoea, rice water stool (w/o inflammatory cekks)Bloody DiarrhoeaShigella (G-ve)Person-to-person spread Campylobacter (G-ve)Watery, foul smelling, bloody diarrhoeaFever and severe abdominal painAssociated with Guillian-Barre SyndromeE.coli (G-ve) Traveller’s diarrhoeaE.coli O157:H7 causes Haemolytic Uremic SyndromeSalmonella enteritidisC. difficile – diagnosed through detection of a cytopathic toxin in the stool. General management for diarrhoeaCiprofloxacin (Quinolone) – Severe bacterialDoxycycline (Tetracycline) – Broad spectrumAmoxicillin (Beta lactam) – Broad spectrum, GI SECodeine – Chronic and persistentTropical Disease / fever in returned travellerEntamboeba Histolytica (Amoebiasis) - faecal/ oral, intermittent fever, swelling in hypochondrium - liver abcess, Trophozoites remain in bowel or invade extra intestinal tissues, leaving“flask-shaped” GI ulcers – severe amoebic dysenteryIntestinal Amoebiasis (Amoebic dysentery)Get tissue ulceration and necrosis. The presentation varies from mild bloody diarrhoea to fulminating colitis, with risk of toxic dilatation, perforation and peritonitisCan get blood and mucus in the stoolIncreased incidence in tropical countriesAmoebic Liver abscessIf enters portal vein and then the liver.Get an abscess (usually single) with tender hepatomegaly, high swinging fever and profound malaise.Amoebic fluorescent antibody test (FAT) is positive in 90% of patients with liver abscess and 70% with active colitis Salmonella typhi (Typhoid – eneteric fever) – Think when has headache and GI symptomsFaecal/ oral spread, high fever, malaise and diarrhoea, CNS and delirium; Gram –ve bacilliHumans are the only known reservoir and spread is faecal-oralIncubation period of 10-14 daysInsidious onset of headache, dry cough and constipationRising fever and relative bradycardia In second week can get an erythematous maculopapular rash that blanches on pressure - rose spots – upper abdomen and thoraxCan get pneumonia; meningitis; acute cholecystitis. Blood count can show leucopenia ShistosomiasisFluke worm (trematode)Disease is caused by inflammatory response to eggs or adult wormsThe earliest symptom is painless terminal haematuria (for haematobium)As bladder inflammation progresses – increased urinary frequency and groin painStrong association with chronic shistosomiasis and squamous cell carcinoma of the bladder.Malaria – Plasmodium Falciparum - flu like illness followed by fever and chills, classic periodic fever and rigors; Signs: anaemia, jaundice and hepatosplenomegaly, no rash or lymphadenopathyOne of the 4 species of plasmodium that infects manMalaria is characterized by headache and episodic very high feversCan get complications with falciparum including severe anaemia or cerebral malariaPlasmodium vivax is not found in West AfricaAlways think of malaria in traveller from an endemic areaThe incubation period is about 10-14 days. Neisseria meningitidis type B : only vaccination against Meng C, high fever, neckstiffness and drowsiness, CSF: Gram –ve diplococciDengue virus: fever, headache, myalgia, rash, thrombocytopenia and leucopeniaLassa Fever: Nigeria, Sierra Leone and Liberia, fever and exudative sore throat, faceoedema and collapseVibrio CholeraProfuse watery diarrhoea!! (not bloody)Rice water stoolInfection is caused by faecal-oral route.Cholera toxin causes massive secretion of isotonic fluid into the intestinal lumenThe incubation period varies from a few hours to 6 daysEffective rehydration is key – mainly oral but in severe cases IV fluids can be givenOral rehydration solutions – high in glucose GiardiasisIt is a cause of travellers diarrhoea and may cause prolonged symptomsGet damage to the small intestineDiarrhoea, nausea, abdominal pain and distention Can get malabsorption and steatorrhoea in somecases No blood or pus in the diarrhoeaCan get wt loss in more than 50% of patients ToxoplasmosisThe primary host is a catDuring first few weeks, infection causes a mild flu like illnessDoesn’t really cause symptoms in otherwise healthy adults.In HIV patients or pregnant women can be fatalComplications include;Encephalits; Chorioretinitis; Can effect the heart and the liver TrypanosomiasisDifferent types of parasitic infectionThe Human African form is transmitted by the Tsetse fly - gives sleeping sicknessEndemic in subsaharan AfricaFirst get fever, headaches, joint pains and itchingThen neurological phase – Confusion, disruption of the sleep cycle with bouts of fatigueLeishmaniasis – Kala-AzarParasitic disease spread by the sand-flyCutaneous leishmaniasis – can give you a skin sore which can progress to an ulcer which takes ages to healCan also get breathing difficultySwallowing difficultSystemic or visceral Leishmaniasis (2-8 months after bite) – fatigue, vomiting, diarrhoea, weaknessNight sweats; abdominal discomfort; weight loss Viral InfectionsCytomegalovirusAlso known as human herpes virus 5 (HHV5)Infections are frequently associated with the salivary glands90% of people are seropositive by the age of 80!Asymptomatic in healthy individualsIn immunocomprimised individuals can get severe disease with fever, diarrhoea, retinitis, hepatitis and encephalitis.Inflammation of the retina leads to a so-called ‘pizza pie’ appearance on fundoscopy (haemorrhages and yellowish retinal infiltrates)Treat - ganciclovir Dengue Fever – Flavi VirusHas an incubation period of 5-6 daysSome patients can present with a biphasic feverThe rash – bright red petechiae usually appears first on lower limbs and chestClassically there is fever with no localising source of infection, rash, thrombocytopneia and leucopenia Found mainly in Africa, central and southern America Herpes Simplex VirusTwo types:I – oral herpes – cold soresII – Genital herpes – transmitted sexually.Get painful genital ulceration, fever and local lymphadenopathy.Anorectal infection may also occurNote that the division between the two is not rigid. Herpes Zoster VirusAfter primary infection (chicken pox) the virus is not eliminated from the body but becomes latent in nerve cell bodies.It can then several years later – travel down nerve axons to cause a viral infection of the skin in the region of the nerveNever crosses the midline!Can get tingling/pain before rashRash consists of papules and vesicles in same dermatome Hepatitis AFaecal-oral spread from ingestion of contaminated food (shellfish/clams and water)Virus excreted in faeces of infected individuals for about 2 weeks before and 7 days after onsetIncubation period averages 30 daysJaundice, fever, malaise, nausea, vomiting and itching.Can get hepatomegaly. Epstien Barr Virus90% of cases of glandular fever is caused by EBV10% of CMVGet fever, sore throat, arthrlagia, myalgia and fatigueCan get splenomegaly There is generalized lymphadenopathy and Paul Bunnel test is +ve!It is an acute disease characterized by fever, swollen lymph nodes and an abnormal increase of monoculcear leucocytes or monocytes in the blood. Atypical lymphocytes on blood film.EBV can also cause Burkitts lymphoma.MeaslesFever, cough, conjunctivitis. Maculopapular rash with Koplik spots being pathognomonic.Koplik spots – small greyish, irregular lesions surrounded by an erythematous base found in greatest number in the buccal cavity Eponymous Syndromes – this are just a few, for a full list please refer to OCHM (there is a whole chapter!!!)Henoch-Schonlein purpuraSystemic vasculitis (IgA complex deposition)Purpura, abdo pain and arthritis (Triad)Kidney involvement common (haematuria)Common post infection, esp resp tractSymptom control, spont resolution within 4/52Pancoast’s syndromeHorner’s (Ptosis, Miosis, Anhydrosis)HPOA (Clubbing, IM wasting, wrist pain)Arm pain/paraesthesiaVocal changeApical lung CA (Often Sq.cell) invades sympathetic chainVwDMost common coag defect (Plt affected)Bleeding tendencyMenstrual, gums, nose bleeds, PPH, easy bruising (not haemophilia!)Blood plasma IxKaposi’s sarcomaTumour, Herpesvirus 8AIDS associatedPapular lesions (lower limbs and intra oral)Airway and GI involvementPeutz-Jegher’s syndromeBenign GI polypsADHyperpig lips and oral mucosal maculesBarrets OesophagusSq to Col epithChronic refluxM 50-70Inc risk dysphagia + (CA)Gardner’sColonic polyps + extracolonic tumours (e.g. osteomas and thyroid)ADFAP similarityAlportsGlomerulonephritis (Haematuria) + RF + Hearing loss (bilateral sensorineural)X LinkedCollagen synthesisOccular lesionsTabes DorsalisSlow degen nerve cells DC= neuro crazinessUnteated syphilis (HIV)Paralysis, dementia, blindnessChrug-straussAsthma + Eosinophilia + vasculitisDressler’s syndromePericardial effusion post MIFelty’s syndromeRheumatoid, splenomegaly and neutropeniaCharcot-Marie-Toothinverted champagne bottle appearance of legs; get foot dropOsler-Weber-Rendu – telangiectasia on the skin and the mucous membranes, which may cause epistaxis, or chronic GI bleeds, with IDAVon-Hippel-Lindau syndrome – Bilateral renal carcinoma and cerebllar haemangioblastoma and phaeochromocytoma.It may present with visual impairment and cerebellar signs.Berger’s Disease IgA nephropathyMost common form of primary glomerular disease Serum IgA increased in 50%Haematuria appears quickly after infections (mostly respiratory25% will develop ESRF in around 25 years Sj?gren’s SyndromeAutoimmune (anti-La, anti-Ro)Chronic inflammatory infiltrate in both lacrimal (dry eyes) and salivary glands (dry mouth)Schirmer’s testMeig’s SyndromeTriad of ovarian fibroma or tumour, ascites and pleural effusionThe removal of the ovarian lesion results in resolution of ascites and pleural effusionZollinger-Ellison SyndromeGastrin-secreting tumourLarge amounts of hydrochloric acid production in gastric antrum leads to recurrent peptic ulceration (often duodenal).Session 8 – Endocrinology, Emergencies and poisoningThyroid DiseaseHyperthyroidism:Primary thyroid diseaseGrave’s diseaseThis is HYPERTHYROIDDiarrhoea, feeling warm, weight loss despite a good appetite and tremor. Specific to graves…Auto-antibodies that stimulate the TSH receptors Pretibial myxoedema=lower limb swelling, waxy, discolored induration of the skin Periorbital myxoedema=exophthalamus Thyroid Acropachy Toxic multinodular goiter…Look for a background of non-toxic mulinodular goiter Plummer’s disease (solitary toxic nodule) Others (still hyperthyroid)De Quervain’s thyroiditisUsually precipitated by a viral infectionInflammation of the thyroid gland…tender Inflammation…transient release of thyroxine…HYPER?No thyroxine left…transient HYPO?Patient then recovers and becomes EUTHYROID TSH secreting tumoursIatrogenic (e.g. amiodarone)Throid Storm (Sever Hyperthyroidism) – treat:Transferred to intensive careFluids and gentle coolingBeta-blockersSodium iopodate (which inhibits thyroxine release) Carbimazole (inhibits synthesis of thyroxine) HypothyroidismChronic autoimmune thyroiditis – Hashimoto’sHypothyroid symptoms…tiredness, cold intolerance, constipation, bradycardia, slow-relaxing reflexes Autoimmune hypothyroiditis…antibodies to thyroid peroxidase Diffusely enlarged rubbery goitreIatrogenic (thyroidectomy)Drugs (e.g. Lithium, amiodarone)Iodine deficiencyMyxoedema ComaSEVERE hypothyroidism Impaired consciousness, hypothermia, bradycardia, and hypoglyceamia Treat:Transferred to intensive careFluidsGentle rewarming IV thyroid hormonesThyroid CancerPapillary -70% - age 30-50Follicular – 15% - age 40-50Medullary - Calcitonin levels importantAnaplastic – Rare - 70s - poor prognosis; aggressiveDiabetes TreatmentT1DM:InsulinT2DM:Risk factor reduction (exercise, smoking cessation, low dose aspirin, BP control, statins)DietHbA1c >7%: Obese: Metformin (biguanide, insulin sensitizer)Non-obese: Sulphonylurea (promotes insulin secretion)If uncontrolled: metformin + SulphonylureaStill uncontrolled: insulinNote:When choosing sulphonylurea…glibenclamide is most popular…but must be avoided in elderly due to its long duration of action…so use Tolbutamide, (potential hypoglyceamia)Metformin contraindicated in renal failure, liver disease and severe heart failure due to risk for lactic acidosis. Make sure you learn the diagnostic criteria Fasting plasma glucose ≥ 7 mmol/LRandom plasma glucose ≥ 11.1 mmol/L One abnormal laboratory value is diagnostic in a patient with typical hyperglycaemic symptoms; two values are needed in asymptomatic people.OGTT, 2 hours after glucose administration ≥11.1 mmol/LImpaired fasting glucose, fasting glucose≥ 6.1 but < 7 mmol/L…high risk of getting DM 2…then do a glucose tolerance test.Impaired glucose tolerance, fasting glucose <7 mmol/L and OGTT 2h glucose ≥7.8mmol/L but <11.1 mmol/L Diabetic Keto-acidosis – only in Type I DM (ie Insulin dependent diabetes) – often first presentationUsually triggered by underlying illness (chest infection), where the insulin requirements increase but the patient does not adjust. Glucose increases…dehydration….rise in ketones and acid. – metabolic acidosis! (reduced renal perfusion)Look for…Kussmaul’s respiration, breath smells of ketones…abdominal pain. Fluid replacement…1L 0.9% saline immediately1L over 1 hour1L over 2 hours1L over 4 hours1L over 6 hoursNote measure glucose hourly, if falls below 12mM then IV fluid change to 5% dextrose+ IV insulin (sliding scale)(potassium replacement)Diagnostic Pitfalls– BM may be normal– Elevated WCC (NOT infection)– Amylase Inc (NOT pancreatitis)– Inc ketones & norm BM ?ETOHHyper-osmotic Non-ketotic Coma (HONK) – only type II diabetes (insulin independent)This is DM Type 2 with HONK (HyperOsmolar Non-Ketotic state)Triggered by underlying illness, large sugar dose…uncontrolled rise in glucose…severe dehydration.Not enough insulin to keep glucose down…but enough to prevent ketone formation! Compare to: DM 1, NO INSULIN at all…ketoacidoses Extra information:Oral hypoglycaemic drugsSecretagogues (Sulphonylureas)ThinniesSensitisers (Biguanides)FattiesGlitazonesCardiac SE, numerous have been withdrawn AcarboseAlpha Glucosidase InhibHyperaldosteronism: Conn’s (primary hyperaldosteronism), CAHLow potassiumCause of hypertensionPhaeochromocytoma –phenoxybenzamine followed by propanolol 10% rule – bilateral, malignant, familial, extra-adrenalVon-Hippel Lindau, neurofibromatosis, MEN IIOther adrenal problems:Waterhouse-Friedrichson syndrome – adrenal haemorrhage following massive G –ive meningitisNelson’s syndrome: pituitary enlargement following bilateral adrenalectomy – high ACTH and pigmentationFailure:Primary – TB, Addison’sSecondary – low ACTh (pituitary failure)Short SynACTHen test – if cortisol rises then the problem is probably in the pituitaryLong SynACTHen test – fails to rise Cushing’sLearn the featuresMay be iatrogenic – Rheum patients!Pseudo-Cushing’s – depression/alcohol with normal cortisol and ACTHCushing’s disease – pituitary over-producing ACTHLow dose dexamethasone suppression test – won’t suppress any hyperACTH stateHigh dose will suppress only Cushing’s disease, not SCC of the lungProlactinomaGalactorrhoea Infertility in womenDA agonists inhibit PL secretion – cabergoline and bromocriptine ...TRH increases it – could be d/t hypothyroidismGrowth HormoneAcromegaly – glucose tolerance test – GH levels fail to suppressBig hands, tongue, hat sizesDiabetes and hypertension; cardiomyopathy AcneArthritisDiabetes InsipidusTwo forms – cranial and nephrogenic ‘Dilute urine’Diagnosed with water deprivation test Getting up at night to drink waterNephrogenic (renal insensitivity) vs centralDDAVP controlled – centralMEN syndromes1 – The Ps – parathyroid, pituitary, pancreatic islet cell2(a) – phaeo! (also parathyroid, medullary thyroid carcinoma)2(b) or 3 – mmmm.... Marfanoid and mucousal neuromas Brief Notes on Emergencies (look at OCHM and other handout notes)Acute Asthma (please see OCHM for details!!)High dose 100% OxygenSalbutomol nebulised with oxygenSteroidCXR to exclude pneumothorax If no real improvement move to ITU and prepare to intubate. Cricothyroidotomy is a small incision in the neck…thus avoiding trauma area. Symptomatic AF:Oxygen heparin synchronised DC shock Chronic / Asymptomatic AF:Rate (Beta-blocker, digoxin) Rhythm (Anti-arrhythmics, Verapamil) Anti-coagulant (warfarin) Hyperkalaemia:Urgent Tx if >7 mmol/L or there are ECG changes1: 10 mL 10% Calcium gluconate IV (Cardioprotective, raises threshold potential, prevent fatal arrythamias)2: Insulin 10 U actrapid and dextrose (Moves K+ from EC->IC)3. Can use B2 agonists (EC->IC), diuretics (K+ loss kidney)Calcium resonium (reduces K+ absorption from GI tract)DialysisHypocalcaemiaMild: Calcium PO, alfacalcidol in CKDSevere: 10 mL of 10% calcium gluconate IV over 30 minutesPoisoning + antidotesPoison / drugAntidoteAspirin <500mg/L – supportive>500 mg/L – alkaline diuresis with i.v sodium bicarbonate>700 mg/L - haemodialysis Diazepam Flumazenil TCA Lorazepam Opiates Naloxone Paracetamol N-Acetylcysteine Heparin Protamine sulphate Warfarin Vit K Methanol Ethanol B-blockers Atropine, Glucagon Organophosphorous poisoning Pralidoxime mesilate CyanideDicobalt EdetateHaemachromatosisDesferrioxamineWilsons disease / mercuryPenicillamineArsenicDimercaprolParaquat / CCBActivated CharcoalLithium DialysisCocaine / extasyDiazepamDrugs and their Side effects*DrugToxicity / SEPhenytoinMacrocytic anaemia, hypocalcaemia, nystagmus, confusion, lethargy, cerebellar signs Cimetidine Gynaecomastia Digoxin Gynaecomastia Spironolactone Gynaecomastia Bendrofluazide Gout Minoxidil Hirsuitism Isoniazid Peripheral neuropathy, hepatitis Ethambutol Retrobulbar palsy Pyrazinamide Gout Neuroleptics Tardive dyskinesia Aspirin Tinnitus, N & V, overbreathing, hyperpyrexia, sweating, tachycardia * These are not the most important or all the side effects of the drugs. For full side effects please see BNF.Warfarin Table of what to when INR is raised. Target INR should be between 2-3 or higher (3-4.5 with a metallic heart valve, or recurrent systemic thromboses). INRAction4.5 – 6Reduce warfarin or omit. Restart when < 56 – 8 Stop warfarin, restart when < 5>8, no bleed or minor bleed Stop warfarin and administer oral vitamin K Major bleed (including intracranial haemorrhage)Stop warfarin, give prothrombin complex. If unavailable, give FFP. MISCELLANEOUSNutritionRDAs:- Sodium: 2.4g, Salt 6g (Salt = sodium x2.5)- Protein (0.8-1.8g/kg)- potassium (3.5kg)Haematological malignanciesMultiple myeloma—60-70 yo. —Aetiology: Proliferation malignant plasma cells (Ab) >10% of BM-> overproduction of monoclonal paraprotein (M protein, IgG 2/3, IgA 1/3), extensive skeletal destruction—Presentation: Incidental 1/3.—Systemic: Bleeding (thrombocytopaenia), infection (leukopenia), anaemia, renal failure (light chain deposition), hypercalcaemia—Pathological fracture (Dx 1/3), bone pain – lumbar spine (lytic lesions), SC compression—Diagnosis: BM > 10% plasma cells + monoclonal globulin spink on serum protein/urine protein electrophoresis + lytic bone lesions—Blood smears: Rouleaux—Bence-Jones proteins: light chains in urine (MM, Waldenstrom’s)—Xrays: Pepperpot skull, vertebral collapse, fractures.—Prognosis: 5 year survival 35%. No cure.Other plasma cell dyscrasias—Monoclonal gammaopathy of unknown significance: Presence of monoclonal immunolgobulin (Ig) in serum or urine without evidence of MM, WM, amyloidosis etc. 1/5 developed MM in next 20 y.—Plasma cell leukaemia: Clinically aggressive variant MM, > 20% circulating plasma cells. Present as MM, advanced stage, significant extramedullary involvement, can include CNS.—Waldenstrom macroglobulinaemia: Chronic, indolent, clonal B cell disease, IgM paraprotein and malignant lymphoplasmacytic cell infiltration in BM and other tissue. Similar presentation MM (hyperviscosity), organomegaly is common, lytic bone lesions uncommon.Vasculitis= Inflammation of vessels leading to occlusion (ischaemia and gangrene) and end organ dysfunction and necrosis.EFFECTS: ANY ORGAN!—SYSTEMIC: fever, malaise, weight loss, arthralgia, myalgia, lethargy, loss of appetite—SKIN: purpura, ulcers, livedo reticularis, nail bed infarcts, digital gangrene—PULMONARY: haemoptysis and dyspnoea—Cardiac: Angina or MI (coronary arteritis), heart failure and pericarditisSo presents as a mutli-system disease.SIZENAMEPresentationIxTxLARGEGiant cell arteritisElderly, temporal headache, scalp tenderness, jaw claudESR, CRP, biopsyHigh dose predTakayasu’s arteritisYoung, Asian, PUO, chest pain, poor distal pulses O/EInflammed aorta, vessels aortic archSteroids in inflammatory phase/surgery in occlusive phaseMEDIUMPolyarteritis nodosaUnwell, skin, renal aneurysmsRenal angiographyImmunosuppresionKawasaki’s diseaseChild, Fever + lymphadenopathy, mucocutaneous erythema, conjunctivitisIV immunoglobulinSMALLWegener’s granulomatosisURT + LRT + glomerulonephritiscANCA 90%Immunosuppsn.Microscopic polyangitisGlomerulonephritis, purpura, haemoptysispANCA 90%Churg-StraussAllergic rhinitis, asthma, sinusitis, eosinophiliaEosinophilia, c/pANCA 40%High dose predMore detail: Wegener’s granulomatosis—Presentation: Rare. —Systemic: Tired, lethargic, fever, purpuric rash, arthralgia. —Triad: —URT symptoms: Epistaxis, nasal septum destruction, rhinorrhoea, laryngeal damage. —LRT symptoms: Haemoptysis, cough, fibrosis, SOB. —Glomerulonephritis: Haematuria, proteinuria, HTn. —Ix: cANCA positive in 90%. —Tx: High dose immunosuppressants e.g. corticosteroids, cyclophosphamide.Churg-Strauss. Allergic granulomatosis.—Presentation: Middle aged: —Allergic rhinitis, asthma.—Eosinophilic disease: eosinophilic pneumonia, gastrenteritis, Eosinophilia >10% peripheral blood. —Systemic vasculitis: nerves, GIT.—Ix: p and cANCA +ve in 40%—Tx: High dose prednisolone—Polyarteritis nodosa, Necrotizing vasculitis -> aneurysms and thrombosis medium sized arteries.—Presentation: Young-middle aged men—Systemically unwell—Skin: haemorrhagic rash, punched out ulcers—Renal aneurysms (75%, main cause of death). Also haematuria, proteinuria and HTn.—Tx: ImmunosuppressionKawasaki disease—Presentation: Child, protracted fever over 5 days - acute systemic febrile vasculitis + 4 of:— Acute cervical lymphadenopathy— Mucocutaneous erythema— Bilateral non-purulent conjunctivitis— Dry, cracked, fissured lips (strawberrry tongue?)— Desquamating rash of palms and soles— Redness, oedema, of palms and soles— Platelets, CRP usually highly raised—Tx: Anti-inflammatories and IV immunoglobulin Condition dangerous as can cause coronary aneurysms).20828047688500Autoantibodies associated with disease (mainly connective tissue disease)Skin manifestations of diseaseAcanthosis nigricans—Presentation: symmetrical, pigmented, velvety thickened skin on neck and flexures eg. Axillae, groin. —Aetiology: Insulin resistance (DM, obesity, Cushing’s), acromegaly, thyroid, GI cancer/malignancy. —Dermatological conditions DIABETES MELLITUS: —Necrobiosis lipoidica: shiny atropic yellow brown patches, can ulcerate. Due to necrosis collagen fibres.—Acanthosis nigricans—Infections e.g. candidiasis, folliculitis—Granuloma annulare: erythematous ring shaped lesions.Gottron’s papules—Diagnosis: Dermatomyositis (Polymyositis + skin involvement)—Presentation: —Skin: Heliotrope rash, Gottron’s papules (violet flat papules)—Muscle: proximal, symmetrical muscle weaknessImportance: Associated with malignancy +/-1 year in 30%. Dermatitis herpetiformis—Presentation: Itchy blisters on elbows, scalp, shoulders, ankles. Found in Coeliac disease—Aetiology: Gluten enteropathy -> circulatinG IgA complexes containing transglutaminase, lodge in skin And cause inflammation—Ix: Coeliac antibodies +ve e.g. antiendomysial—Tx: Gluten free diet life long. Dapsone.Erythema nodosum. Nodular, red, raised, tender, not itchy, ill-defined, typically shin. Due to panniculitis = fat inflammation. —Associations: —Infections: TB, post-streptococcus—Drugs: OCP, antibiotics. —Systemic: SLE, sarcoidosis, IBD—Pregnancy & idiopathic ................
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