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OSCEazy SBA series x Cardiff Medsoc Case 1 Nicole Lau Question 1 A Greenstickfracture Which of the following options is this statementdescribing? B Comminutedfracture A fracture wherethe bone is broken at least three or more positions. Spiral fracture C D Crush fracture E Buckle fracture Question 1 A Greenstickfracture Which of the following types of fracturesis this statementdescribing? B Comminuted fracture A fracture wherethe bone is broken at least three or more positions. Spiral fracture C D Crush fracture E Buckle fracture Greenstickfracture Comminutedfracture An incomplete break in the bone, where the The bone is shattered into three or more fragments. bone bends and cracks on one side, but does This is in contrast to a simple fracture, where the not break all the way through. This type of bone breaks into two main pieces. fracture is common in children whose bones are more flexible. Spiral fracture Crushfracture https://www.researchgate.net/figure/ A spiral fracture is a type of break where the This name was made up fracture_fig2_318492019laced- bone fractures in a spiral or twisting pattern, often due to a rotating force applied to the limb. This type of fracture can occur in the long bones of the arms or legs. Bucklefracture A type of incomplete break where one side of the bone bends or buckles, but the bone does not break all the way through. This is common in the bones of children. https://commons.m.wikimedia.org/wiki/File:Buckle_Fracture.jpg#mw-jump-to-license Question 2 A 5, 3, 4, 1, 6, 2 Placethestagesofbonehealinginthecorrect order: B 3, 5, 4, 1, 6, 2 1.Callus 2.Remodelling 3.Haematoma C 4, 3, 5, 1, 6, 2 4.Inflammation 5.Granulation 6.Consolidation D 3, 4, 5, 1, 6, 2 E 4, 5, 6, 3, 1, 2 Question 2 A 5, 3, 4, 1, 6, 2 Placethestagesofbonehealinginthecorrect order: B 3, 5, 4, 1, 6, 2 1.Callus 2.Remodelling 3.Haematoma C 4, 3, 5, 1, 6, 2 4.Inflammation 5.Granulation 6.Consolidation D 3, 4, 5, 1, 6, 2 E 4, 5, 6, 3, 1, 2 1. Haematoma 2. Inflammation Caused by blood vessel tearing which results in local bleeding The defectbetween fractured ends is filled with the blood clot The injury results in acute inflammation Macrophages invade the clot and start the destruction 3. Granulation 4. Callus Vascularin growth (growth of capillaries) • Islandsof cartilage appear (specially near the periosteum) By day 5 the granulation tissue has replaced the clot and extends • fracture ends are now united by vascularisedgranulation tissue into the marrow cavity and cartilage= provisional callus In the granulation tissue, small groups of cartilage begin to form • Day 7: calcium is deposited in the cartilage and the osteoblasts start to produce a seam of osteoids across the fracture 5. Consolidation 6. Remodelling Endocondral ossification is established and adds to the new Woven bone (immature bone) is replaced by lamellar bone bone. (bone containing osteoblasts and osteoclasts) The callus calcifies and the end of the fracture unite with bony Excess bone is slowly resorbed callus This process can take years to complete and is often incomplete Question 3 Initiation,amplification, A Whichofthefollowingisthecorrectorderof proliferation eventsinthecell-basedmodelforclot Initiation,proliferation, formation? B amplification Initiation,propagation, C amplification Initiation,amplification, D propagation E Propagation,initiation, amplification Question 3 Initiation,amplification, A Whichofthefollowingisthecorrectorderof proliferation eventsinthecell-basedmodelforclot Initiation,proliferation, formation? B amplification Initiation,propagation, C amplification Initiation,amplification, D propagation E Propagation,initiation, amplification Smallamounts of coagulationfactors(II, VII, IX and X) diffuseacross the vesselwallinto the surroundingtissue. Initiation Theybecomenonspecificallyactivated. They formthe extrinsic pathway, but it is of very low activity due to the absenceof Fva anddue to the low concentrationof coagulant factors beingpresent. Only a small amount of thrombin is produced. Amplificationstartswhen the vesselis damagedand blood enters the surroundingtissue. Thesmallamount of thrombinfromthe initiationstageactivates manyof the incomingcoagulationfactors and thesego on to activateothercoagulationfactors. Amplification In this stage, the IXa.VIIIa complex which has an affinity for a negatively charged environment, binds to the negatively charged phospholipid surface. Propagation It is much more active in this environment and efficiently converts FX to F Xa. The FX a thencomplexeswith anyFva thatis presentandthis complexbindsto the negativelychargedphospholipidsurface. It is more active in thisenvironmentand efficientlyconvertsFII to FIIa. Co-localisation of IXa.VIIIa and Xa.Va adds to the efficiency and results in rapid and quantitative production of thrombin, known as the thrombin burst. The large amount of thrombin quantitatively converts fibrinogen to fibrin for the clot. Question 4 A HaemophiliaA A7-year-oldboypresentswithahistoryof prolongedbleedingepisodes.Laboratory testsrevealadecreasedleveloffactorIX B HaemophiliaB activity.Whichofthefollowingconditiondoes thisboyhave? C HaemophiliaC D HaemophiliaD Question 4 A HaemophiliaA A7-year-oldboypresentswithahistoryof prolongedbleedingepisodes.Laboratory testsrevealadecreasedleveloffactorIX B HaemophiliaB activity.Whichofthefollowingconditiondoes thisboyhave? C HaemophiliaC D HaemophiliaDClassical coagulation model https://www.osmosis.org /answers/coagulation- cascade Haemophilia A Haemophilia B It is characterisedby a deficiencyor dysfunctionof It is characterisedby a deficiency or dysfunctionof factor VIII. factor IX. lesscommonthanhemophiliaA but presentswith similarsymptomsof prolonged bleeding Haemophilia C It is a milder formof hemophiliacaused by a deficiencyof factorXl. It is relativelyrareandtypicallypresents with less severebleedingsymptomscomparedto hemophiliaA andB. Question 5 Spinothalamic,enkephalin, A serotonin,ventral The periaqueductal gray (PAG) receives information from the ascending pain and temperature fibres of the (1) tract. Spinothalamic,nociceptin, Stimulation of the PAG activates (2)-releasing neurons that projnoradrenaline,dorsal the raphe nucleus in the brainstem. This leads to the release of (3) which descends and binds tC Spinocerebellar,enkephalin, interneurone in the substantia gelatinosa of the (4) horn. noradrenaline,ventral Upon activation, the interneurone releases endogenous opioid Spinothalamic,enkephalin, neurotransmitters that to Mu opioid receptors on the axons Df serotonin,dorsal incoming Ad and C fibres. Mu opioid receptors inhibit the release of substance P inhiEiting thethalamic,enkephalin, experience of pain noradrenaline,dorsal Question 5 Spinothalamic,enkephalin, A serotonin,ventral The periaqueductal gray (PAG) receives information from the ascending pain and temperature fibres of the (1) tract. Spinothalamic,nociceptin, Stimulation of the PAG activates (2)-releasing neurons that projnoradrenaline,dorsal the raphe nucleus in the brainstem. This leads to the release of (3) which descends and binds tC Spinocerebellar,enkephalin, interneurone in the substantia gelatinosa of the (4) horn. noradrenaline,ventral Upon activation, the interneurone releases endogenous opioid Spinothalamic,enkephalin, neurotransmitters that to Mu opioid receptors on the axons Df serotonin,dorsal incoming Ad and C fibres. Mu opioid receptors inhibit the release of substance P inhiEiting thethalamic,enkephalin, experience of pain noradrenaline,dorsal PAG is the primary control centre for the descending pain modulatory system Pain Modulation The PAG receives information from the ascending pain and temperature fibres of the spinothalamic tract. Stimulation of the PAG activates enkephalin-releasing neurons that project to the raphe nucleus in the brainstem. This leads to the release of serotonin which descends and binds to interneurone in the substantia gelatinosa of the dorsal horn. Upon activation, the interneurone releases opioid neurotransmitters that bind to Mu opioid receptors on the axons of incoming A delta and C fibres. Mu opioid receptors inhibit the release of substance P inhibiting the experience of pain Question 6 A PGHS-2 Which of the following options causes platelet aggregation and local vasoconstriction? B PGHS-1 C PGE2 D PGI2 E TXA2 Question 6 A PGHS-2 Which of the following options causes platelet aggregation and local vasoconstriction? B PGHS-1 C PGE2 D PGI2 E TXA2 Phospholipase A2 leaves the fatty acid tails of the phospholipids by separating the fatty acids from the phosphate and glycerol. These FA are a precursor to prostaglandins Prostaglandin production Arachidonic acid (AA) is a polyunsaturated omega-6 FA (20:4 w-6) It has 20 carbon atoms and 4 C=C double bonds. The double bonds allow the molecule to be modified to form different prostaglandins. Prostaglandin H synthase has two catalytic domains. The cyclo-oxygenase domain converts AA and O2 into two initial endoperoxides which can then be modified into cell specific prostaglandins. Prostaglandins are eventually responsible for causing local pain. Prostaglandin H synthase has 3 distinct isoforms: PGHS-1, PGHS- 2 and PGHS-3. Prostaglandin roles PGHS-2 PGHS-1 Pghs-2, is the inducible cyclooxygenase isoform. Its PGHS-1, is the constitutively expressed expression is induced by inflammation, growth factors, cyclooxygenase isoform. It maintains normal and other stimuli. Pghs-2 produces prostaglandins physiological functions like protecting the involved in pathological processes like inflammation, stomach, regulating kidney blood flow, and pain, and fever. Selective Pghs-2 inhibition is a target sustaining platelet activity. Pghs-1 is considered a for anti-inflammatory and pain medications. "housekeeping" enzyme. PGE2 PGI2 Produced in the GI mucosa and causes uterine Inhibits platelet aggregation and causes local contraction. It is a pain sensitiser and inflammatory vasodilation mediator (causing location vasodilation, histamine and bradykinin release, and eosinophil and basophil chemotaxis) PGE2 normally sensitises Ad and C nociceptive neurons to serotonin, bradykinins and substance P. Prostaglandin roles TXA2 Causes platelet aggregation and local vasoconstriction Question 7 Which of the following option describes the mechanismof A Opioid receptor agonist actionof paracetamol? Glucocorticoid steroid receptor agonist B C Reversible inhibition of the peroxidase domain activity in PGHS-2 Competitive inhibitor of COX domain in D PGHS E Irreversible inhibitor of COX domain in PGHS Question 7 Which of the following option describes the mechanismof A Opioid receptor agonist actionof paracetamol? Glucocorticoid steroid receptor agonist B Reversible inhibition of the C peroxidase domain activity in PGHS-2 Competitive inhibitor of COX domain in D PGHS E Irreversible inhibitor of COX domain in PGHS Medications Codeine Prednisolone Codeine is an opioid receptor agonist. It is a glucocorticoid steroid receptor agonist. ADRs include constipation dizziness drowsiness and ADRs include Cushing’s syndrome and immune dependence suppression It is contraindicated if there is acute respiratory Contraindicated if there is acute infection. depression or a coma Paracetamol Ibuprofen Paracetamol may be chosen before NSAIDs as it can The S-enantiomer is the active NSAID. have better analgesic and anti-pyretic effects. But it It competes with AA for the COX domain active site has very little anti-inflammatory action. of PGHS 1/2. It is a reversible competitive inhibitor Paracetamol’s MOA although not clear is thought to of PGHS. inhibit the peroxidase domain activity in PGHS-2, or PGHS-3 in the CNS. Medications Aspirin Acetyl Salicylic Acid is the only irreversibleinhibitor of PGHS. It acts by causing the acetylation of a serine residue in the COX domain active site. It is derived from willow tree bark (which contains salicin). Question 8 A 3, 4, 1, 2 Please arrange the following steps of the migration of neutrophils during inflammation in the correctorder: B 3, 1, 4, 2 1. Diapedesis 2.Migration 3. Rolling adhesion C 2, 3, 4, 1 4. Tight binding. D 2, 1, 3, 4 E 2, 3, 1, 4 Question 8 A 3, 4, 1, 2 Please arrange the following steps of the migration of neutrophils during inflammation in the correctorder: B 3, 1, 4, 2 1. Diapedesis 2.Migration 3. Rolling adhesion C 2, 3, 4, 1 4. Tight binding. D 2, 1, 3, 4 E 2, 3, 1, 4 In response to an inflammatory stimulus, cells in the affected area release IL-8 and TNF-a. IL-8 specifically plays a role in regulating neutrophil migration. NeutrophilMigrationduring Inflammation TNF-a acts on endothelial cells lining the blood vessels, increasing the expression of selectins.Selectins are cell adhesion molecules that slow down passingneutrophils, allowing them to interact with the vessel wall. TNF-alpha also makes the blood vessels slightly more permeable, facilitatingthe migration of immune cells. Secreted IL-8 attaches to cell surfaces, including endothelial cells, and the extracellular matrix (ECM) in the vicinity of the inflammation site. The interaction betweenIL-8 and IL-8 receptors on neutrophils in the blood triggers the activation of adhesion molecules on the surface of neutrophils. These adhesion molecules promote the tight binding of neutrophils to the endothelial cells lining the blood vessels,preparing them for migration. Neutrophils undergo diapedesis, which is the process of squeezing between the endothelial cells and migrating out of the blood vessel into the subendothelial space. In the subendothelial space, neutrophils follow a gradient of IL-8 towards the infected or inflamed site. The concentration of IL-8 is highest in the area of inflammation, creating a chemotactic gradient that guides the neutrophils towards NeutrophilMigrationduring the source of infection. InflammationOSCEazy SBA series Cases 3 Question 1 A Stronger, more, skeletal Comparedto the trachea,tertiary bronchioleshave ( ) cartilaginous rings and ( ) elastin. Tertiary bronchioles also B Weaker, less,smooth have ( ) muscles,allowing contraction and relaxation of these bronchioles. Weaker, more, smooth C D Weaker, less,smooth E Stronger, less,skeletal Question 1 A Stronger, more, skeletal Comparedto the trachea,tertiary bronchioleshave ( ) cartilaginous rings and ( ) elastin. Tertiary bronchioles also B Weaker, less,smooth have ( ) muscles,allowing contraction and relaxation of these bronchioles. Weaker, more, smooth C D Weaker, less,smooth E Stronger, less,skeletal Definitions Trachea Tertiarybronchioles • Has 20 C-shaped cartilaginous rings made up of • Have weaker cartilaginous rings compared to the hyaline cartilage central airways • A wide and flexible tube but it is a strong structure • Have more elastin, particularly in the sub mucosa which to prevent it from collapsing when you breathe out allows more flexibility and the epithelium in the tertiary • The gaps between the cartilaginous rings are filled bronchi is tall columnar and have fewer numbers of with the trachealis muscle and there are glands goblet cells than the trachea surrounding the lumen of the trachea which produce • The bronchial smooth muscle is important in terms of mucus which is important in trapping various the prescribing medication and treatment for airway diseases. These bronchial smooth muscle can contract different particles and pathogens. making the airways narrower and vice versa. Question 2 A Acinus Match the following description to the correct option: • rounded cells in the alveoli with cytoplasms rich in mitochondria • are responsible for secreting surfactant (reduces surface tension) C Type 1 pneumocyte D Type 2 pneumocyte E Alveolar macrophages Question 2 A Acinus Match the following description to the correct option: • rounded cells in the alveoli with cytoplasms rich in mitochondria • are responsible for secreting surfactant (reduces surface tension) C Type 1 pneumocyte D Type 2 pneumocyte E Alveolar macrophages Acinus Segment Part of the airway that is involved in gas exchange, A segment is a functionally independent unit of the e.g. respiratory bronchioles, alveolar ducts and lung supplied with its own lymphatic drainage and alveolar sacs innervation. https://radiopaedia.org/cases/secondary-pulmonary-lobule-illustration https://images.app.goo.gl/ek81iwYrtFwx2LgG8 https://radiologyassistant.nl/chest/lung-anatomy/lung-segments Type 1 and 2 pneumocytes TypeI pneumocytesare flat cells with large cytoplasms which make up 40% of the cells and make up 90% of the surface lining TypeII pneumocytesare rounded cells with cytoplasms rich in mitochondria make up 60% of the cells and are responsible for secreting surfactant (reduces surface tension) Illustrationof alveoles.The Sars-CoV-2-Virus can attachon type II pneumocytes © Diane Schad MPIIB Alveolar macrophages Alveolarmacrophageswhich are derived from circulating monocytes which enter the alveoli and phagocytose foreign material Question 3 A Passive,ascends, internal, downwards Expirationis a ( 1 ) process Thediaphragmrelaxesand2 ) to originaldome shapedposition Active,ascends,internal, The( 3 ) intercostalmusclesrelax andthe ribs)ove( 4 B atmosphereein the thoraxincreasesandairis forcedout intothe downwards Passive,descends,external, C downwards D Passive,ascends, external, downwards Passive,ascends, external, E upwards Question 3 A Passive,ascends, internal, downwards Expirationis a ( 1 ) process Thediaphragmrelaxesand2 ) to originaldome shapedposition Active,ascends,internal, The( 3 ) intercostalmusclesrelax andthe ribs)ove( 4 B atmosphereein the thoraxincreasesandairis forcedout intothe downwards Passive,descends,external, C downwards D Passive,ascends, external, downwards Passive,ascends, external, E upwards Definitions Inspiration Expiration Expiration is a passive process which relies on the The diaphragm contracts, flattens and moves downwards elastic recoil of the lungs and chest walls The external intercostal muscles contract, pulling the ribs upwards The diaphragm relaxes and ascends to original dome and outwards shaped position This causes an increase in the volume of the chest cavity which The external intercostal muscles relax and the ribs results in a decrease in the pressure inside the chest cavity and move downwards air rushes into the lungs The volume of the chest cavity decreasesand the pressure in the thorax increases and air is forced out into the atmosphere Question 4 A Complete pulmonary obstruction Which of the following scenarios cause V/Q ratio to become infinite? Lung fibrosis B C Pulmonary embolism D Severe bronchospasm E Severe pulmonary oedema Question 4 A Complete pulmonary obstruction Which of the following scenarios cause V/Q ratio to become infinite? B Lung fibrosis C Pulmonary embolism D Severe bronchospasm E Severe pulmonary oedema The ventilation-perfusion ratio is the amount of air entering the alveoli, dividedby the amount of blood flowing into the alveoli. The V Q ratio can vary considerably from infinity (ventilated alveoli that are not perfused) to zero ( blood that flows through the lungs without coming into contact with the alveolar air). In reality it can be distinguished between three V/Q Ratio situations: Well-ventilated alveoli that are well perfused with blood (V/Q ratio is almost 1). Poorly ventilated alveoli that are well perfused with blood (V/Q ratio is less than one). Well-ventilated alveoli that are poorly perfused with blood (V/Q ratio greater than 1). Completelung obstruction Lungfibrosis there will be no ventilation (airflow) to lung tissue becomes scarred and stiff that area Areas of the lung affected by fibrosis Blood flow (perfusion) may still occur through the pulmonary arteries, may have decreased or absent ventilation, resulting in a V/Q ratio of 0. V/Q is reduced/0 Pulmonaryembolism Severe bronchospasms occurs when a blood clot (typically originating from the deep veins of the significant constriction of the legs) travels to the lungs and blocks a bronchioles,leading to pulmonary artery. decreasedor absentventilation to the affected areas.V/Q ratio Ventilation continues, but there is no of 0 in those regions blood flow to that region, V/Q = infinite Pulmonaryoedema severe pulmonary edema: fluid accumulates within the alveoli, impairing gas exchange. This can lead to a decreased or absent ventilation in the affected areas while blood flow continues, resulting in a V/Q ratio of 0. Question 5 DecreasedpH andincreasedPCO2 shift A the oxygen-hemoglobin dissociation curve Which of the following best describes the Bohr to the right. effect on oxygen binding in peripheral tissues? IncreasedpHanddecreasedPCO2 shift the (Think about the oxyhemoglobin dissociation curve) oxygen-hemoglobin dissociation curve to B the left. IncreasedpHandincreasedPCO2 shift the C oxygen-hemoglobin dissociation curve to the right. Decreased pH and decreased PCO2have no D effect on the oxygen-hemoglobin dissociationcurve. Question 5 DecreasedpH andincreasedPCO2 shift A the oxygen-hemoglobin dissociation curve Which of the following best describes the Bohr to the right. effect on oxygen binding in peripheral tissues? IncreasedpHanddecreasedPCO2 shift the (Think about the oxyhemoglobin dissociation curve) oxygen-hemoglobin dissociation curve to B the left. IncreasedpHandincreasedPCO2 shift the C oxygen-hemoglobin dissociation curve to the right. Decreased pH and decreased PCO2have no D effect on the oxygen-hemoglobin dissociationcurve.Oxygen dissociation curve Decreased PCO2: In the lungs, the PCO2 is lower compared to other tissues in the body. This decrease in PCO2 leads to increased pH in the blood. The higher pH causes a shift of the oxygen- Bohr’ s effect in lungs hemoglobin dissociation curve to the left, indicating increased affinity of hemoglobin for oxygen. This shift allows for efficient oxygen uptake in the lungs. more oxygen can be loaded onto hemoglobin in the lungs, facilitating oxygenation of the blood. byproduct. This leads to an increase in carbon dioxide levels and subsequent production of carbonic acid. Carbonic acid dissociates into hydrogen ions (H+) and bicarbonate ions (HCO3-), resulting in a decrease in tissue pH. The lower pH causes a rightward shift of the oxygen- hemoglobin dissociation curve, indicating decreased affinity Bohr’ s effect in of hemoglobin for oxygen. peripheral tissues This shift promotes the offloading of oxygen from hemoglobin to the surrounding tissues. This shift promotes the offloading of oxygen from hemoglobin to the surrounding tissues. Question 6 A Non-respiratory portion of the lungs Which of the following best describes physiological dead space in the lungs? The portion of the lungs with impaired B perfusion and ventilation The portion of lungs with no gas C exchange due to impaired perfusion and air in non-respiratory parts of the lung D The region where oxygen is removed from the blood. The area of the lungs where ventilation E is absent Question 6 A Non-respiratory portion of the lungs Which of the following best describes physiological dead space in the lungs? The portion of the lungs with impaired B perfusion and ventilation The portion of lungs with no gas exchange due to impaired perfusion and C air in non-respiratory parts of the lung D The region where oxygen is removed from the blood. The area of the lungs where ventilation E is absent Definitions Anatomical dead space • the portion of the respiratory system where there is no gas exchange. It includes the conducting airways, such as the trachea, bronchi, and bronchioles, that do not contain respiratory surfaces (alveoli). • Although air is inhaled into these airways, it does not participate in gas exchange with the blood. • fixed volume that is approximately 150 mL in a healthy adult Physiological dead space • Anatomical dead space + functionaldead space • portionof the respiratorysystemwhere ventilationoccurs but does not contributeto gas exchange due to inadequate perfusion.It representsthe mismatch between ventilationand perfusion. • can occur when there is reduced or absent blood flow to certainareas of the lung, such as in pulmonary embolismor lung diseases. • alveoli are ventilated,they do not receive adequate blood supply, resultingin inefficient gas exchange. Question 7 Confusion, restlessness, cyanosis, asterixis A Which of the following options correctly describes symptoms of high CO2 levels in a patient? Drowsiness, headache, agitation, B bounding pulse, asterixis C Confusion, restlessness, cyanosis, tachypneoa Drowsiness, headache, agitation, D tachypneoa, asterixis E Confusion, restlessness, cyanosis, headache Question 7 Confusion, restlessness, cyanosis, asterixis A Which of the following options correctly describes symptoms of high CO2 levels in a patient? Drowsiness, headache, agitation, B bounding pulse, asterixis C Confusion, restlessness, cyanosis, tachypneoa Drowsiness, headache, agitation, D tachypneoa, asterixis E Confusion, restlessness, cyanosis, headache Definitions Symptomsof Low Oxygen Symptomsof highCO2 • Confusion • Drowsiness/daytime sleepiness • Restlessness (hypersomnelence) • Cyanosis • Confusion • Tachypneoa (increased respiratory rate) • Headache (worse in the mornings due to overnight hypoventilation) • Agitation • Bounding pulse • Hand flap (asterixis) Question 8 Matchthis descriptionwith the correct answer: A Stretch receptors Thesereceptorsare located in regionsof highbloodflow Proprioceptors A decreasein PO2, or an increasein PCO2, causes increased firing B of impulses Theseact rapidlyandare sensitive to evensmalloscillations which C PeripheralChemoreceptors occurduringbreathing Thesearemost sensitive to low levelsof oxygenin the blood D CentralChemoreceptors E Juxta- pulmonary receptors Question 8 A Stretch receptors Thesereceptorsare located in regionsof highbloodflow A decreasein PO2, or an increasein PCO2, causes increased firing of impulses B Proprioceptors Theseact rapidlyandare sensitive to evensmalloscillations which occurduringbreathing Thesearemost sensitive to low levelsof oxygenin the blood C PeripheralChemoreceptors D CentralChemoreceptors E Juxta- pulmonary receptors Receptors involved in breathing Stretch receptors Proprioceptors • Mechanosensitive receptors which sense • Located in the Golgi Tendon Organs of the expansion of the lung and they prevent joints. over inflation of the lungs • When exercising these relay information to the brainstem so that minute ventilation • Activates in the end inspiratory phase can be increased Peripheralchemoreceptors Centralchemoreceptors • Located in the carotid and aortic bodies (regions of high • Located in the brainstem in the regions concerned blood flow) with the regulation of breathing, near the • A decrease in PO2, or an increase in PCO2/[H+], causes ventrolateral surface of the medulla. increased firing of impulses • These act rapidly and are sensitive to even small • Sensitive to changes in the pH of the cerebrospinal oscillations which occur during breathing fluid (CSF) • These are most sensitive to low levels of oxygen in the • A relatively slow response time and are relatively blood insensitive to the changes in PO2 Receptors involved in breathing Juxta- pulmonaryreceptors • “J” receptors-pulmonary C fibres sensitive to pressure changes • sensory nerve endings located within the alveoli walls in juxtaposition to the pulmonary capillaries of the lungs • Responds, to events, like pulmonary oedema, pulmonary emboli, pneumonia etc • The stimulation of J receptors causes a reflex increase in breathing Question 9 Which of the following is the mechanism of action of A Short-term beta-2 adrenergic, receptor agonist ipratropium? Long-term beta-2 adrenergic, B receptor agonist C Steroid Short-term muscarinic acetylcholine D antagonist Long- term muscarinic acetylcholine E antagonist Question 9 Which of the following is the mechanism of action of A Short-term beta-2 adrenergic, receptor agonist ipratropium? Long-term beta-2 adrenergic, B receptor agonist C Steroid Short-term muscarinic acetylcholine D antagonist Long- term muscarinic acetylcholine E antagonist Medications Short-term beta-2 adrenergic, Long-term beta-2 adrenergic, receptor agonist receptor agonist E.g. Salbutamol E.g.Salmeterol Causesbronchodilationandsmooth muscle relaxation Causesbronchodilation Activation causes adenylyl cyclase to convert ATP to cAMP, Activationcausesadenylylcyclaseto convertATPto cAMP, increases uptakeof Ca2+in sarcoplasmicreticulum, reducing increasesuptakeof Ca2+in sarcoplasmicreticulum,reducingactin myosininteraction,musclerelaxes actin myosin interaction, muscle relaxes Steroids Short-term muscarinic acetylcholine antagonist E.g. Ipratropium E.g. Fluticasone It leads to decreased contraction of the smooth Forms of complex with glucocorticoid receptor, is muscles which then act as a transcriptional regulatory and reduces inflammation It blocks cholinergic receptors,which decreasesthe production of cGMP, inhibiting bronchoconstriction Medications Long-term muscarinic acetylcholine antagonist E.g. tiotropium It leadsto decreasedcontractionof the smoothmuscles It blocks cholinergicreceptors,whichdecreasestheproductionof cGMP,inhibiting bronchoconstriction Question 10 A Respiratory acidosis Which of the following options matches with the ABG pattern down below: B Respiratory alkalosis • pH: low or normal • pCO2: low • HCO3: low C Metabolic acidosis Metabolic alkalosis D Question 10 A Respiratory acidosis Which of the following options matches with the ABG pattern down below: B Respiratory alkalosis • pH: low or normal • pCO2: low • HCO3: low C Metabolic acidosis Metabolic alkalosis D Carbonic acid is the most important buffer in the body CO2+H2O=H2CO3=H++HCO3- Changes in CO2 can be controlled by ventilation (increased or decreasing the respiratory rate and depth). This is called respiratory compensations and occurs rapidly within hours or minutes Changes in HCO3- can be controlled through renal reabsorption / excretion. This is called metabolic compensation and it is a slow Acid-base balance process and can take days to come into effect. -abnormal CO2 clearance from the lungs ;Respiratory acidosis and alkalosis -abnormalities in the regulation of bicarbonate; metabolic acidosis and alkalosis Therefore acidosis or alkalosis implies that the compensation is failing Respiratory acidosis Respiratoryalkalosis There is a reduction in pH and increase in PaCO2 There is an increase in Ph and a decrease in PaCO2 Metabolicacidosis Metabolicalkalosis There is a decrease in pH and a negative base There would be an increase in PH and BE and HCO3 excess and a reduction in HCO3 levels. There may be respiratory compensation E.g. vomiting, diuretics (Less sodium and water reabsorbed, reduction of blood pressure, renin- E.g. hypoperfusion of tissues,diabetic ketoacidosis, renalfailure angiotensin aldosterone system activated, K+ and H+ removed, HCO3 increases in concentration) Question 11 A Conn’s syndrome Which of the following options causes metabolic alkalosis? B Renal failure C Type 2 respiratory failure D Panic attacks E Overdose of salicylates Question 11 A Conn’s syndrome Which of the following options causes metabolic alkalosis? B Renal failure C Type 2 respiratory failure D Panic attacks E Overdose of salicylates Medications Conn’s syndrome Renal failure • Leads to metabolic alkalosis due to aldosterone's effects on the kidneys. 1. Impaired acid-base regulation by the kidneys 2. Reduced bicarbonate reabsorption • Aldosterone increases sodium reabsorption, which drives potassium excretion. • To maintain electrical neutrality, bicarbonate is also reabsorbed, causing an 3. Impaired ammonium excretion increase in blood pH and bicarbonate levels, resulting in metabolic alkalosis. 4. Decreased titratable acid excretionThese factors collectively cause a decrease in blood bicarbonate and an increase in hydrogen ions, resulting in metabolic acidosis. Type 2 respiratory failure Panic attacks • Impaired ventilation leads to CO2 accumulation, increasing carbonic acid Panic attacks cause hyperventilation, which reduces CO2 levels and increases and causing respiratoryacidosis. blood pH, leading to respiratory alkalosis. The kidneys try to compensate, but • The kidneys compensate by increasing bicarbonate reabsorption,but the the initial response is elevated pH and decreased CO2. initial response is the drop in blood pH due to excess CO2. Medications Overdose of salicylate • Causes respiratory alkalosis by stimulating the respiratory center, leading to hyperventilation. • This excessive removal of CO2 from the body decreases blood CO2 levels, shifting the pH balance towards alkalinity. References • https://www.osmosis.org/answers/coagulation-cascade • IAvailable from: https://www.researchgate.net/figure/X-ray-2-comminuted-displaced-fracture_fig2_318492019[accessed 25 May, 2024]ResearchGate. • https://upload.wikimedia.org/wikipedia/commons/5/57/Gruenholzfraktur_-_Unterarmfraktur.jpg • Bone Structure,Development and Bone Biology: Bone Pathology - ScientificFigure on ResearchGate. Available from: https://www.researchgate.net/figure/Diagram-of-immature-and-mature-bone-Immature-woven-bone-displays-a-disorganized_fig2_224929158 [accessed 25 May, 2024] • https://upload.wikimedia.org/wikipedia/commons/7/71/Buckle_Fracture.jpg • Gaillard F, Secondary pulmonary lobule (illustration). Case study, Radiopaedia.org (Accessed on 25 May 2024) https://doi.org/10.53347/rID-8760 • Other images are from Cardiff University lecturesPLEASE FILL OUT THE FEEDBACK FORM PLEASE TUNE IN TO OUR REMAINING SESSIONS THIS WEEK