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LO 1,3,4,9 LO PRESENTED BYYEW-ERNAU LO 1 LO PRESENTED BYYEW-ERNAU A patient presents with a shortened,abducted and externally rotated leg.What is the likely fracture that has occurred? A Fibular fracture B Hip fracture C Shaft of femur fracture D Tibial tuberosity fracture E Neck of femur fracture A patient sustained a fall and landed on their left hip and now presents with a shortened,abducted and externally rotated leg.What is the likely fracture that has occurred? A Fibular fracture B Hip fracture C Shaft of femur fracture D Tibial tuberosity fracture E Neck of femur fracture What muscle is primarily responsible for extension of the knee? A Quadriceps B Biceps femoris C Gracilis D Sartorius E Semitendinosus What muscle is primarily responsible for extension of the knee? A Quadriceps B Biceps femoris C Gracilis D Sartorius E Semitendinosus From lateral to medial,what is the order of the femoral triangle contents? A Vein,Nerve, Artery,Empty space,Lymphatics B Nerve,Artery,Vein,Empty space,Lymphatics C Artery,Nerve,vein,Lymphatics,Empty space D Nerve,Vein,Artery,Empty space,Lymphatics E Lymphatics,Empty space,Artery,Vein,Nerve From lateral to medial,what is the order of the femoral triangle contents? A Vein,Nerve, Artery,Empty space,Lymphatics B Nerve,Artery,Vein,Empty space,Lymphatics C Artery,Nerve,vein,Lymphatics,Empty space D Nerve,Vein,Artery,Empty space,Lymphatics E Lymphatics,Empty space,Artery,Vein,Nerve What muscles attach onto the PesAnserine? A Gluteus maximus,Gluteus minimus,Gluteus medius B Semitendinosus,Semimembranosus,Biceps femoris C Rectus femoris,Rectus lateralis,Rectus medialis,Rectus intermedius D Sartorius,Gracilis,Semitendinosus E Gracilis, Adductor magnus,Adductor brevis,Adductor longus,Obturator externus What muscles attach onto the PesAnserine? A Gluteus maximus,Gluteus minimus,Gluteus medius B Semitendinosus,Semimembranosus,Biceps femoris C Rectus femoris,Rectus lateralis,Rectus medialis,Rectus intermedius D Sartorius,Gracilis,Semitendinosus E Gracilis, Adductor magnus,Adductor brevis,Adductor longus,Obturator externus A patient presents with swelling in the back of the knee,this is known as a Baker’s cyst.What is the space in which the swelling is present called? A Femoral canal B Popliteal fossa C Flexor retinaculum D Tibialis longus E Inguinal canal A patient presents with swelling,and this is known as a Baker’s cyst.What is the space in which the swelling is present called? A Femoral canal B Popliteal fossa C Flexor retinaculum D Tibialis longus E Inguinal canal You are studying the anatomy of the lower limb and recall that a muscle has the superior gluteal nerve above it and the inferior gluteal nerve below it.What muscle is this? A Gluteus maximus B Gluteus Medius C Gluteus Minimus D Piriformis E Superior Gemellus You are studying the anatomy of the lower limb and recall that a muscle has the superior gluteal nerve above it and the inferior gluteal nerve below it.What muscle is this? A Gluteus maximus B Gluteus Medius C Gluteus Minimus D Piriformis E Superior Gemellus A patient presents with the inability to plantarflex after an injury that they sustained during their training for an upcoming competition.They are a competitive sprinter but have recently taken a course of Ciprofloxacin for a recent infection.They have a past medical history ofAnkylosing Spondylitis.What is the most likely injury sustained? A Damage to the tibial nerve B Damage to the common peroneal nerve C Ruptured achilles tendonitis D ACL injury E Injury to the popliteal fossa A patient presents with the extreme pain and inability to plantarflex after an injury that they sustained during their training for an upcoming competition.They are a competitive sprinter but have recently taken a course of Ciprofloxacin for a recent infection. They have a past medical history ofAnkylosing Spondylitis.What is the most likely injury sustained? A Damage to the tibial nerve B Damage to the common peroneal nerve C Ruptured achilles tendonitis D ACL injury E Injury to the popliteal fossa A patient has become acutely confused and kicked a brick with their inner sole.He now complains of numbness to his plantar aspect of the foot. What nerve is damaged? A Femoral nerve B Deep peroneal nerve C Tibial nerve D Superficial peroneal nerve E Sural nerve A patient has become acutely confused and kicked a brick with their inner sole.He now complains of numbness to his plantar aspect of the foot. What nerve is damaged? A Femoral nerve B Deep peroneal nerve C Tibial nerve D Superficial peroneal nerve E Sural nerve LO 3 LO PRESENTED BYYEW-ERNAU You are a medical student preparing for your neurology block on placement. As part of this you are attempting to illicit the ”ankle reflex”.What nerve roots are responsible for this? A S1-S2 B S3-S4 C L3-L4 D L4-L5 E T12-L1 You are a medical student preparing for your neurology block on placement. As part of this you are attempting to illicit the ”ankle reflex”.What nerve roots are responsible for this? A S1-S2 B S3-S4 C L3-L4 D L4-L5 E T12-L1 A patient has come intoA&E with a posterior hip dislocation.What is the most likely nerve damaged? A Sciatic nerve B Femoral nerve C Obturator nerve D Tibial nerve E Common peroneal nerve A patient has come intoA&E with a posterior hip dislocation and is now unable to extend their hip.Plantarflexion and dorsiflexion is also absent.What is the most likely nerve damaged? A Sciatic nerve B Femoral nerve C Obturator nerve D Tibial nerve E Common peroneal nerve A patient has presented with damage to their superficial peroneal nerve.What is the most likely clinical presentation of this? st A Numbness to the 1 web space of the dorsum of the foot B Inability to dorsiflex,weakness in inversion C Inability to plantarflex,inability to evert foot D Numbness to the medial foot E Weakness in plantarflexion,weakness in eversion A patient has presented with damage to their superficial peroneal nerve.What is the most likely clinical presentation of this? st A Numbness to the 1 web space of the dorsum of the foot B Inability to dorsiflex,weakness in inversion C Inability to plantarflex,inability to evert foot D Numbness to the medial foot E Weakness in plantarflexion,weakness in eversion What is the nerve roots responsible for the“knee jerk” reflex? A S3-S4 B L1-L2 C L3-L4 D T5-T6 E L5-S1 What is the nerve roots responsible for the“knee jerk” reflex? A S3-S4 B L1-L2 C L3-L4 D T5-T6 E L5-S1 A patient presents with the inability to adduct their hip and has complained of medial thigh numbness.What nerve is most likely damaged? A Femoral nerve B Sciatic nerve C Obturator nerve D Saphenous nerve E Gluteal nerve A patient presents with the inability to adduct their hip and has complained of medial thigh numbness.What nerve is most likely damaged? A Femoral nerve B Sciatic nerve C Obturator nerve D Saphenous nerve E Gluteal nerve LO 4 LO PRESENTED BYYEW-ERNAU What are you likely to find in a histological sample of the vastus rectus muscle? A Intercalated disks,mildly striated,mono-nucleated B No striations,mono-nucleated C Highly striated,uniform pattern,multi-nucleated D Intercalated disks,highly striated E No striations,intercalated disks What are you likely to find in a histological sample of the vastus rectus muscle? A Intercalated disks,mildly striated,mono-nucleated B No striations,mono-nucleated C Highly striated,uniform pattern,multi-nucleated D Intercalated disks,highly striated E No striations,intercalated disks What does this sample represent? A Tendon B Bone C Cartilage D Skeletal muscle E Dermis What does this sample represent? A Tendon B Bone C Cartilage D Skeletal muscle E Connective tissue LO 9 LO PRESENTED BYYEW-ERNAU What does this sample represent? A Tendon B Bone C Cartilage D Skeletal muscle E Connective tissueWHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY? Pelvic X-RayAP 4 y/o male patientWHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY?WHAT ISTHE PATHOLOGY? LO 5 LO OUTLINETHE PHYSIOLOGY OF PAIN MECHANISMS PRESENTED BY… OUTLINETHE PHYSIOLOGY OF PAIN MECHANISM Pain: How we feel pain;a subjective experience with emotional,motivational and cognitive components Nociception: Process through which potentially damaging stimuli are detected 4 Phases of Nociception: 1. Transduction – exposure to noxious stimulus producesAP at nociceptors in the periphery 2. Transmission – travels along nerve fibres to the dorsal horn,along the spinothalamic tracts of the spinal cord to the brain 3. Perception – individual experiences discomfort/ pain 4. Modulation – response to the pain- facilitation or inhibition of nociceptive input.TYPES OF SENSORY FIBRES A 19-YEAR-OLDWOMAN GETSA PAPER CUTWHILE ORGANIZING SOME PAPERWORK.SHE EXPERIENCES SUDDEN,SHARP PAINATTHE SITE OFTHE CUT. WHICHTYPE OF NERVE FIBRE IS RESPONSIBLE FORTRANSMITTINGTHIS SENSATIONTOTHE BRAIN? A A-alpha B A-beta C A-delta D C-fibre E D-fibre A 19-YEAR-OLDWOMAN GETSA PAPER CUTWHILE ORGANIZING SOME PAPERWORK.SHE EXPERIENCES SUDDEN,SHARP PAINATTHE SITE OFTHE CUT. WHICHTYPE OF NERVE FIBRE IS RESPONSIBLE FORTRANSMITTINGTHIS SENSATIONTOTHE BRAIN? A A-alpha B A-beta C A-delta D C-fibre E D-fibre TYPES OF SENSORY FIBRES Fast pain is conducted byA-delta fibres.WHICH NERVE ENDINGSARE SENSITIVETOTHERMAL PAIN? A Merkel’s disks B Ruffini’s corpuscles C Free nerve endings D Pacinian corpuscles E Hair follicle receptorsWHICH NERVE ENDINGSARE SENSITIVETOTHERMAL PAIN? A Merkel’s disks B Ruffini’s corpuscles C Free nerve endings D Pacinian corpuscles E Hair follicle receptorsWHICH NERVE ENDINGSARE SENSITIVETOTHERMAL PAIN?A 40-YEAR-OLD GENTLEMAN STUBBED HISTOE ONA DOORSTEP.ASA RESULT,NOCICEPTIVE STIMULITRAVEL FROM HIS LEFTTOETO HIS RIGHT POST-CENTRAL GYRUS,ALONG HIS SPINAL CORD. WHERE DOTHESE FIBERS DECUSSATION? A At the medullary pyramids B At Lissauer’s tract C At the medulla after synapsing with the cuneate or gracile nucleus D A few vertebral levels above or below their entry point into the spinal cord E At the inferiomedial cortex through the internal capsuleA 40-YEAR-OLD GENTLEMAN STUBBED HISTOE ONA DOORSTEP.ASA RESULT,NOCICEPTIVE STIMULITRAVEL FROM HIS LEFTTOETO HIS RIGHT POST-CENTRAL GYRUS,ALONG HIS SPINAL CORD. WHERE DOTHESE FIBERS DECUSSATION? A At the medullary pyramids B At Lissauer’s tract C At the medulla after synapsing with the cuneate or gracile nucleus D A few vertebral levels above or below their entry point into the spinal cord E At the inferiomedial cortex through the internal capsule A 40-YEAR-OLD GENTLEMAN STUBBED HISTOE ONA DOORSTEP.ASA RESULT,NOCICEPTIVE STIMULITRAVEL FROM HIS LEFTTOETO HIS RIGHT POST-CENTRAL GYRUS,ALONG HIS SPINAL CORD. THROUGHWHICH STRUCTURE DOTHESE NOCICEPTIVE FIBRES DECUSSATE? THE SPINOTHALAMICTRACT Conveys pain,temp and crude touch. 1. Information is sent from nociceptors to where the cell bodies lie in the dorsal root ganglion. 2. The neurone enters the spinal cord and ascends or descends for one or two levels through Lissauer’s fasciculus . 3. It then synapses onto a cell body in the dorsal horn of the grey matter,in an area called the substantia gelatinosa. 4. The axon then decussates and ascends in the spinothalmic fasciculus.The decussation occurs through the‘anterior white commissure’. 5. Spinothalamic tract then ascends through brainstem and synapses onto thalamus. 6. Thalamus sends projections to post-central gyrus in the cortex i.e. the primary sensory area.WHICH OFTHESE IS NOTAN EXAMPLE OF HOW PAIN MODULATION CAN REDUCEYOUR PERCEPTION OF PAIN? A Rubbing the site of pain to stimulate the DCML pathway B In response to feeling anger or tiredness C Release of opioids in the substantia gelatinosa D Increased GABA activity in the substantia gelatinosa E Use ofTENS machinesWHICH OFTHESE IS NOTAN EXAMPLE OFWHEN PAIN MODULATION REDUCESYOUR PERCEPTION OF PAIN? A Rubbing the site of pain to stimulate the DCML pathway B In response to feeling anger or tiredness C Release of opioids in the substantia gelatinosa D Increased GABA activity in the substantia gelatinosa E Use ofTENS machinesWHICH OFTHESE IS NOTAN EXAMPLE OF HOW PAIN MODULATION CAN REDUCEYOUR PERCEPTION OF PAIN? •Anger and feeling fatigued can actually exacerbate your perception of pain intensityOUTLINETHE MOLECULARAND CELLULAR BASIS OF INFLAMMATIONOUTLINETHE MOLECULARAND CELLULAR BASIS OF INFLAMMATION Acute Inflammation Vascular Changes ¡ Transient vasoconstriction followed by vasodilation ¡ Increased permeability of vessels- causing fluid and plasma protein exudation ¡ Stasis and concentration RBCs Cellular Changes ¡ Neutrophil migration to site,extravasation into tissues,phagocytosis of pathogens and cellular debris ¡ Release of inflammatory mediators i.e.histamine,serotonin,PGs,LTs,ROS,NO,cytokines,complementOUTLINETHE MOLECULARAND CELLULAR BASIS OFWOUND HEALING STAGES OF HEALING BY FIRST INTENTION 1. Haemostasis – initial vasoconstriction to allow fibrin clot formation,limiting blood loss at the affected area 2. Inflammation 3. Proliferation – proliferation of fibroblasts to form granulation tissue 4. Remodelling – organization of collagen fibres and apoptosis of fibroblasts OUTLINETHE MOLECULARAND CELLULAR BASIS OFWOUND HEALING STAGES OF HEALING BY SECOND INTENTION 1. Haemostasis – initial vasoconstriction to allow clot formation,limiting blood loss at the affected area 2. Inflammation 3. Proliferation – granulation tissue forms from the bottom of the wound upwards.Myofibroblasts (modified smooth muscle cells containing actin and myosin) contract to bring the wound edges together. 4. Remodelling DESCRIBE SKIN STRUCTUREAND FUNCTION ¡ Skin is composed of epidermis,dermis and hypodermis ¡ It also contains many sensory receptors: Receptor Name Location Sensation detected Hair follicle Dermis Light touch Meissner corpuscle Dermal papilla Discriminative touch/ vibration Pacinian corpuscle Deep dermis Vibration Merkel cell Basal epidermis Light touch/ textural discrimination Ruffini ending Dermis Stretch Free nerve ending Epidermis Pain STRUCTURE OFTHE EPIDERMIS Main cell type is keratinocytes,but also contains: ¡ Melanocytes (pigment production) ¡ Langerhans cells (dendritic cells) ¡ Merkel cells (mechanoreceptors) The epidermis has up to 5 sublayers: 1. Stratum basale – mitosis of keratinocytes 2. Stratum spinosum – desmosomes form between cells 3. Stratum granulosum – secrete lipids for waterproofing, ……………………….formation of tight junctions 4. Stratum lucidum – loss of nuclei,keratin production 5. Stratum corneum – loss of all organelles,keratin production Remember the pneumonic: Come Lets Get Some Beer STRUCTURE OFTHE DERMIS The papillary dermis is the thin layer that is composed of loose connective tissue and is highly vascular;it functions to provide nutrients to the lower epidermis. The reticular layer is the deep layer,forming a thick layer of dense connective tissue that constitutes the bulk of the dermis.It’s function is to add strength and pliability to the skin. Fibroblasts are the most abundant cells in the dermis,which generate connective tissue fibres. Collagen (type I and type III) is found in abundance in the dermis. Elastic fibres also play an important structural role – degeneration of elastin over time leads to the sagging of the skin and wrinkling. KELOID SCARSARE GENERATED DUETOA PROLONGED INFLAMMATORY PHASE OFWOUND HEALING, WHICH LEADSTO EXCESSING FIBROBLASTACTIVITYAND DEPOSITION OF COLLAGEN BEYONDTHE ORIGINALWOUND MARGINS.WHICH OFTHE FOLLOWING IS NOTA RISK FACTOR FOR KELOID SCARS? A Being ofAsian ethnicity B Age between 20 and 30 C Being male D Sustaining a burn injury E Location of injury being on the sternal notch KELOID SCARSARE GENERATED DUETOA PROLONGED INFLAMMATORY PHASE OFWOUND HEALING, WHICH LEADSTO EXCESSING FIBROBLASTACTIVITYAND DEPOSITION OF COLLAGEN BEYONDTHE ORIGINALWOUND MARGINS.WHICH OFTHE FOLLOWING IS NOTA RISK FACTOR FOR KELOID SCARS? A Being ofAsian ethnicity B Age between 20 and 30 C Being male D Sustaining a burn injury E Location of injury being on the sternal notch KELOID SCARSARE GENERATED DUETOA PROLONGED INFLAMMATORY PHASE OFWOUND HEALING, WHICH LEADSTO EXCESSING FIBROBLASTACTIVITYAND DEPOSITION OF COLLAGEN BEYONDTHE ORIGINALWOUND MARGINS.WHICH OFTHE FOLLOWING IS NOTA RISK FACTOR FOR KELOID SCARS? Risk Factors The major risk factors for keloid formation are: •Ethnicity – most common in Black African or Caribbean and Asian populations •Age – the highest incidence occurring between 20- 30yrs •Cause of injury – burns carry the highest risk •Anatomical site – most commonly occur in scars on the ear lobe, shoulders, and sternal notch •Previous keloid formation Keloid formation affects both men and women equally.DURINGA POWER CUT, ALEXATTEMPTSTO FINDA BOX OF MATCHES INTHE DRAWERTO LIGHTA CANDLE.WHICH MECHANORECEPTOR,WHICH IS HIGHLYABUNDANT INTHE FINGERTIPS,HELPSTHEM TO FINDTHE CORRECT OBJECT? A Merkel disks B Naked endings C Pacinian corpuscles D Meissner corpuscles E Ruffini endingsDURINGA POWER CUT, ALEXATTEMPTSTO FINDA BOX OF MATCHES INTHE DRAWERTO LIGHTA CANDLE.WHICH MECHANORECEPTOR,WHICH IS HIGHLYABUNDANT INTHE FINGERTIPS,HELPSTHEM TO FINDTHE CORRECT OBJECT? A Merkel disks B Naked endings C Pacinian corpuscles D Meissner corpuscles E Ruffini endings DURINGA POWER CUT, ALEXATTEMPTSTO FINDA BOX OF MATCHES INTHE DRAWERTO LIGHTA CANDLE.WHICH MECHANORECEPTOR,WHICH IS HIGHLYABUNDANT INTHE FINGERTIPS,HELPSTHEM TO FINDTHE CORRECT OBJECT? Receptor Name Location Sensation detected Hair follicle Dermis Light touch Meissner corpuscle Dermal papilla Discriminative touch/ vibration Pacinian corpuscle Deep dermis Vibration Merkel cell Basal epidermis Light touch/ textural discrimination Ruffini ending Dermis Stretch Free nerve ending Epidermis Pain THE LECTURER EXPLAINSTHAT KERATINOCYTES DUPLICATE INTHE STRATUM BASALE,BEFORE TRAVELLING UPWARDSTOWARDSTHE SURFACE,MATURINGALONGTHEWAY.HOW LONG DOES ITTAKE FORA KERATINOCYTETOTRAVEL FROMTHE STRATUM BASALETOTHE STRATUM CORNEUM OFTHE EPIDERMIS? A 20-30 days B 30-40 days C 40-50 days D 50-60 days E 60-70 days HOW LONG DOES ITTAKE FORA KERATINOCYTETOTRAVEL FROMTHE STRATUM BASALETOTHE STRATUM CORNEUM? A 20-30 days B 30-40 days C 40-50 days D 50-60 days E 60-70 days HOW LONG DOES ITTAKE FORA KERATINOCYTETOTRAVEL FROMTHE STRATUM BASALETOTHE STRATUM CORNEUM? ¡ It takes 30-40 days for a keratinocyte to make the journey from basale to corneum ¡ After formation of the waterproofing layer at the stratum granulosum,the keratinocytes die as they are cut off from oxygen and nutrition ¡ Once at the surface,the dead cells flake off in tiny specks call dander (dandruff is accumulation of dander held together by sebum/oil) ¡ In a healthy adult,it takes between 4-6 weeks to completely renew the cells of the skin! INTERMS OF CELLULAR BIOLOGY, WHY DO SOME INDIVIDUALSAT BIRTH HAVEA LIGHTER SHADE OF SKINTHAN OTHERS? A They have less melanocytes B They have a thinner epidermal layer C They have less keratinocytes D They receive less in-utero nutrition E Their melanocytes produce less melanin INTERMS OF CELLULAR BIOLOGY, WHY DO SOME INDIVIDUALSAT BIRTH HAVEA LIGHTER SHADE OF SKINTHAN OTHERS? A They have less melanocytes B They have a thinner epidermal layer C They have less keratinocytes D They receive less in-utero nutrition E Their melanocytes produce less melaninINTERMS OF CELLULAR BIOLOGY, WHY DO SOME INDIVIDUALSAT BIRTH HAVEA LIGHTER SHADE OF SKINTHAN OTHERS? • In different ethnicities, the number of melanocytes is THE SAME. • In light skinned people, the melanin is concentrated deep in the epidermis, particularly in the stratum basale layer. • Differences in skin colour depend on how much melanin is produced. OUTLINETHE MOA OF COMMONANALGESICS ANDANTI-INFLAMMATORY DRUGS PARACETAMOL • Paracetamol is an effective analgesic and antipyretic,that has only weak anti-inflammatory properties. • It’s mechanism of action is not fully understood. • It is thought to act on the central nervous system by inducing effects on pathways involving prostaglandin, serotonin, endogenous opioids, NO and cannabinoids.NSAIDs Steroids Work by reversibly inhibiting cyclo-oxygenase (COX) enzymes. There are 2 main types used medicinally: Examples: • Mineralocorticoid mimetics- used to maintain fluid and electrolyte balance in patients with ibuprofen. hypoaldosteronism naproxen. diclofenac. • Glucocorticoid mimetics- for insufficiencies, anti- inflammatory and immunosuppression. Can be further subdivided based on duration of effect: •Short-acting – Hydrocortisone (1st drug of choicefor replacement therapy) •Intermediateacting – Prednisolone •Long-acting – DexamethasoneOpioids • Bind to opioid receptors in the brain, spinal cord and GI tract • Stop inhibitory neurons from releasing GABA, which promotes the release of dopamine, noradrenaline and serotonin • Pain processing regions (in the thalamus, brainstem and spinal cord) release more serotonin and NA that reduces sensitivity to pain • Reward regions (such as nucleus accumbens, VTA and prefrontal cortex) release more dopamine that results in feeling calm and euphoricAYOUNG CHILD DID NOT RECEIVETHEIR RECOMMENDED COURSE OFVACCINATIONSAND CONSEQUENTLY HAS CONTRACTED MEASLES.HER GP PRESCRIBES CALPOL (LIQUID PARACETAMOL) FORTHE CHILD AS SHE IS SPIKINGA FEVER.WHICH PROTEIN IS RESPONSIBLE FOR HER ELEVATED BODYTEMPERATURE? A PGI2 B Enorphin C PGD2 D Prostacyclin E PGE2AYOUNG CHILD DID NOT RECEIVETHEIR RECOMMENDED COURSE OFVACCINATIONSAND CONSEQUENTLY HAS CONTRACTED MEASLES.HER GP PRESCRIBES CALPOL (LIQUID PARACETAMOL) FORTHE CHILD AS SHE IS SPIKINGA FEVER.WHICH PROTEIN IS RESPONSIBLE FOR HER ELEVATED BODYTEMPERATURE? A PGI2 B Enorphin C PGD2 D Prostacyclin E PGE2AYOUNG CHILD DID NOT RECEIVETHEIR RECOMMENDED COURSE OFVACCINATIONSAND CONSEQUENTLY HAS CONTRACTED MEASLES.HER GP PRESCRIBES CALPOL (LIQUID PARACETAMOL) FORTHE CHILD AS SHE IS SPIKINGA FEVER.WHICH PROTEIN IS RESPONSIBLE FOR HER ELEVATED BODYTEMPERATURE? A common effect of increased PGE2 production is fever.JOHN ISAN IV DRUG USERWHOWANTSTO GIVE UP USING HEROINE. HE PRESENTSTOTHE EDWITH TERRIBLE SYMPTOMS OFWITHDRAWAL FROM OPIOIDS. WHAT ISTHE FIRST LINE MEDICAL TREATMENT INTHIS CASE? A Methadone B Tramadol C Codeine D Low-dose morphine E ParacetamolJOHN ISAN IV DRUG USERWHOWANTSTO GIVE UP USING HEROINE. HE PRESENTSTOTHE EDWITHTERRIBLE SYMPTOMS OFWITHDRAWAL FROM OPIOIDS .WHAT ISTHE FIRST LINE MEDICALTREATMENT INTHIS CASE? A Methadone B Tramadol C Codeine D Low-dose morphine E ParacetamolMethadone is an opioid that can be taken orally as a liquid or tablet. It reduces the withdrawal symptoms and cravings for opioids. It does not result in the feeling of euphoria that most opioids generate,making it the best choice for people who need medical help with their detoxification.A 50YO PATIENT PRESENTSTOTHE GPWITH LOWER BACK PAIN,WHICHTHE GP BELIEVES IS FROM MUSCLE STRAIN. THE PATIENT HASA PMH OF DEPRESSION,GASTRIC ULCERATIONAND HYPERTENSION.WHICH OFTHE FOLLOWING MEDICATIONSARE CONTRAINDICATED INTHIS CASE? A Paracetamol B Naproxen C Codeine D Deep heat cream E AspirinA 50YO PATIENT PRESENTSTOTHE GPWITH LOWER BACK PAIN,WHICHTHE GP BELIEVES IS FROM MUSCLE STRAIN. THE PATIENT HASA PMH OF DEPRESSION,GASTRIC ULCERATIONAND HYPERTENSION.WHICH OFTHE FOLLOWING MEDICATIONSARE CONTRAINDICATED INTHIS CASE? A Paracetamol B Naproxen C Codeine D Deep heat cream E Aspirin• Naproxen is a long-acting NSAID. • Like other NSAIDs, it upregulates the production of leukotrienes as a result of shunting in the AA cascade. • Leukotrienes act on parietal cells to increase HCl production, which can lead to an exacerbation of peptic ulcer disease. • This patient has a PMH of peptic ulcer disease and so naproxen would be counter-indicated.FLUDROCORTISONE MIMICSTHEACTIONS OFALDOSTERONE,BUT FROMWHERE INTHEADRENAL GLAND ISALDOSTERONE RELEASED FROM? A Zona glomerulosa B Zona fasciculata C Zona reticularis D Adrenal medulla E Zone minulataFLUDROCORTISONE MIMICSTHEACTIONS OFALDOSTERONE,BUT FROMWHERE INTHEADRENAL GLAND ISALDOSTERONE RELEASED FROM? A Zona glomerulosa B Zona fasciculata C Zona reticularis D Adrenal medulla E Zone minulataFLUDROCORTISONE MIMICSTHEACTIONS OFALDOSTERONE,BUT FROMWHERE INTHEADRENAL GLAND ISALDOSTERONE RELEASED FROM? Zona glomerulosaMRS HUWS IS STARTED ONA SHORT -TERM COURSE OF PREDNISOLONETO HELPWITH HER FLARE UP OF RHEUMATOIDARTHRITIS.WHICH OFTHE FOLLOWING IS SHE MOST LIKELYTO BEADVISEDABOUT? A That she should not take them before driving,as they induce drowsiness B That she should aim to take them on an empty stomach,to promote absorption C That she may experience weight loss,as they reduce appetite D That she may need to monitor her blood pressure,as they induce hypertension E That long-term use can cause hearing lossMRS HUWS IS STARTED ONA SHORT -TERM COURSE OF PREDNISOLONETO HELPWITH HER FLARE UP OF RHEUMATOIDARTHRITIS.WHICH OFTHE FOLLOWING IS SHE MOST LIKELYTO BEADVISEDABOUT? A That she should not take them before driving,as they induce drowsiness B That she should aim to take them on an empty stomach,to promote absorption C That she may experience weight loss,as they reduce appetite D That she may need to monitor her blood pressure,as they induce hypertension E That long-term use can cause hearing lossLO Outlinethephysiologyofbone health PresentedbyRachaelDavisCellularcomponentsofbone Therearethreecelltypeinbone: • Osteoclasts-resorbsbone Blast=Build • Osteoblasts-formsbone • Osteocytes-maintainsbone Clast=Collapse ⚬ (differentiatedfromosteoblasts) Boneremodellingiscontinuous-especiallyinareasunderstress,tostrengthenthe bone Healthybonehasabalanceofosteoclastandosteoblastactivity Osteoporosisresultsfromosteoclastactivityoutweighingosteoblastactivity Structur eofbone IlikecanaliculiFr actur ehealing 1.Haematoma Days 2.Inflammation 3.Granulation 4.Callus (sofhard) 5.Consolidation Weeks 6.Remodelling YearsAmedicalstudentfracturestheirhumerusinaskatingaccident.Aftertheinjury,shetriestorememberthestagesof bonehealing.Sheknowsthebonewillhaveformedahaematoma,butcannotrememberwhatthenextstageis. Whatisthesecondstageofbonehealing? A Callus formation B Remodelling C Granulation D Consolidation E InflammationAmedicalstudentfracturesherhumerusinaskatingaccident.Aftertheinjury,shetriestorememberthestagesof bonehealing.Sheknowsthebonewillhaveformedahaematoma,butcannotrememberwhatthenextstageis. Whatisthesecondstageofbonehealing? A Callus formation B Remodelling C Granulation D Consolidation E InflammationA5-year-oldboypresentswithhismotherinatraumaandorthopedicsclinicforacheckup2weeksafterfracturing histibiaandfibula.Thedoctoremphasisestheimportanceofcalciumintaketopromotebonehealing.Duringwhich stageofbonehealingdoescalcificationofimmatureboneoccur? A Callus formation B Remodelling C Granulation D Consolidation E InflammationA5-year-oldboypresentswithhismotherinatraumaandorthopedicsclinicforacheckup2weeksafterfracturing histibiaandfibula.Thedoctoremphasisestheimportanceofcalciumintaketopromotebonehealing.Duringwhich stageofbonehealingdoescalcificationofimmatureboneoccur? A Callus formation B Remodelling C Granulation D Consolidation E InflammationAn80yearoldwomanexperiencesapathologicalfractureofherhumerus.FromaDEXAscan,sheisfoundtohave lowbonedensityandisdiagnosedwithosteoporosis. Over-activityofwhichcellcausesosteoporosis? A Osteoclasts B Osteoblasts Osteocytes C D Osteons Osteoprogenitor cells EAn80yearoldwomanexperiencesapathologicalfractureofherhumerus.FromaDEXAscan,sheisfoundtohave lowbonedensityandisdiagnosedwithosteoporosis. Over-activityofwhichcellcausesosteoporosis? A Osteoclasts B Osteoblasts Osteocytes C D Osteons Osteoprogenitor cells EA65yearoldfemalepatientpresentsinherGPpracticewithconcernsaboutherriskofdevelopingosteoporosis. SheaskshowshemightbeabletoreduceherriskandtheGPtellsherthatweight-bearingexercisessuchas jumping,running,andwalkingwouldhelpastheyincreasetheactivityofacertaincellularcomponentofbone. WhichcellistheGPreferringto? A Osteoclasts B Osteoblasts Osteocytes C D Osteons Osteoprogenitor cells EA65yearoldfemalepatientpresentsinherGPpracticewithconcernsaboutherriskofdevelopingosteoporosis. SheaskshowshemightbeabletoreduceherriskandtheGPtellsherthatweight-bearingexercisessuchas jumping,running,andwalkingwouldhelpastheyincreasetheactivityofacertaincellularcomponentofbone. WhichcellistheGPreferringto? A Osteoclasts B Osteoblasts Osteocytes C D Osteons Osteoprogenitor cells EAmedicalstudentisdiscussingthemicroanatomyofbonewithahistologist.Shecannotrecallthenameofthe structurethatosteocyteprojectionspassthrough. Whatisthisstructurecalled? A Lacunae B Canaliculi C Osteons D Haversian canals Volkmann's canals EAmedicalstudentisdiscussingthemicroanatomyofbonewithahistologist.Shecannotrecallthenameofthe structurethatosteocyteprojectionspassthrough. Whatisthisstructurecalled? A Lacunae B Canaliculi C Osteons D Haversian canals Volkmann's canals ELO Describethephysiologyofbruising PresentedbyRachaelDavis Bruisingtimeline Bruise/ contusion = haematoma under the skin due to damage to capillariesBruisingphysiology vert BiliVERdin A7-year-oldboysustainsaninjurytohiskneeafterfallingfromhisbike.Theskinisnotbroken,butquickly hasalargebruiseformonhisknee.After10days,henoticesthebruisehaschangedcolourandnowhas yellowedges. Whichprocessisresponsibleforthebruisechangingcolour? A Deoxygenation of red blood cells B Release of iron from haemoglobin Breakdown of haemoglobin into biliverdin C D Breakdown of biliverdin into bilirubin E Breakdown of bilirubin into hemosiderin A7-year-oldboysustainsaninjurytohiskneeafterfallingfromhisbike.Theskinisnotbroken,butquickly hasalargebruiseformonhisknee.After10days,henoticesthebruisehaschangedcolourandnowhas yellowedges. Whichprocessisresponsibleforthebruisechangingcolour? A Deoxygenation of red blood cells B Release of iron from haemoglobin Breakdown of haemoglobin into biliverdin C D Breakdown of biliverdin into bilirubin E Breakdown of bilirubin into hemosiderinA30-year-oldmansustainsaninjurywhilstplayingcricketwhenacricketballstrikeshimwithforceonhis rightarm. Whichtypeofinjuryishemostlikelytohavesustained? A Abrasion B Incision Contusion C D Laceration Avulsion EA30-year-oldmansustainsaninjurywhilstplayingcricketwhenacricketballstrikeshimwithforceonhis rightarm. Whichtypeofinjuryishemostlikelytohavesustained? A Abrasion B Incision Contusion C D Laceration Avulsion ELO Identifydifferenttypesofblood disorderthatmayalternormal haemostasisandbruising PresentedbyRachaelDavisCoagulation disorders Symptoms • Epistaxis(nosebleeds) • Easybruising • Gumbleeding • Menagorrhea(heavymenstrual Differentials bleeding) • HaemophiliaA • SERIOUS-jointbleeding, • HaemophiliaB haematuria,rectalbleeding • HaemophiliaC • vonWillebrandDisease • VitaminKdeficiencyHaemophilia 1/5000 HaemophiliaA inherit,female carriers) Haemophilia 1/25000 B 1/100000 HaemophiliaCVitamin K deficiency Greenleafyvegetables K e.g.kale,spinach, K K cabbagsproutsoliand 2 ,7 ,9 ,1 0 K "2plus7is9NOT10"ApatientpresentsintheirGPforareviewoftheirwarfarinandisfoundtohaveaconcerninglyreducedINR,leavingthem athighriskofbloodclots.Fromfurtherconversation,thepatientrevealsthattheyhavealteredtheirdietrecentlytotryand leadahealthierlifestyle.Theyindicatethattheynowhave3spinach,kaleandapplesmoothiesperdayandtrytohave sproutsorbroccoliwithasmanymealsaspossible.WhatisitaboutthesefoodsthatcouldhavecausedareducedINR? A TheyarehighinVitaminKwhichisacompetitiveinhibitorofwarfarin B TheyarehighinVitaminKandsoincreaseprothrombinproduction C TheyhavenoVitaminKsothepatienthasaVitaminKdeficiency D TheyarehighinVitaminKwhichinhibitsclottingfactorII E TheyarehighinVitaminKandclottingfactorXIisVitaminKdependentApatientpresentsintheirGPforareviewoftheirwarfarinandisfoundtohaveaconcerninglyreducedINR,leavingthemat highriskofbloodclots.Fromfurtherconversation,thepatientrevealsthattheyhavealteredtheirdietrecentlytotryandlead ahealthierlifestyle.Theysaythattheynowhave5spinach,kaleandapplesmoothieseveryday.Howmightthesefoods causeareducedINR? A TheyarehighinVitaminKwhichisacompetitiveinhibitorofwarfarin B TheyarehighinVitaminKandsoincreaseprothrombinproduction C TheyhavenoVitaminKsothepatienthasaVitaminKdeficiency D TheyarehighinVitaminKwhichinhibitsclottingfactorII E TheyarehighinVitaminKandclottingfactorXIisVitaminKdependentAmotherbringshertoddlertotheGPashehadsustainedagrazeonhislegwhichdidn’tstopbleeding.Thedoctor orderedbloodandgenetictestsandconfirmedthatthetoddlerhasVonWillebrand‘sdisease.Sheexplainsthat therearedifferentpathwaysinvolvedintheclottingcascadeandthatoneofthemistheintrinsicpathway.Whatare the4clottingfactorsinvolvedinthepathwaymentioned? A 9,8,2,1 B 10,9,7,2 C 11,10,9,8 D 12,11,9,8 E 13,11,10,9AmotherbringshertoddlertotheGPashehadsustainedagrazeonhislegwhichdidn’tstopbleeding.Thedoctor orderedbloodandgenetictestsandconfirmedthatthetoddlerhasVonWillebrand‘sdisease.Sheexplainsthat therearedifferentpathwaysinvolvedintheclottingcascadeandthatoneofthemistheintrinsicpathway.Whatare the4clottingfactorsinvolvedinthepathwaymentioned? A 9,8,2,1 B 10,9,7,2 C 11,10,9,8 D 12,11,9,8 E 13,11,10,9 ApatientpresentsintheirGPwithahistoryofuncontrolledbleedingandeasybrusing. The GPdoessometestsandfindsthepatientisdeficientincoagulationfactor9(IX). Whatconditionisthiscalled? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiency ApatientpresentsintheirGPwithahistoryofuncontrolledbleedingandeasybruising. The GPdoessometestsandfindsthepatientisdeficientincoagulationfactor9(IX). Whatconditionisthiscalled? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiencyApatientmentionsfrequentnosebleedsandheavymenstrualperiodstotheirGP .Uponinvestigation,theyare foundtohaveanincreasedbleedingtimebutanormalprothrombintimeandAPTT. Whatconditiondotheseresultsindicate? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiency ApatientmentionsfrequentnosebleedsandheavymenstrualperiodstotheirGP .Uponinvestigation,theyare foundtohaveanincreasedbleedingtimebutanormalprothrombintimeandAPTT. Whatconditiondotheseresultsindicate? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiencyOnatriptothedentist,apatientisfoundtohavepoordentalhygiene.Whenaskingabouttheirbrushinghabits, thepatientrevealstheyrarelybrushtheirteethastheyarenervousaboutcausingableedintheirgumsasthey have"Christmasdisease". Whatisthisconditionalsoknownas? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiencyOnatriptothedentist,apatientisfoundtohavepoordentalhygiene.Whenaskingabouttheirbrushinghabits, thepatientrevealstheyrarelybrushtheirteethastheyarenervousaboutcausingableedintheirgumsasthey have"Christmasdisease". Whatisthisconditionalsoknownas? A HaemophiliaA B HaemophiliaB C HaemophiliaC D Von-WillebrandDisease E VitaminKdeficiency