2024.2 MCQ Flashcards

Question

#25. Which increases the risk of blood product related graft vs host disease - genetic variability between donor and recipient - irradiated - leukodepleted - Immunodeficiency - transfusion of non-cellular product

Answer 1

- genetic variability between donor and recipient - irradiated - leukodepleted - Immunodeficiency - transfusion of non-cellular product **Immunideficiency?** ## Footnote "Lifeblood: https://www.lifeblood.com.au/health-professionals/clinical-practice/adverse-events/TA-GVHD#:~:text=The%20three%20primary%20risk%20factors,diversity%20between%20donor%20and%20recipient. The three primary risk factors for developing TA-GVHD are: 1. **degree of immunodeficiency of the recipient.** 2. **number of viable T lymphocytes transfused** (affected by the age of the blood transfused, degree of leucodepletion and irradiation status), and 3. genetic diversity between donor and recipient. **Greatest risks are donations from blood relatives and with HLA-matched blood** products."

Answer 2

The correct answer is **6h**[2]. Fibrinogen concentrates such as RiaSTAP® have specific post-reconstitution stability periods dictated by their product monographs. According to the Australian prescribing information for RiaSTAP®, reconstituted fibrinogen concentrate **must be stored below 25°C and used within 6 hours**[2]. This contrasts with stability data from other jurisdictions (e.g., 8 hours in the U.S. and Canada)[3][5], but the Australian guidelines explicitly specify a 6-hour window to mitigate microbiological risks and ensure efficacy. Studies demonstrating extended stability under refrigeration (e.g., Fibryga® for up to 7 days at 4°C[1]) apply to specific formulations and storage conditions not universally adopted. For the Australian clinical context, adherence to the 6-hour limit aligns with local regulatory standards[2]. Citations: [1] https://pubmed.ncbi.nlm.nih.gov/36804189/ [2] https://www.cslbehring.com.au/-/media/cslb-australia/documents/aus-pis-and-cmis/riastap-au-pi-v1000.pdf [3] https://transfusionontario.org/wp-content/uploads/2023/10/Transfusionists-Talk-2023-Sep_FC-PCC_Final_Sept-27_website.pdf [4] https://pubmed.ncbi.nlm.nih.gov/33196820/ [5] https://labeling.cslbehring.com/pi/us/riastap/en/riastap-prescribing-information.pdf [6] https://www.riastap.com/professional/about-riastap/convenience.aspx [7] https://www.bloodtransfusion.it/public/pre2018archives/2012/BloodTransfus2012_Vol10_Issue_1_023-027_015-11.pdf [8] https://nibsc.org/documents/ifu/09-242.pdf [9] https://www.rch.org.au/bloodtrans/about_blood_products/Clotting_Factor_Concentrates/ [10] https://litfl.com/fibrinogen-concentrate/ [11] https://academic.oup.com/milmed/article/183/suppl_1/183/4959968 [12] https://www.fda.gov/media/73604/download [13] https://www.albertahealthservices.ca/assets/wf/lab/if-lab-clin-tm-riastap.pdf [14] https://academic.oup.com/milmed/article/186/3-4/286/5983609 [15] https://www.rch.org.au/bloodtrans/about_blood_products/clotting_factor_concentrates/ [16] https://aci.health.nsw.gov.au/__data/assets/pdf_file/0004/716566/ACI-Fibrinogen-administration-in-prehospital-trauma.pdf 8h -- -- -- looks like 6 hours according to an australian resource - LITFL says 8 hours, however they reference the American datasheet, whereas NZ and Oz datasheets say 6 hours. Research also states 8 hours." ## Footnote "RIASTAP product info: If it is not administered immediately, it must be stored below 25oC and used within 6 hours of reconstitution. The reconstituted solution should not be stored in the refrigerator"

Answer 3

LAA parachute

Answer 4

Withhold warfarin?? Can't actually find a guideline on this anywhere **Answer:** **Just withhold the warfarin** **Rationale:** For patients with an On-X mechanical aortic valve (without additional thromboembolic risk factors) undergoing surgery, current evidence supports withholding warfarin without bridging anticoagulation when the INR is appropriately managed. 1. **On-X Valve-Specific Guidelines** The On-X valve allows for lower INR targets (1.5–2.0) compared to older mechanical valves[8][12]. Bridging is not required in low-risk patients (aortic position, no additional risk factors) if warfarin is interrupted for ≤48 hours and INR is <1.5 preoperatively[11][12]. 2. **INR Trajectory** Warfarin’s half-life (~40 hours) means withholding it 48 hours preoperatively will further reduce the INR (already 1.5 at the time of decision-making), minimizing perioperative thromboembolic risk while avoiding excessive bleeding[5][16]. 3. **Bridging Risks** Bridging with enoxaparin or heparin increases bleeding complications without reducing thromboembolic events in low-risk On-X aortic valve patients[6][12]. The PROACT trial and 2024 registry data confirm the safety of omitting bridging in this population[8][12]. **Conclusion:** Withholding warfarin aligns with On-X valve guidelines and minimizes bleeding risks, as the INR is already at the lower target threshold. Bridding is unnecessary in this low-risk scenario. **Sources:**[6][8][11][12] Citations: [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC11024885/ [2] https://pmc.ncbi.nlm.nih.gov/articles/PMC11715504/ [3] https://www.ahajournals.org/doi/10.1161/circulationaha.111.084517 [4] https://thischangedmypractice.com/perioperative-anticoagulation-management-in-mechanical-heart-valves/ [5] https://pubmed.ncbi.nlm.nih.gov/18704620/ [6] https://www.bmj.com/content/bmj/373/bmj.n1205.full.pdf [7] https://www.ahajournals.org/doi/10.1161/circulationaha.105.598268 [8] https://www.jacc.org/doi/10.1016/j.jacc.2018.03.535 [9] https://onlinelibrary.wiley.com/doi/10.1111/jcpt.13164 [10] https://pmc.ncbi.nlm.nih.gov/articles/PMC3835169/ [11] http://www.heartvalvechoice.com/wp-content/uploads/2021/05/On-X-Valve-Patient-FAQs.pdf [12] https://pmc.ncbi.nlm.nih.gov/articles/PMC11136449/ [13] https://www.nps.org.au/assets/9bf65e3bdcbf0fe0-ac62d69f22ee-c0d8a6fa7795b1097b2afb4eab5437f708fbaaa4536a31d33e077815d2ee.pdf [14] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?format=pdf [15] https://www.cec.health.nsw.gov.au/__data/assets/pdf_file/0006/458988/Guidelines-on-perioperative-management-of-anticoagulant-and-antiplatelet-agents.pdf [16] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?lang=en [17] https://pmc.ncbi.nlm.nih.gov/articles/PMC9387617/ [18] https://www.ncbi.nlm.nih.gov/books/NBK557590/ [19] https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2020/12/16/22/01/2020-ACC-AHA-VHD-GL-Pt-3-GL-VHD [20] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000923 [21] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-20/prosthetic-heart-valves-part-2-antithrombotic-management [22] https://academic.oup.com/ejcts/article-pdf/65/5/ezae117/57986671/ezae117.pdf [23] https://www.mtw.nhs.uk/wp-content/uploads/2015/09/Algorithm-for-Perioperative-Management-of-Anticoagulation1.pdf [24] https://pmc.ncbi.nlm.nih.gov/articles/PMC10360928/ [25] https://pmc.ncbi.nlm.nih.gov/articles/PMC3312231/ [26] https://www.health.qld.gov.au/__data/assets/pdf_file/0015/1152213/statewide-anticoagulant-guideline.pdf [27] https://www.researchgate.net/publication/23172264_Inguinal_hernia_repair_in_the_anticoagulated_patient_A_retrospective_analysis [28] https://emedicine.medscape.com/article/285265-overview ## Footnote Only heart valve marketed for low INR 1.5-2 The patient with a mechanical aortic valve undergoing inguinal hernia repair in 48 hours and an INR of 1.5 requires bridging anticoagulation. Mechanical heart valves are thrombogenic, necessitating perioperative management to balance thromboembolic and bleeding risks. Current guidelines recommend bridging therapy with low-molecular-weight heparin (LMWH) or unfractionated heparin (UFH) when INR is subtherapeutic in high-risk patients[1][7][9]. **Key considerations:** - **INR target:** For mechanical aortic valves without additional risk factors, the target INR is typically 2.5[1][11]. An INR of 1.5 indicates subtherapeutic anticoagulation, increasing thromboembolic risk. - **Bridging necessity:** Bridging is recommended for mechanical valves during periods of subtherapeutic INR, particularly for procedures with intermediate/high bleeding risk[7][9]. Inguinal hernia repair, while lower risk, still requires bridging in this context due to the valve’s thrombogenicity[8][9]. - **LMWH vs. UFH:** - LMWH (e.g., enoxaparin) is commonly used for bridging due to outpatient feasibility and predictable pharmacokinetics[7][10]. It is typically discontinued 24 hours before surgery[2][10]. - UFH may be preferred in high-bleeding-risk scenarios due to its shorter half-life and reversibility, but it requires inpatient monitoring[9]. **Conclusion:** Bridging with **enoxaparin** is appropriate here, as the patient’s INR is already subtherapeutic, and LMWH provides effective anticoagulation until 24 hours preoperatively[2][7][9]. Withholding warfarin alone without bridging would leave the patient unprotected against thromboembolism[1][7]. Citations: [1] https://www.acc.org/latest-in-cardiology/articles/2015/05/18/09/58/anticoagulation-for-valvular-heart-disease [2] https://www.cec.health.nsw.gov.au/__data/assets/pdf_file/0006/458988/Guidelines-on-perioperative-management-of-anticoagulant-and-antiplatelet-agents.pdf [3] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?format=pdf [4] https://www.scielo.br/j/ramb/a/Nd9KFJxS9GgWYPzFq5VsbSz/?lang=en [5] https://www.ahajournals.org/doi/10.1161/circulationaha.105.598268 [6] https://pmc.ncbi.nlm.nih.gov/articles/PMC8182532/ [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC3835169/ [8] https://pubmed.ncbi.nlm.nih.gov/18704620/ [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC11024885/ [10] https://www.ouh.nhs.uk/services/referrals/specialist-medicine/documents/anticoagulant-protocols.pdf [11] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-20/prosthetic-heart-valves-part-2-antithrombotic-management [12] https://www.thrombosiscanada.ca/guides/pdfs/Warfarin_perioperative_management.pdf [13] https://pmc.ncbi.nlm.nih.gov/articles/PMC9387617/ [14] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/anticoag16.pdf [15] https://www.ncbi.nlm.nih.gov/books/NBK557590/ [16] https://thrombosiscanada.ca/guides/pdfs/Mechanical_Valves.pdf [17] https://www.ahajournals.org/doi/10.1161/circulationaha.111.084517 [18] https://www.health.qld.gov.au/__data/assets/pdf_file/0015/1152213/statewide-anticoagulant-guideline.pdf [19] https://ashpublications.org/blood/article/120/15/2954/30631/How-I-treat-anticoagulated-patients-undergoing-an [20] https://pubmed.ncbi.nlm.nih.gov/30107917/ [21] https://www.heart.org/-/media/Files/Professional/Quality-Improvement/Get-With-the-Guidelines/Get-With-The-Guidelines-AFIB/Anticoagulation-Toolkit/Bridging-Warfarin-with-Parenteral-AgentsPeriProcedural-Management-of-Anticoagulation-and-Subtherapeu.pdf [22] https://www.health.qld.gov.au/__data/assets/pdf_file/0025/443806/warfarin-guideline.pdf [23] https://pubmed.ncbi.nlm.nih.gov/26178802/ [24] https://pubmed.ncbi.nlm.nih.gov/19492151/ --- Answer from Perplexity: pplx.ai/share

Answer 5

"- TR - MR"

Answer 6

"- RV - RA ."

Answer 7

"🌮 Inconclusive" ## Footnote "https://youtu.be/bv9GXUbqyfs https://www.nature.com/articles/s41416-022-01937-w For interpretation of results as this Q was likely showing a diagram that you had to interpret"

Answer 8

Spont breathing patient ## Footnote "https://litfl.com/airway-pressure-release-ventilation/#:~:text=PROS%20AND%20CONS,requirements%20to%20allow%20spontaneous%20breathing pressure-controlled mode of ventilation that delivers an almost continuous positive pressure with intermittent, time-cycled, short releases at a lower pressure - aim high mean airway pressures for thoeretic alveolar recruitment, FRC preservation, lung homogeneity https://www.bjaed.org/article/S2058-5349(19)30178-7/fulltext"

Answer 9

Transgastric mid papillary ## Footnote "TOE was found to be good at detecting new left ventricular RWMAs, associated with ischaemia. In particular the transgastric short axis mid view of the left ventricle demonstrates areas of myocardium subtended by each of the three coronary arteries. It is therefore the most frequently used view for intraoperative monitoring of left ventricular ischaemia." https://www.sciencedirect.com/science/article/pii/S0007091217351863#:~:text=In%20particular%20the%20transgastric%20short,monitoring%20of%20left%20ventricular%20ischaemia.

Answer 10

This is an X-ray image showing the placement of leads from a cardiac device, such as a pacemaker or an implantable cardioverter-defibrillator (ICD). The labeled components include: - **Right atrial lead**: Positioned in the right atrium to monitor and regulate atrial activity. - **Right ventricular lead**: Positioned in the right ventricle to manage ventricular activity. - **LV (left ventricular) coronary sinus lead**: Positioned via the coronary sinus to stimulate the left ventricle, often used in cardiac resynchronization therapy (CRT). The visible device in the upper chest area is likely the pulse generator of the pacemaker or ICD. This setup is commonly used for patients with heart rhythm disorders or heart failure requiring synchronized ventricular contraction. Citations: [1] https://pplx-res.cloudinary.com/image/upload/v1741690186/user_uploads/tfvkBcBtKFnfTJd/image.jpg --- Answer from Perplexity: pplx.ai/share

Answer 11

RCH guideline says milk is "first choice", the dental article says 1. HBSS 2. milk 3. sterile saline. UTD also milk The optimal storage medium for an avulsed tooth must preserve periodontal ligament (PDL) cell viability to maximize the success of replantation. Among the options provided—**chlorhexidine**, **saline**, **balanced salt solution**, **fresh bovine milk**, and **water**—**fresh bovine milk** is the most recommended choice based on current evidence and clinical guidelines. Key Findings Fresh bovine milk demonstrates superior efficacy in maintaining PDL cell viability compared to other readily available media. Systematic reviews highlight milk as the most frequently recommended individual storage medium due to its physiological compatibility, ease of access, and cost-effectiveness[1][3][6]. Hank’s balanced salt solution (HBSS), a synthetic medium, is equally effective but less practical for laypeople due to limited availability outside clinical settings[1][6]. Saline and water are suboptimal, as their hypo-osmolarity accelerates PDL cell lysis[3][6]. Chlorhexidine, not validated in major studies, is unsuitable for this purpose. Mechanistic Basis for Milk’s Efficacy Milk’s osmolarity (~275 mOsm/kg) closely matches that of PDL cells, minimizing osmotic stress[6]. Its nutrient composition—including amino acids, carbohydrates, and growth factors—supports cellular metabolism during extra-alveolar storage[4]. Additionally, refrigeration extends milk’s efficacy, with studies showing viable PDL cells after 4–8 hours of storage[4][7]. Comparative Analysis of Alternatives 1. **Balanced Salt Solution (HBSS)**: While HBSS is the gold standard in clinical settings, its reliance on specialized storage and limited shelf life restricts widespread use[5][8]. Modified HBSS formulations with additives like vitamin C show enhanced cell viability but remain impractical for emergency use[5]. 2. **Saline**: Normal saline’s low osmolarity (~154 mOsm/kg) causes rapid PDL cell swelling and necrosis, reducing replantation success[3][6]. Meta-analyses indicate significantly lower cell viability in saline compared to milk[3]. 3. **Water**: Distilled water’s extreme hypo-osmolarity (<50 mOsm/kg) induces catastrophic cell rupture, rendering it the least suitable option[3][6]. 4. **Chlorhexidine**: No robust evidence supports chlorhexidine as a storage medium. Its antimicrobial properties do not offset cytotoxic effects on PDL cells[6]. Clinical Recommendations For immediate replantation, fresh bovine milk is the preferred medium due to its balance of efficacy and accessibility[1][6][8]. HBSS remains ideal in dental clinics, but milk’s widespread availability makes it the pragmatic choice for public health contexts. Avoid saline, water, or unvalidated agents like chlorhexidine. **Correct Answer**: Fresh bovine milk. **Rationale**: Milk’s physiological properties, clinical validation, and practicality align with guidelines from the International Association of Dental Traumatology and the American Academy of Pediatric Dentistry[6][8]. While HBSS is equally effective, its limited accessibility outside clinical environments positions milk as the superior choice for most scenarios. Citations: [1] https://onlinelibrary.wiley.com/doi/10.1111/edt.12382 [2] https://journals.lww.com/senj/fulltext/2015/05020/natural_products_as_storage_media_for_avulsed.2.aspx [3] https://onlinelibrary.wiley.com/doi/10.1111/edt.12564 [4] https://pubmed.ncbi.nlm.nih.gov/12669877/ [5] https://onlinelibrary.wiley.com/doi/10.1111/edt.13010 [6] https://pmc.ncbi.nlm.nih.gov/articles/PMC5571385/ [7] https://bestbets.org/bets/bet.php?id=187 [8] https://www.aapd.org/media/policies_guidelines/e_avulsion.pdf [9] https://pubmed.ncbi.nlm.nih.gov/39578673/ [10] https://www.distinguished-dental.com/blog/2019/11/14/emergency-dentist-putting-a-tooth-in-milk/ [11] https://www.aapd.org/globalassets/media/policies_guidelines/r_traumaflowsheet.pdf [12] https://www.scielo.br/j/bdj/a/8c8n6p3BG4jNZGgGz3KXbZq/?format=pdf&lang=en [13] https://pmc.ncbi.nlm.nih.gov/articles/PMC3809259/ [14] https://www.idjsronline.com/html-article/13809 [15] https://www.dental-update.co.uk/content/dental-traumatology/an-anaphylactic-replantation-milk-allergy-tooth-avulsion-and-appropriate-storage-media/ [16] https://www.dental-update.co.uk/content/technique-tips/technique-tips-replantation-and-stabilization-of-avulsed-permanent-teeth/ [17] https://themamadentist.com/shop/save-a-tooth-hanks-balanced-salt-solution/ [18] https://www.libertyendo.com/files/2014/06/Avulsed-permanent-teeth-new-treatment-guidelines.pdf [19] https://bondidental.com.au/first-aid-for-a-knocked-out-tooth/ [20] https://www.researchgate.net/publication/228474005_Study_of_storage_media_for_avulsed_teeth ## Footnote "https://www.aapd.org/globalassets/media/publications/archives/ram-26-03.pdf, https://www.rch.org.au/clinicalguide/guideline_index/Dental_trauma/ UTD: Place the tooth in a storage solution – As soon as possible, place the tooth in a storage solution to maintain the viability of the periodontal ligament on the tooth's surface [42-44]. We suggest cold milk, oral rehydration solution (eg, Ricelyte or Pedialyte), or a cell culture medium (Hank's balanced salt solution or Viaspan) used in avulsed tooth preservation kits. Cold milk is usually most readily available [44]. If milk or specialized mediums are not available, have the child spit into a container or place the tooth in saline instead. "

Answer 12

Neuraxial ok - no correlation between relapses of MS. NMBD caution - ND may have prolonged effects, hyperK from denervation/misuse myopathy, resis to NMBA ?due to extrajunctional receps The optimal anesthetic technique for a Category 1 cesarean section in a pregnant woman with multiple sclerosis (MS) requires balancing urgency with neurological safety. **Spinal anesthesia** is the most appropriate choice in this scenario, supported by current evidence and clinical guidelines[1][3][4][6][8]. Rationale 1. **Urgency of Category 1 Section**: A Category 1 cesarean section mandates delivery within 30 minutes due to immediate threat to maternal or fetal life. Spinal anesthesia provides rapid onset (typically within 3–5 minutes) and reliable surgical conditions, making it faster than epidural catheter placement or titration[6][7]. While general anesthesia (GA) is traditionally considered the fastest option, it carries significant risks in obstetric patients, including difficult airway management, aspiration, and postoperative respiratory complications[7]. 2. **Safety of Neuraxial Anesthesia in MS**: Historical concerns about neuraxial techniques exacerbating MS relapses due to local anesthetic neurotoxicity in demyelinated regions have been disproven by recent studies[1][3][4][6][8]. For example: - A cohort study of 155 MS patients undergoing cesarean delivery found no increased relapse risk with epidural or spinal anesthesia compared to GA[8]. - Case reports demonstrate successful spinal anesthesia in MS patients without postoperative neurological deterioration[6]. - Theoretical risks of spinal anesthesia (higher intrathecal local anesthetic concentration) are offset by clinical evidence showing no correlation with relapse rates[4][6]. 3. **Advantages Over GA**: GA introduces risks such as autonomic instability, hyperkalemia from succinylcholine in patients with spasticity, and immune modulation from volatile agents[4][6]. Spinal anesthesia avoids these issues while providing superior postoperative analgesia and earlier maternal-neonatal bonding[6][8]. 4. **Epidural vs. Spinal Considerations**: While epidural anesthesia is often preferred in elective cases for its titratability, spinal anesthesia is more practical in emergencies due to faster onset[6]. The literature confirms that both techniques are safe, but spinal anesthesia aligns better with time constraints in Category 1 scenarios[4][6]. 5. **Methylprednisolone Prophylaxis**: Prophylactic steroids lack robust evidence for preventing relapses in this context and are not routinely recommended[4][8]. Their use should be reserved for treating acute exacerbations rather than as a pre-anesthetic measure. Conclusion For a Category 1 cesarean section in a pregnant woman with MS, **spinal anesthesia** is the optimal choice. It balances rapid execution with safety, avoiding the risks of GA while adhering to contemporary evidence supporting neuraxial techniques in MS[6][8]. **Correct Answer**: Spinal anesthesia. **Sources**:[1][3][4][6][8] Citations: [1] https://www.elsevier.es/en-revista-colombian-journal-anesthesiology-342-articulo-management-anesthesia-during-c-section-multiple-S2256208714001096 [2] https://www.revcolanest.com.co/index.php/rca/article/view/495 [3] https://rapm.bmj.com/content/48/Suppl_1/A96.3 [4] https://resources.wfsahq.org/atotw/anesthetic-considerations-for-pregnant-women-with-multiple-sclerosis/ [5] https://pmc.ncbi.nlm.nih.gov/articles/PMC4141396/ [6] https://besarpp.adagiocreate.com/wp-content/uploads/2020/12/01-rayyan.pdf [7] https://pubmed.ncbi.nlm.nih.gov/31634161/ [8] https://pmc.ncbi.nlm.nih.gov/articles/PMC6160638/ [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC7199839/ [10] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.13729 [11] https://academic.oup.com/bja/article/doi/10.1093/bja/el_9820/2451457 [12] https://academic.oup.com/bmb/article/101/1/105/262350 [13] https://www.pregnancybirthbaby.org.au/emergency-caesarean [14] https://www.wjgnet.com/2307-8960/full/v10/i14/4563.htm ## Footnote "BJA Ed 2021 Anaesthesia and neurological disorders in pregnancy PRIMS study"

Answer 13

60mmHg (product guide) ## Footnote https://www.lmaco.com/sites/default/files/31817-LMA-Classic-A4Data-0214-LORES-fnl.pdf

Answer 14

**Answer:** **A. Modified valsalva** **Rationale:** In a hemodynamically **stable** patient with narrow complex tachycardia (NCT), **vagal maneuvers** such as the modified Valsalva maneuver are first-line therapy, as per ACC/AHA/HRS guidelines[12]. The modified Valsalva (supine positioning with leg elevation post-strain) has demonstrated higher efficacy than standard techniques[3][8]. While adenosine is effective, it is typically reserved for cases where vagal maneuvers fail[12][15]. Direct current cardioversion (DCCV) is reserved for hemodynamically **unstable** patients (e.g., shock, altered mental status, severe hypotension)[4][6]. This patient’s SBP of 90 mmHg is at the threshold for stability; however, in the absence of additional signs of shock (e.g., altered consciousness, chest pain, or respiratory distress), modified Valsalva remains appropriate initial management. Postoperative NCT often responds well to non-pharmacological interventions, and adenosine or DCCV can be escalated if needed[4][9]. --- **Key Evidence:** 1. **Vagal maneuvers** (e.g., modified Valsalva) are recommended first-line for stable NCT[12][15]. 2. **Adenosine** follows if vagal maneuvers fail[12][15]. 3. **DCCV** is indicated only for hemodynamic instability[4][6]. 4. Postoperative NCT management prioritizes conservative measures before pharmacological or electrical interventions[4][9]. **Conclusion:** The modified Valsalva maneuver (A) is the correct initial treatment in this scenario. Citations: [1] https://patient.info/doctor/narrow-complex-tachycardias [2] https://www.acc.org/Latest-in-Cardiology/ten-points-to-remember/2019/09/10/12/36/2019-ESC-Guidelines-for-Supraventricular-Tachycardia [3] https://www.thelancet.com/journals/lancet/article/PIIS0140-67361561485-4/fulltext [4] https://e-safe-anaesthesia.org/e_library/11/Supraventricular_tachyarrhythmias_and_their_management_in_the_perioperative_period.pdf [5] https://www.resus.org.uk/sites/default/files/2021-04/Tachycardia%20Algorithm%202021.pdf [6] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-9-managing-acute-dysrhythmias/ [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC2907092/ [8] https://resus.com.au/modified-valsalva-plus-adenosine-for-reverting-svt/ [9] https://www.cancertherapyadvisor.com/home/decision-support-in-medicine/critical-care-medicine/svt-in-a-cardiac-surgery-patient/ [10] https://www.mayoclinic.org/diseases-conditions/supraventricular-tachycardia/diagnosis-treatment/drc-20355249 [11] https://www.rch.org.au/clinicalguide/guideline_index/supraventricular_tachycardia_svt/ [12] https://www.ahajournals.org/doi/10.1161/cir.0000000000000311 [13] https://pmc.ncbi.nlm.nih.gov/articles/PMC3375013/ [14] https://pubmed.ncbi.nlm.nih.gov/3502542/ [15] https://aci.health.nsw.gov.au/networks/eci/clinical/tools/cardiology/supraventricular-tachycardia-svt [16] https://www.racgp.org.au/getattachment/55d4f29f-65bb-4bac-ba42-35407dbee553/attachment.aspx [17] https://www.racgp.org.au/clinical-resources/clinical-guidelines/handi/handi-interventions/procedures/modified-valsalva-manoeuvre-for-supraventricular-t [18] https://academic.oup.com/bjaed/article/15/2/90/248695 [19] https://pmc.ncbi.nlm.nih.gov/articles/PMC8832017/ [20] https://pmc.ncbi.nlm.nih.gov/articles/PMC5613596/ [21] https://pmc.ncbi.nlm.nih.gov/articles/PMC1964549/ [22] https://www.analesdepediatria.org/en-modified-valsalva-manoeuvre-in-paroxysmal-articulo-S2341287923001539 [23] https://www.escardio.org/static-file/Escardio/Subspecialty/EACPR/Education/Test%20your%20knowledge/guidelines-sva-es.pdf [24] https://academic.oup.com/qjmed/advance-article/7905488 [25] https://www.ncbi.nlm.nih.gov/books/NBK557830/ [26] https://www.ahajournals.org/doi/10.1161/CIR.0000000000000549 [27] https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.7.2.192 [28] https://my.clevelandclinic.org/health/treatments/24605-svt-ablation [29] https://www.ncbi.nlm.nih.gov/books/NBK507699/ ## Footnote I'm guessing because not unstable, go with modified valsalva first?

Answer 15

"G6PD " Methemoglobinemia Risk Prilocaine is associated with an increased risk of methemoglobinemia, especially in G6PD-deficient individuals: • Prilocaine is metabolized to o-toluidine, which can oxidize hemoglobin and lead to methemoglobin formation. • G6PD-deficient patients are more susceptible to developing methemoglobinemia when exposed to oxidative stressors like prilocaine. • Methemoglobinemia can occur even at lower doses in G6PD-deficient patients compared to the general population. ## Footnote https://www.orphananesthesia.eu/en/rare-diseases/published-guidelines/glucose-6-phosphate-dehydrogenase-deficiency/193-glucose-6-phosphate-dehydrogenase-deficiency/file.html

Answer 16

Gelofusine (due to the gelatin!) ## Footnote Journal of Clinical Immunology 1993, Journal of Military medicine 2020

Answer 17

Pleural effusion

Answer 18

Adenosne 4x increase in SA & AV nodal blocking effect "denervation supersensitivity" ## Footnote BJA https://watermark.silverchair.com/020074.pdf

Answer 19

Long thoracic - does motor to serratus anterior ## Footnote The innervation of the breast is supplied mainly by the 1. anterior branches of the 4th, 5th and 6th intercostal nerves which arise from the thoracic spinal nerves (T4-6). 2. the apex of the axilla is supplied by the intercostobrachialis nerve; this is a cutaneous branch of the second intercostal nerve (T2). 4. the pectoral major and minor muscles are innervated by the lateral pectoral nerve (C5-7) and medial pectoral nerve (C8-T1). Terminal branches of the supraclavicular nerves (C3-4) innervate the upper part of the breast and this should be taken into account when the surgical procedure involves this area, because Pecs blocks will not block the supraclavicular nerve. Breast surgery however, is rarely performed at this level. BMJ Nerves that DOES NOT innervate the breast 1. Long thoracic - motor to Serr ant 2. Lat pec - motor to pec major/minor 3. Thoracodorsal - motor to lat dorsi 4. Posterior "cutaneous"

Answer 20

"Ex-preterm infants at risk of postoperative apnoea should not be considered for same day discharge unless they are medically fit and have reached a **postmenstrual age of 54 weeks."** | Term - PMA 46 weeks Ex-prem - PMA 54 weeks ## Footnote https://www.anzca.edu.au/getContentAsset/aae56c4d-8983-47db-97c7-0366e9f6f271/80feb437-d24d-46b8-a858-4a2a28b9b970/PG29(A)-Guideline-for-the-provision-of-anaesthesia-care-to-children-2020.PDF?language=en&view=1

Answer 21

ergometrine ## Footnote https://www.bjaed.org/action/showPdf?pii=S1743-1816%2817%2930438-9

Answer 22

inferior alveolar nerve ## Footnote https://radiopaedia.org/articles/mental-nerve

Answer 23

Buccal/ intranasal 0.3x20 = 6mg IV/ IO 0.15x20= 3mg IM 0.2x20= 4mg *needle = 0.15 *no needle = 0.3 but IM = 0.2 ## Footnote https://www.childrens.health.qld.gov.au/__data/assets/pdf_file/0021/174180/status-epilepticus-flowchart-and-medications.pdf

Answer 24

- underweight < 18.5 ## Footnote BJA anaesthesia for the obese patient 2020

Answer 25

-Dose expected higher because of up-regulation of acetylcholine receptors

Answer 26

2 ## Footnote "https://www.asahq.org/standards-and-practice-parameters/statement-on-asa-physical-status-classification-system. Mild diseases only without substantive functional limitations. Current smoker, social alcohol drinker, pregnancy, obesity (3040) = ASA 3"

Answer 27

the only proven therapy is an ** implantable cardioverter – defibrillator (ICD) ** ## Footnote LITFL Brugada syndrome

Answer 28

LBW is a more appropriate dosing scalar Mnemonic: TBW = Xa (TXa) ABW = PINSA (A PINS) prop inf/neo/suga/anti ## Footnote SOBA https://www.sobauk.co.uk/_files/ugd/373d41_eebe369c3c6b4021bff6f3da059aa796.pdf

Answer 29

Sensitive to ND, resistant to depol ## Footnote "BJA Myaesthenia gravis and periop rx 1/10 normal Roc/ (NDNMBD)"

Answer 30

Resp dep postop - mcq group Wrong! **Reduced MAC requirements** ## Footnote "https://pmc.ncbi.nlm.nih.gov/articles/PMC6319973/#:~:text=Albrecht%20et%20al%20reviewed%2025,any%20reported%20serious%20adverse%20effects. Albrecht et al reviewed 25 RCTs including 1461 patients and concluded that perioperative intravenous magnesium can **reduce opioid consumption and pain scores in the first 24 hours postoperatively without any reported serious adverse effects** https://www.mdpi.com/2072-6643/16/14/2375 administration of magnesium sulfate **1. reduces the intraoperative opioid use, 2. decreases the pain severity within the first 24 h postoperatively, and 3. reduces the incidence of PONV while exerting a minimal effect on the length of stay in the PACU. ** Mg in toxic doses can cause respiratory depression"

Answer 31

5 mmol bolus of K+ ## Footnote ALS 2 Handbook P. 134

Answer 32

63mL/h of 0.9% saline with 5% dex --> Give 2/3 maintenance once resus'd because prone to secreting ADH+++, and never give hypotonic solution to children!! ## Footnote RCH Guidelines: The preferred fluid type for IV maintenance is sodium chloride 0.9% with glucose 5% Alternative maintenance fluid options include: Plasma-Lyte 148 with glucose 5% (contains 5 mmol/L of potassium) - generally stocked in tertiary paediatric centres and intensive care Hartmann's with glucose 5% 4-2-1 rule = 4mL/h x 10kg + 2mL/h x 10kg + 1mL/h x 3 kg = 40+20+3 =63mL/h

Answer 33

Prostaglandin Try sedation, beta blockers, IVF bolus, phenylephrine/metaraminol ## Footnote Craig Sims P. 386 https://www.rch.org.au/clinicalguide/guideline_index/Cyanotic_Episodes_in_Congenital_Heart_Disease/ Try sedation, beta blockers, IVF bolus, phenylephrine/metaraminol"

Answer 34

Pethidine ## Footnote "NPS Tramadol + MAOIs = highest risk SS Some opioids such as tramadol, pethidine, dextromethorphan and tapentadol increase serotonergic activity. Fentanyl and methadone also do this but to a lesser extent. Pethidine: The highest risk opioid drugs are tramadol, pethidine and dextromethorphan. Tapentadol: Currently, it is unclear if tapentadol has a greater risk of serotonin toxicity than other opioids. Methadone: Methadone has been associated with serotonin toxicity when given with other serotonergic medicines but the risk appears low Sux: Fent: Co-administration with an SSRI has been reported to cause an agitated delirium consistent with serotonin toxicity.2"

Answer 35

Cyclizine ## Footnote "https://www.drugs.com/drug-interactions/apomorphine-with-ondansetron-224-0-1752-0.html States not for apomorphine + ondans apo + ondans = hypotension PD pt not for antiD2 drugs therefore no droperidol or metoclopramide"

Answer 36

??tachycardia # Vagus Nerve Stimulator (VNS) Inadvertent Firing in Refractory Epilepsy: Mechanisms and Likely Triggers The inadvertent firing of a vagus nerve stimulator (VNS) in patients with refractory epilepsy is a critical clinical concern. Among the potential triggers—hypertension, tachycardia, bradycardia, hypotension, and hyperthermia—**tachycardia** is the most likely culprit. This conclusion is supported by extensive evidence from clinical studies, device functionality, and physiological mechanisms outlined in the provided search results. Physiological Basis of VNS Activation Modern VNS systems, such as the AspireSR® (Model 106), incorporate an **AutoStim Mode** designed to detect **ictal tachycardia**, a rapid increase in heart rate associated with seizures. This feature triggers automatic stimulation when a ≥20% relative heart rate increase is detected, aiming to abort or mitigate seizure activity[2][4][6]. The rationale stems from the observation that approximately two-thirds of focal seizures correlate with tachycardia, making heart rate a reliable biomarker for seizure onset[2][8]. Key Evidence Supporting Tachycardia as the Primary Trigger 1. **AutoStim Functionality**: - The AspireSR® generator uses tachycardia detection to deliver responsive stimulation. In clinical trials, 34.8% of seizures were treated via AutoStim, with 61.3% of these seizures terminating during stimulation[2][4]. - False-positive activations can occur due to physiological or pathological tachycardia unrelated to seizures (e.g., exercise, anxiety), potentially leading to unintended stimulation[11]. 2. **Clinical Outcomes**: - Switching from traditional VNS to responsive VNS (rVNS) with AutoStim resulted in a **28% additional reduction in seizure frequency** for patients not fully controlled by conventional therapy[8]. - Device-triggered stimulation during ictal tachycardia reduced seizure severity and improved quality of life in long-term studies[4][8]. 3. **Exclusion of Other Triggers**: - **Bradycardia**: While VNS malfunction (e.g., cyclic asystole) can cause symptomatic bradyarrhythmias[1][3], this represents a **complication of overstimulation**, not a trigger for inadvertent firing. - **Hypertension/Hypotension**: No evidence links blood pressure fluctuations to VNS activation. The device’s sensing mechanism focuses on cardiac rhythm, not vascular tone[6][9]. - **Hyperthermia**: Temperature changes are not integrated into VNS algorithms[11]. Safety Considerations and Device Limitations The AutoStim feature is contraindicated in patients with **chronotropic incompetence** (e.g., sustained bradycardia <50 bpm) or those reliant on beta-blockers, as these conditions may impair heart rate responsiveness[11]. Furthermore, manufacturing defects in leads (e.g., PerenniaDURA models) or MRI-related interference could theoretically cause erratic stimulation, but these are hardware-specific issues rather than physiological triggers[10][11]. Conclusion In patients with refractory epilepsy and a VNS, **tachycardia** is the most likely cause of inadvertent device firing. This aligns with the intentional design of AutoStim-enabled generators to respond to ictal heart rate increases. Clinicians should educate patients on recognizing non-seizure-related tachycardia (e.g., during exercise) and consider adjusting stimulation parameters to minimize false activations. Regular device interrogation and adherence to implantation protocols remain essential to mitigate risks[5][11]. Citations: [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC10285099/ [2] https://pmc.ncbi.nlm.nih.gov/articles/PMC5064739/ [3] https://pmc.ncbi.nlm.nih.gov/articles/PMC5419945/ [4] https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/ner.12376 [5] https://thejns.org/pediatrics/view/journals/j-neurosurg-pediatr/18/1/article-p97.xml [6] https://www.epilepsy.org.uk/info/treatment/vagus-nerve-stimulation [7] https://www.livanova.com/epilepsy-vnstherapy/getmedia/a0f9e731-f117-4948-896e-abcfb377eb3f/IM-7601065-EPI_SenTecGd19U1-Rev-B_Sentival-Technical-Guide.pdf [8] https://pubmed.ncbi.nlm.nih.gov/32759064/ [9] https://www.rch.org.au/Vagus_nerve_stimulation.aspx [10] https://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfRes/res.cfm?id=191291 [11] https://www.livanova.com/epilepsy-vnstherapy/en-au/safety-information [12] https://my.clevelandclinic.org/health/treatments/17598-vagus-nerve-stimulation [13] https://www.frontiersin.org/journals/medical-technology/articles/10.3389/fmedt.2021.696543/full ## Footnote Vague mention of tachycardia in UTD but I haven't foudn anything definitive

Answer 37

Age >3 then? Given that the alternative is post pubertal girls ## Footnote "RCH website: Risk Factors Age > 3, Past history of PONV, History of motion sickness, Post-pubertal girls, Preoperative anxiety Surgery type Strabismus, Otoplasty, Adenotonsillectomy, Surgery requiring postoperative inpatient (vs day stay),Volatile anaesthesia"

Answer 38

**Sternohyoid** An infrahyoid muscle that depresses the hyoid bone rather than elevating it5. Its primary role is to lower the hyoid after swallowing/speaking, opposing elevation56. The sterno-hyoid option --> Depresses hyoid bone after swallowing ## Footnote Various anatomy websites

Answer 39

RR >16 not mentioned in that list so I guess I'll go with that despite the articel being about children, not neonates ## Footnote "https://www.bjaed.org/article/S2058-5349(21)00133-5/fulltext Eight features have been found to be associated with successful awake extubation in children: 1. eye opening, 2. facial grimace, 3. movement of the patient other than coughing, 4. conjugate gaze, 5. purposeful movement, 6. low end-tidal anaesthetic concentration (< 0.2% for sevoflurane, < 0.15% for isoflurane and < 1% for desflurane), 7. Spo2 > 97%, 8. tidal volume 5 ml kg−1 and a positive laryngeal stimulation test."

Answer 40

Greater auricular - comes off C2-C3 of cervical plexus

Answer 41

L posterior cerebral artery? Posterior Cerebral Artery Infarction: Neuroanatomical Correlates of Right Homonymous Hemianopia and Right Hemisensory Loss The constellation of right homonymous hemianopia and right hemisensory loss localizes to infarction in the territory of the **left posterior cerebral artery (PCA)**. This conclusion is supported by anatomical and clinical-pathological correlations derived from neurovascular anatomy, lesion localization studies, and clinical stroke syndromes. --- Neurovascular Anatomy of the Posterior Cerebral Artery The posterior cerebral artery arises from the basilar artery and supplies the occipital lobes, medial temporal lobes, thalamus, and rostral brainstem. Critical branches include: 1. **Cortical branches**: Supply the primary visual cortex (calcarine cortex) and optic radiations. 2. **Thalamogeniculate arteries**: Penetrate the thalamus, supplying the ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei, which process somatosensory information[1][2]. Occlusion of the left PCA disrupts perfusion to these regions, producing contralateral (right-sided) visual and sensory deficits[3][8]. --- Pathophysiology of Right Homonymous Hemianopia Homonymous hemianopia arises from damage to the **optic radiations** or **primary visual cortex** (Brodmann area 17) in the left occipital lobe[4][7]. The left PCA supplies these structures, and infarction interrupts the visual pathway posterior to the optic chiasm, resulting in loss of the right visual field in both eyes. Clinical studies report that **88.9% of patients with superficial PCA (SPCA) infarcts** exhibit contralateral homonymous hemianopia due to occipital lobe involvement[3][8]. --- Mechanisms of Right Hemisensory Loss Hemisensory loss in PCA territory strokes originates from infarction of the **thalamus**, specifically the VPL and VPM nuclei. These nuclei receive somatosensory input from the contralateral body via the medial lemniscus and spinothalamic tracts. Occlusion of thalamogeniculate arteries—branches of the left PCA—causes ischemia in these nuclei, leading to contralateral sensory deficits[2][5]. - **Pure sensory stroke**: Isolated sensory loss due to small thalamic infarcts[2][5]. - **Sensory-motor stroke**: Combined sensory loss and motor weakness from larger infarcts involving the adjacent internal capsule[2][5]. In the context of left PCA infarction, **60–72% of patients with proximal PCA (PPCA) or combined (P+SPCA) infarcts** exhibit sensory deficits[3][8]. --- Differential Diagnosis of Artery-Specific Syndromes 1. **Left Anterior Cerebral Artery (ACA)**: - Supplies medial frontal and parietal lobes. - Infarction causes contralateral leg weakness/sensory loss, executive dysfunction, and apraxia. **No visual deficits**[7]. 2. **Superior Cerebellar Artery (SCA)**: - Supplies superior cerebellum and dorsolateral pons. - Infarction causes ipsilateral limb ataxia, dysarthria, and vertigo. **No sensory or visual deficits**[7]. 3. **Left Anterior Inferior Cerebellar Artery (AICA)**: - Supplies lateral pons and inferior cerebellum. - Infarction causes vertigo, hearing loss, and facial weakness. **No hemianopia or hemisensory loss**[7]. --- Clinical-Pathological Correlation The combination of right homonymous hemianopia and right hemisensory loss is pathognomonic for **left PCA infarction**, as no other artery supplies both the occipital cortex and thalamus. This is validated by: - **Imaging studies**: CT/MRI showing left occipital and thalamic infarcts[1][8]. - **Angiographic findings**: Occlusion of the left PCA or its branches[3][5]. - **Stroke registries**: 56.4% of PCA infarcts present with motor/sensory deficits, and 52.5% with visual field abnormalities[3][8]. --- Conclusion **Left posterior cerebral artery infarction** is the definitive etiology of right homonymous hemianopia and right hemisensory loss. This syndrome reflects dual involvement of the occipital cortex (visual loss) and thalamus (sensory loss), territories exclusively supplied by the PCA. Clinicians should prioritize neuroimaging (MRI/CT angiography) to confirm the diagnosis and guide thrombolytic or endovascular therapy within appropriate time windows[1][8]. **Correct Answer**: Left posterior cerebral artery. Citations: [1] https://radiopaedia.org/articles/posterior-cerebral-artery-pca-infarct [2] https://pubmed.ncbi.nlm.nih.gov/3046580/ [3] https://jamanetwork.com/journals/jamaneurology/fullarticle/788716 [4] https://en.wikipedia.org/wiki/Homonymous_hemianopsia [5] https://jamanetwork.com/journals/jamaneurology/fullarticle/588031 [6] https://pmc.ncbi.nlm.nih.gov/articles/PMC2077751/ [7] https://www.strokenetworkseo.ca/sites/default/files/files/stroke_school_brockville_part_3.pdf [8] https://radiopaedia.org/articles/posterior-cerebral-artery-pca-infarct?embed_domain=hackmd.io%25252525252525252F%252525252525252540yipuafecsl2jsu8smr5njq%25252525252525252Fbnjhjgjghjghjgh&lang=us [9] https://academic.oup.com/braincomms/article/5/2/fcad050/7059656 [10] https://journals.sagepub.com/doi/full/10.1177/11206721211046146 [11] https://www.ahajournals.org/doi/10.1161/01.str.0000087786.38997.9e [12] https://www.heart.org/-/media/files/affiliates/mwa/nebraska-ml-stroke/posterior-circulation-stroke-pam-stout-msn-rn-scrn.pdf?la=en [13] https://www.ncbi.nlm.nih.gov/books/NBK532296/ [14] https://jamanetwork.com/journals/jamaneurology/fullarticle/775182 [15] https://www.ijceo.org/html-article/20023 [16] https://www.ncbi.nlm.nih.gov/books/NBK558929/ [17] https://emedicine.medscape.com/article/2128100-overview

Answer 42

Hypokalaemia ## Footnote "LITFL: Laboratory hyponatraemia (dilutional effect of a large volume of absorbed irrigation fluid, but later due to natriuresis) iso-osmolar (or mildly hypo-osmolar) increased osmolar gap from absorbed glycine hyperglycinaemia (up to 20 mM; normal is 0.15-0.3mmol/L) hyperserinaemia (major metabolite of glycine) hyperammonaemia (due to deamination of glycine and serine) hyperoxaluria and hypocalcaemia (glycine is metabolised to glycoxylic acid and oxalic acid, the latter forms calclium oxalate crystals in the urinary tracts and may contribute to renal failure) metabolic acidosis haemodilution and haemolysis ?more likely to get hyPERkalaemia from cell lysis"

Answer 43

- 100 x PPmax-PPmin/ PPmean

Answer 44

SV and periph O2 extraction ## Footnote Novel techniques for quantifying oxygen pulse curve characteristics during cardiopulmonary exercise testing in tetralogy of fallot 2024 - "Oxygen pulse (O2P) is the CPET surrogate for stroke volume and peripheral oxygen extraction."

Answer 45

Pulm hemorrhage ## Footnote "UTD: The diffusing capacity of the lungs for carbon monoxide (DLCO) is designed to reflect properties of the alveolar-capillary membrane, specifically the ease with which oxygen moves from inhaled air to the red blood cells in the pulmonary capillaries. Increased DLCO — Disorders to consider when the DLCO is near or above the upper limit of the normal range include the following [17,72,73]: ●Obesity ●Asthma ●High altitude ●Polycythemia ●Pulmonary hemorrhage ●Left-to-right intracardiac shunting ●Mild left heart failure (due to increased pulmonary capillary blood volume) ●Exercise just prior to the test session (due to increased cardiac output) ●Supine position; Mueller maneuver"

Answer 46

K 2.7 ## Footnote SCARF Sodium./K 120/150 2.8/6.0 Chest inf Arr Reversible coag Fixable ketoacidosis "AAGBI 7 acceptable reasons for delaying NOF 1. Hb <80 2. Acute CCF 3. Uncontrolled DM 4. Correctable cardiac arrhythmia with vent rate >120bpm 5. Na <120 or >150, K <2.8 or >6 6. Reversible coagulopathy 7. Chest infection with sepsis"

Answer 47

Ant axillary line 5th intercostal space ## Footnote "12-lead Precordial lead placement V1: 4th intercostal space (ICS), RIGHT margin of the sternum V2: 4th ICS along the LEFT margin of the sternum V4: 5th ICS, mid-clavicular line V3: midway between V2 and V4 V5: 5th ICS, anterior axillary line (same level as V4) V6: 5th ICS, mid-axillary line (same level as V4)"

Answer 48

Conclusion **NT-proBNP >300 pg/mL** is the most sensitive predictor of 30-day mortality and MACE, supported by its strong prognostic performance across diverse surgical populations and consistency in guidelines15913. DASI ≤34 and AT <11 mL/kg/min provide incremental risk stratification but are less sensitive. Clinicians should prioritize NT-proBNP measurement in high-risk patients undergoing noncardiac surgery to guide perioperative management. Rationale for Excluding Other Options: **DASI score 55**: Incorrect cutoff; studies use ≤34. **VO₂ <11**: Predicts complications, not mortality/MACE. **AT <11**: Lacks sensitivity for short-term events. 6MWT: No direct evidence in provided studies. Final Answer: proBNP >30015913. ## Footnote "https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31131-0/abstract UTD re: METS trial *Subjective assessment did not predict postoperative myocardial infarction (MI), myocardial injury, or myocardial complications. *Lower DASI scores predicted 30-day death or MI and 30-day death or myocardial injury. *Reduced peak oxygen consumption and anaerobic threshold measured by CPET were not associated with postoperative MI or myocardial injury. *Higher NT-proBNP levels predicted 30-day death or MI and one-year death."

Answer 49

VO2 max ~32 ## Footnote "V˙o2 peak (ml kg−1 min−1) = (0.43 × DASI) + 9.6 [VO2max = half DASI + 10]"

Answer 50

Milrinone as an inodilator ## Footnote Dopamine low dose = no effect PVR Dopamine high dose = incr PVR Vaso low dose = no effect PVR NAd = incr PVR and SVR Dobutamine low dose = reduces PVR as per (Hemmings and Egan)

Answer 51

UO ## Footnote "For adults iwth sepsis or septic shock, we suggest using dynamic measures to guide fluid resuscitation over physical examination or static parameters alone. Weak recommendation, v low quality evidence. Dynamic parameters = passive leg raise, fluid bolus, SV, SVV, PPV, echo"

Answer 52

Probs observe as per algorithm. "Consider CPAP" ## Footnote "https://www.anzcor.org/assets/Uploads/Newborn-Life-Support-August-2023-1-v4.pdf The determining factor after 1min is whether HR <100. This neonate's parameters all seem very normal!"

Answer 53

Give adrenaline CALS 1. VF/VT --> 3 seq shock --> amiodarone 2. Asystole --> pacing external 3. PEA --> turn off pacing if paced CPR until resternotomy DO not give adrenaline An emergency resternotomy should be an integral part of the CALS arrest management for all patients within 10 days of their last operation. Beyond the tenth postoperative day, a senior clinician should decide whether emergency resternotomy is to be performed Cardiac arrests in patients after cardiac surgery are often quickly reversible and circulating standard advanced life support doses of epinephrine/adrenaline (ie, 1 mg intravenous) can therefore cause excessive hypertension and arrhythmias when achieving ROSC. Therefore, only small doses of adrenaline (eg, 50–100 micrograms i.v.) should be given. Amiodarone should be considered for refractory shockable rhythms ## Footnote https://www.sciencedirect.com/science/article/pii/S1441277223000492#ec0010 BJA During early resternotomy for VF/VT, 1. a bolus of 300 mg of amiodarone should be administered with a further dose of 150 mg in refractory cases. 2. Lidocaine at a dose of 1 mg kg 1 is a suitable alternative. https://www.bjaed.org/article/S2058-5349(17)30182-8/fulltext

Answer 54

"PCWP high Because TRALI is clinical Dx with the criteria to the L" ## Footnote "UTD: TRALI is a clinical diagnosis made using the criteria outlined by the NHLBI's working group on TRALI or the Canadian Consensus Conference (CCC) on TRALI The diagnostic criteria for TRALI and possible TRALI share the following features: acute onset of hypoxemia, bilateral infiltrates on frontal chest radiograph, and absence of circulatory overload as the primary etiology of respiratory insufficiency. For a diagnosis of TRALI to be made, all of these features must be present. In addition, there should be no pre-existing ALI/ARDS risk factors at the time of transfusion"

Answer 55

**Answer:** The correct components of the 4Ts score for heparin-induced thrombocytopenia (HIT) diagnosis are **thrombocytopenia, timing of platelet count fall, thrombosis/other sequelae, and absence of other causes of thrombocytopenia**. The platelet serotonin release assay (SRA) is **not part of the 4Ts score** but is a confirmatory laboratory test used after clinical assessment. **Rationale:** 1. The **4Ts scoring system** is a clinical pretest probability tool with four criteria ([1][6][10]): - **Thrombocytopenia**: Magnitude of platelet count fall and nadir (scored 0–2). - **Timing**: Onset relative to heparin exposure (scored 0–2). - **Thrombosis/other sequelae**: Presence of new thrombosis, skin necrosis, or systemic reactions (scored 0–2). - **Other causes**: Likelihood of alternative explanations for thrombocytopenia (scored 0–2). 2. **Platelet serotonin release assay (SRA)** is a functional laboratory test to confirm HIT in patients with intermediate/high 4Ts scores ([3][8][14]). It is not a component of the 4Ts score itself. **Conclusion:** The 4Ts score comprises **only the four clinical criteria** listed above. SRA is a subsequent diagnostic step for laboratory confirmation. **Sources:**[1][6][10] (4Ts criteria),[3][8][14] (SRA role). **Correct Answer:** **Thrombocytopenia, Timing of PLT drop, Thrombosis, and Other causes of thrombocytopenia** (4Ts criteria). The serotonin release assay is a confirmatory test, not part of the 4Ts score. Citations: [1] https://www.hematology.org/-/media/hematology/files/education/clinicians/guidelines-quality/documents/ash_vte_hit_pocketguide.pdf [2] https://documents.cap.org/documents/Heparin-Induced_Thrombocytopenia.pdf [3] https://onlinelibrary.wiley.com/doi/10.1002/ajh.24006 [4] https://bestpractice.bmj.com/topics/en-gb/1202 [5] https://ashpublications.org/blood/article/140/Supplement%201/5656/489804/Correlation-between-the-4T-Score-Enzyme-Linked [6] https://medschool.co/tools/fourtscore [7] https://pubmed.ncbi.nlm.nih.gov/20149589/ [8] https://news.mayocliniclabs.com/hematology/coagulation-disorders/serotonin-release-assay/ [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC9197915/ [10] https://pubmed.ncbi.nlm.nih.gov/22990018/ [11] https://academic.oup.com/ajcp/article/161/2/122/7344335 [12] https://pubmed.ncbi.nlm.nih.gov/31621093/ [13] https://academic.oup.com/ajcp/article/162/Supplement_1/S183/7823015 [14] https://news.mayocliniclabs.com/2022/08/01/heparin-induced-thrombocytopenia-hit-and-the-role-of-serotonin-release-assay-sra/ [15] https://onlinelibrary.wiley.com/doi/full/10.1002/ajh.25660 [16] https://pmc.ncbi.nlm.nih.gov/articles/PMC11665626/ [17] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/SESLHDGL%20123%20-%20Heparin%20Induced%20Thrombocytopaenia%20-%20Diagnosis%20and%20Management.pdf [18] https://pubmed.ncbi.nlm.nih.gov/25775976/ [19] https://www.ncbi.nlm.nih.gov/books/NBK482330/ [20] https://pmc.ncbi.nlm.nih.gov/articles/PMC3501714/ [21] https://www.health.qld.gov.au/__data/assets/pdf_file/0035/1178486/hit-guideline.pdf [22] https://ashpublications.org/blood/article/135/14/1082/454154/Diagnosing-HIT-the-need-for-speed [23] https://practical-haemostasis.com/Clinical%20Prediction%20Scores/Formulae%20code%20and%20formulae/Formulae/HIT/4T_HIT_score_2.html [24] https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2816742 [25] https://ashpublications.org/blood/article/126/5/563/126419/Toward-improved-diagnosis-of-HIT [26] https://ashpublications.org/ashclinicalnews/news/4980/How-Common-Is-Serotonin-Release-Assay-Negative"Platelet serotonin release assay - this is the gold standard test but not part of the 4Ts score." ## Footnote "UTD: Thrombocytopenia *Platelet count fall >50 percent and nadir ≥20,000/microL – 2 points *Platelet count fall 30 to 50 percent or nadir 10 to 19,000/microL – 1 point *Platelet count fall < 30 percent or nadir < 10,000/microL – 0 points ●Timing of platelet count fall *Clear onset between days 5 and 10 or platelet count fall at ≤1 day if prior heparin exposure within the last 30 days – 2 points *Consistent with fall at 5 to 10 days but unclear (eg, missing platelet counts), onset after day 10, or fall ≤1 day with prior heparin exposure within 30 to 100 days – 1 point *Platelet count fall at < 4 days without recent exposure – 0 points ●Thrombosis or other sequelae *Confirmed new thrombosis, skin necrosis, or acute systemic reaction after intravenous unfractionated heparin bolus – 2 points *Progressive or recurrent thrombosis, non-necrotizing (erythematous) skin lesions, or suspected thrombosis that has not been proven – 1 point *None – 0 points ●Other causes for thrombocytopenia *None apparent – 2 points *Possible – 1 point *Definite – 0 points" "- thrombocytopenia - Timing of PLT drop - History of thrombus - Other cause of thrombocytopenia - Platelet serotonin release assay"

Answer 56

Unassisted diastole

Answer 57

7.5mmHg ## Footnote "Association of Anaes doc https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.15817 Amplitude rises during exhalation and falls during inspiration. Consistent or increasing amplitude over at least seven breaths [74, 91]. Peak amplitude more than 1 kPa (7.5 mmHg) above baseline [74, 94]. Reading is clinically appropriate."

Answer 58

Healthy person less than 40yo

Answer 59

#5. In patients with DES-PCI who require time-sensitive NCS with interruption of ≥1 antiplatelet agents, NCS may be considered ≥3 months after PCI if the risk of delaying surgery outweighs the risk of MACE.5,23,24 ## Footnote 2024 AHA/ACC 7.5

Answer 60

AION ## Footnote "UTD: Both PION and AION have painless visual loss and both have afferent defect Although anterior ischemic optic neuropathy (AION) appears to be more common than PION after cardiac surgery, PION is relatively more common in cases of spine surgery and radical neck dissection - "

Answer 61

COPD ## Footnote "Airway abnormality eg muscous plugging causes matched defect secondary to HPV vs Flow abnormality eg PE/infarct causes a mismitch V/Q because you can stop blood flow but lung will remain ventilated"

Answer 62

60min ## Footnote "Blue Book 2023 Heparin 25iU/kg --> t1/2 30min 100IU/kg --> 60min 400IU/kg --> 150min"

Answer 63

The **posterior cutaneous nerve** does not innervate the knee joint, making it the correct answer. Here’s the rationale based on the provided sources: Knee Innervation Overview The knee joint receives **articular branches** from multiple nerves, primarily: - **Obturator nerve**: Supplies the anteromedial and posteromedial aspects of the knee capsule[7][9][14]. - **Tibial nerve**: Innervates the posterior capsule and infrapatellar fat pad[4][7][13]. - **Common peroneal (fibular) nerve**: Provides branches to the anterolateral capsule and tibial periosteum[7][10]. Posterior Cutaneous Nerve The **posterior cutaneous nerve of the thigh** (posterior femoral cutaneous nerve) is a **sensory nerve** that supplies: - Skin over the **posterior thigh** and **lower gluteal region**[1][5][8]. - Cutaneous sensation near the knee but **no articular branches to the knee joint itself**[8]. While it innervates the skin overlying the posterior knee, it does not contribute to joint innervation[7][8]. Key Distinction - **Cutaneous vs. Articular Innervation**: The posterior cutaneous nerve’s role is limited to **skin sensation**, whereas the obturator, tibial, and peroneal nerves directly innervate the **joint capsule, ligaments, and periosteum**[7][9][10][13]. Conclusion The **posterior cutaneous nerve** is excluded from knee joint innervation, as it lacks articular branches. The obturator, tibial, and peroneal nerves all participate in knee joint innervation. **Answer**: Posterior cutaneous nerve. Citations: [1] https://www.kenhub.com/en/library/anatomy/posterior-femoral-cutaneous-nerve [2] https://www.orthobullets.com/anatomy/10112/obturator-nerve [3] https://www.hopkinsmedicine.org/health/conditions-and-diseases/peroneal-nerve-injury [4] https://www.orthobullets.com/anatomy/10116/tibial-nerve [5] https://teachmeanatomy.info/lower-limb/nerves/cutaneous-innervation/ [6] https://pubmed.ncbi.nlm.nih.gov/27015545/ [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC7807845/ [8] https://teachmeanatomy.info/encyclopaedia/p/posterior-cutaneous-nerve-of-the-thigh/ [9] https://www.physio-pedia.com/Obturator_Nerve?lang=en [10] https://en.wikipedia.org/wiki/Common_fibular_nerve [11] https://www.kenhub.com/en/library/anatomy/tibial-nerve [12] https://ekja.org/journal/view.php?number=7167 [13] https://teachmeanatomy.info/lower-limb/nerves/tibial-nerve/ [14] https://www.physio-pedia.com/Obturator_Nerve [15] https://pmc.ncbi.nlm.nih.gov/articles/PMC10366308/ [16] https://www.kenhub.com/en/library/anatomy/obturator-nerve [17] https://www.physio-pedia.com/Common_Peroneal_Nerve [18] https://www.physio-pedia.com/Posterior_Femoral_Cutaneous_Nerve [19] https://teachmeanatomy.info/lower-limb/nerves/obturator-nerve/ [20] https://www.ncbi.nlm.nih.gov/books/NBK549859/ [21] https://www.ncbi.nlm.nih.gov/books/NBK537028/ [22] https://www.physio-pedia.com/Posterior_Cutaneous_Nerve_of_Thigh [23] https://my.clevelandclinic.org/health/body/22348-obturator-nerve [24] https://radiopaedia.org/articles/common-peroneal-nerve [25] https://my.clevelandclinic.org/health/body/21962-tibial-nerve [26] https://www.ncbi.nlm.nih.gov/books/NBK532301/ [27] https://www.ncbi.nlm.nih.gov/books/NBK482431/ [28] https://academic.oup.com/bjaed/article/12/1/38/260058 [29] https://www.medbox.org/index.php/dl/5e148832db60a2044c2d209a [30] https://academic.oup.com/bjaed/article/5/5/166/283234 [31] https://www.ncbi.nlm.nih.gov/books/NBK500017/ [32] https://pmc.ncbi.nlm.nih.gov/articles/PMC8693230/ [33] https://www.openanesthesia.org/keywords/peripheral-nerve-injuries-from-positioning/ [34] https://www.ncbi.nlm.nih.gov/books/NBK532887/ [35] https://usra.ca/regional-anesthesia/specific-blocks/lower-limb/obturatornerve.php [36] https://www.youtube.com/watch?v=xdj-yL7LqVc/?Peroneal ## Footnote NYSORA - unclear

Answer 64

Facial nerve Cranial Nerve Injury Risks Associated with Supraglottic Airway Device Insertion Supraglottic airway (SGA) devices are widely used in clinical anesthesia, but their insertion carries risks of cranial nerve injuries due to anatomical proximity and mechanical compression. Based on systematic reviews and case reports, the trigeminal (inferior alveolar and infra-orbital branches), glossopharyngeal, vagus (recurrent laryngeal branch), and hypoglossal nerves are commonly implicated in such injuries[1][2][3][5][7]. The lingual nerve, a branch of the trigeminal nerve, is the most frequently injured[1][7]. However, the **facial nerve (CN VII)** is not anatomically positioned in the regions affected by SGA placement, and no cases of facial nerve injury have been reported in the literature[1][2][3][5][7]. This absence of association makes the facial nerve the correct answer. **Answer:** Facial **Rationale:** The facial nerve (CN VII) is not anatomically proximate to SGA insertion sites and is not cited in any reported cases of nerve injury from SGAs, unlike the trigeminal, glossopharyngeal, vagus, and lingual nerves[1][2][3][5][7]. Citations: [1] https://pubmed.ncbi.nlm.nih.gov/25376257/ [2] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.12917 [3] https://www.scirp.org/journal/paperinformation?paperid=100681 [4] https://www.jkns.or.kr/journal/view.php?number=7579 [5] https://pmc.ncbi.nlm.nih.gov/articles/PMC10664044/ [6] https://www.nature.com/gimo/contents/pt1/full/gimo36.html [7] https://www.lmaco.com/evidence/lingual-nerve-injury-following-use-i-gel%E2%84%A2-laryngeal-mask [8] https://my.clevelandclinic.org/health/body/22269-glossopharyngeal-nerve [9] https://journals.sagepub.com/doi/10.1177/17504589241270238?icid=int.sj-abstract.citing-articles.2 [10] https://emedicine.medscape.com/article/1875813-overview [11] https://pmc.ncbi.nlm.nih.gov/articles/PMC4691459/ [12] https://www.researchgate.net/publication/267812551_Cranial_nerve_injuries_with_supraglottic_airway_devices_A_systematic_review_of_published_case_reports_and_series [13] https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/abs/10.1111/anae.12917 [14] https://www.researchgate.net/publication/356593603_Unilateral_lingual_nerve_and_hypoglossal_nerve_injury_caused_by_a_novel_laryngeal_mask_airway_a_case_report [15] https://journals.lww.com/ejanaesthesiology/fulltext/2009/11000/cranial_nerve_injuries_from_a_laryngeal_mask.16.aspx [16] https://academic.oup.com/bjaed/article/15/4/184/305721

Answer 65

Inf gluteal ## Footnote inf gluteal = motor to glute, no sensory Genitofemoral L1-L2 PCN of thigh S1-3 Pudendal S2-4

Answer 66

Inferior alveolar ...or is this one mental n. because it hasn't specified a tooth they're taking out? Numbness Over the Lower Chin Following Dental Extraction: Identification of the Affected Nerve Dental extraction procedures, while routine, carry inherent risks of iatrogenic nerve injury due to the close anatomical relationship between dental structures and peripheral nerve pathways. The presentation of postoperative numbness over the lower chin—colloquially termed "numb chin syndrome" or mental nerve neuropathy—directly implicates injury to sensory nerves supplying the mandibular region. Through analysis of clinical literature and neuroanatomical principles, this report identifies the mental nerve as the primary structure damaged in such cases, while contextualizing its relationship to the inferior alveolar nerve and broader diagnostic considerations. Anatomical Foundations of Mandibular Sensory Innervation The Trigeminal Nerve and Its Mandibular Division The trigeminal nerve (cranial nerve V) provides sensory innervation to the face via three divisions: ophthalmic (V1), maxillary (V2), and mandibular (V3). The mandibular division gives rise to the inferior alveolar nerve, which enters the mandibular foramen and courses through the mandibular canal[3][4]. Approximately at the level of the second premolar, the inferior alveolar nerve bifurcates into two terminal branches: 1. **Mental nerve**: Exits via the mental foramen to supply sensory fibers to the skin of the chin, lower lip, and labial gingiva of anterior teeth[3][4]. 2. **Incisive nerve**: Continues anteriorly within the incisive canal to innervate mandibular incisors and canines[3][4]. This anatomical arrangement means that while the inferior alveolar nerve serves as the parent trunk, the mental nerve acts as its terminal cutaneous branch responsible for chin sensation[3][4]. Vulnerability During Dental Procedures The mental foramen's position—typically between the apices of the first and second premolars—places the mental nerve at risk during procedures involving these teeth or their surrounding tissues[3][4]. However, posterior extractions (e.g., molars) may indirectly affect the nerve through manipulation of the inferior alveolar trunk within the mandibular canal, as the mental nerve derives from this structure[5][8]. Mechanisms of Post-Extraction Nerve Injury Direct Trauma to the Mental Nerve Surgical extraction of premolars or anterior teeth poses the highest risk of direct mental nerve injury due to: - **Periosteal elevator slippage** during flap reflection near the mental foramen[4][8]. - **Root fragment displacement** into the mental foramen during apical curettage[1][5]. - **Local anesthetic needle penetration** into the foramen during inferior alveolar nerve blocks[4][8]. Such mechanical insults can induce neuropraxia (conduction block without axonal disruption) or, in severe cases, axonotmesis (axonal degeneration with intact endoneurium)[5][8]. Indirect Injury via Inferior Alveolar Nerve Trauma Molar extractions—particularly impacted third molars—frequently endanger the inferior alveolar nerve due to: - **Compression** from apical root displacement into the mandibular canal[2][5]. - **Thermal injury** from osteotomy burrs during bone removal[5][8]. - **Postoperative edema** or hematoma formation within the canal[2][8]. While these mechanisms primarily affect the inferior alveolar trunk, the resulting sensory deficits encompass all its terminal territories, including the mental nerve distribution (chin and lower lip)[2][8]. This explains why molar extractions may manifest with chin numbness despite the injury site being posterior to the mental foramen. Clinical Differentiation Between Mental and Inferior Alveolar Neuropathies Symptomatology - **Isolated mental nerve injury**: Numbness strictly localized to the chin and ipsilateral lower lip vermilion[1][3]. Gingival sensation remains intact if the incisive nerve is unaffected[3][4]. - **Inferior alveolar nerve injury**: Numbness involving the chin, lower lip, **and** labial/buccal gingiva of mandibular teeth anterior to the injury site[2][8]. Concomitant incisive nerve dysfunction may cause dental hypersensitivity due to pulp innervation disruption[2]. Diagnostic Testing 1. **Pinprick testing**: Maps sensory loss boundaries; mental nerve deficits spare the gingiva[3][4]. 2. **Two-point discrimination**: Impaired in the lower lip with inferior alveolar involvement[8]. 3. **Dental vitality testing**: Positive response in anterior teeth rules out incisive nerve injury, localizing damage to the mental branch[2][8]. Management Considerations Acute Phase (0-8 Weeks Post-Injury) - **Corticosteroids** (e.g., dexamethasone 4-8 mg/day tapered over 5 days) to reduce inflammatory compression[1][8]. - **Antioxidants** (alpha-lipoic acid 600 mg/day) to mitigate oxidative neuronal damage[1][5]. - **Low-level laser therapy** to enhance axonal regeneration[1][8]. Persistent Neuropathy (>3 Months) - **Pulsed radiofrequency ablation** of the mental nerve for refractory neuropathic pain[1][5]. - **Microneurosurgical repair** via direct neurorrhaphy or autografting for transected nerves[4][8]. Conclusion Numbness over the lower chin following dental extraction overwhelmingly implicates **mental nerve injury**, whether through direct trauma at the mental foramen (anterior procedures) or indirect insult via the inferior alveolar trunk (posterior extractions). Clinicians must recognize that while the inferior alveolar nerve serves as the anatomical origin, the mental nerve's terminal distribution dictates the chin-specific symptomatology. Timely diagnosis—supported by sensory mapping and dental testing—enables targeted interventions to optimize functional recovery. Citations: [1] https://pubmed.ncbi.nlm.nih.gov/24850119/ [2] https://jdapm.org/DOIx.php?id=10.17245%2Fjdapm.2021.21.2.173 [3] https://en.wikipedia.org/wiki/Mental_nerve [4] https://selectedreadingsoms.com/wp-content/uploads/2019/05/Numb-Tongue-Numb-Lip-Numb-Chin-What-to-Do-When-Updated.pdf [5] https://www.woodviewos.com/dental-paresthesia-nerve-damage-complication-wisdom-tooth-extraction-dental-injection [6] https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2017.00343/full [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC5526228/ [8] https://www.blvddentistry.com/managing-nerve-pain-after-tooth-extraction-a-guide/ [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC10141477/ [10] https://www.lenus.ie/bitstream/handle/10147/333831/OctArticle2.pdf?sequence=1&isAllowed=y [11] https://www.cambridge.org/core/services/aop-cambridge-core/content/view/383E302FCA45F0D2F01AF93249063483/S1481803500008460a.pdf/mental-nerve-neuropathy-case-report-and-review.pdf [12] https://www.baoms.org.uk/patients/procedures/23/removal_of_impacted_wisdom_teeth [13] https://www.painphysicianjournal.com/current/pdf?article=MjEwOA%3D%3D&journal=82 [14] https://www.ncbi.nlm.nih.gov/books/NBK589668/ [15] https://www.medicalnewstoday.com/articles/numb-chin [16] https://www.nycoms.com/management-injury-nerves-maxillofacial-region/ [17] https://pmc.ncbi.nlm.nih.gov/articles/PMC6031975/ [18] https://www.oralsurgerysouth.com/procedures/wisdom-teeth/after-extraction-of-wisdom-teeth/ [19] https://www.healthline.com/health/numb-chin [20] https://www.baoms.org.uk/patients/procedures/44/coronectomy

Answer 67

FIX --- Mnemonic: III F VIII XIII Fibro x2 vwF ## Footnote Cryo contains: vwF, fibronectin, fibrinogen (I), VIII, XIII

Answer 68

Deep posterior ## Footnote The PTN is one of the two terminal divisions of the sciatic nerve and consists of muscular, cutaneous, and articular branches. It extends from the arch of the soleus muscle to the tibiotalocalcaneal canal. In the upper two-thirds of the leg the nerve is located deep in the posterior compartment.

Answer 69

Speed of muscle akinesis ## Footnote HYALASE is used as an aid in different medical conditions to allow injected substances to be rapidly dispersed and absorbed. https://www.nps.org.au/medicine-finder/hyalase-injection

Answer 70

Reduced rate of anaphylaxis ## Footnote "https://www.nationalauditprojects.org.uk/downloads/NAP6%20Chapter%2018%20-%20Patent%20Blue%20dye.pdf https://pubmed.ncbi.nlm.nih.gov/28355372/ Methylene blue is more widely available and less expensive than patent blue, with an apparently lower risk of anaphylaxis. Patent blue = easier to see the nodes"

Answer 71

- Rectal indomethacin ## Footnote "NEJM APMSE - Rectal diclofenac and indomethacin"

Answer 72

Lower dose, same conc ## Footnote "Epipen = 300microg 1:1000 = 1mg 1000microg/mL ANAPEN 500mcg adrenaline (epinephrine) 500 micrograms/0.3 mL solution for injection pre-filled syringe (auto-injector) Epipen 300mcg Ad in 0.3mL " A device containing either 300 micrograms ( EpiPen®) OR a device containing 500 micrograms (Anapen®) should be used. EpiPen® = one dose of 0.3 mg epinephrine, USP 0.3 mg/0.3 mL EpiPen Jr® = one dose of 0.15 mg epinephrine, USP 0.15 mg/0.3 mL Anapen 150/300/500 microg / 0.3mL All 0.3mL Vetted by perplexity

Answer 73

Soap and water "Laryngoscope handles, being non-critical devices, should be cleaned with detergent and water between each patient use. If contaminated with blood, they should be washed and disinfected" ## Footnote PG 28 2015 P.4

Answer 74

dexamethasone ## Footnote "https://www.bjaed.org/action/showPdf?pii=S2058-5349%2819%2930079-4 Dexamethasone --> Dexmed --> Clonidine "

Answer 75

High PEEP ## Footnote "Blue Book 2017 PEEP prevents de-recruitment of alveoli at the end of each expiration thus maintaining functional residual capacity (FRC). Patients with ARDS often receive PEEP of 5 to 20 cm of water. Higher PEEP levels may improve oxygenation but may also cause circulatory depression and lung injury from over distention. Thus, optimal PEEP is that which prevents atelectrauma and at the same time prevents over distension of normal alveoli – it needs to be individualised to the patient’s respiratory mechanics. How to set “optimal PEEP” remains controversial."

Answer 76

0.5% chlorhex/ 70% alcohol. For skin preparation, 0.5 per cent chlorhexidine in alcohol, where available, is recommended for neuraxial techniques ## Footnote PG 28 Infection control https://www.anzca.edu.au/getattachment/e4e601e6-d344-42ce-9849-7ae9bfa19f15/PG28(A)-Guideline-on-infection-control-in-anaesthesia

Answer 77

100ml/kg | Parameters for pregnant lady ## Footnote https://www.ahajournals.org/doi/10.1161/circulationaha.114.009029

Answer 78

PSA RM rate modulation multichamber pacing ## Footnote https://litfl.com/pacemaker-rhythms-normal-patterns/

Answer 79

5 mins ## Footnote """neutralizing their anticoagulant effect immediately after administration"" Praxbind website https://pro.boehringer-ingelheim.com/us/products/praxbind/idarucizumab/reversing-pradaxa# 2021 Blue book - Almost immediate"

Answer 80

TRE: traps --> rhomboids --> erector spinae in that order

Answer 81

maximum of 8-9mg/kg lignocaine can be used for topicalisation ## Footnote https://www.anzca.edu.au/resources/sig-resources/2019-airway-management-sig-afoi-topicalisation-sed

Answer 82

Physical dependence

Answer 83

cardiothoracic anaesthesia (~1:8,600) ## Footnote "NAP 5 2014 GA CS 1:670 Paralysed pt 1:8000 In general for GA with paralysis 1: 20,000 GA without paralysis 1:136,000"

Answer 84

major haemorrhage | NAP 7 ## Footnote NAP 7 2023: The most common causes of perioperative cardiac arrest were major haemorrhage (17%), bradyarrhythmia (9.4%) and cardiac ischaemia (7.3%) but varied by surgical specialty

Answer 85

Haemophilia B ## Footnote "BJA + UTD DDAVP stim factor VIII"

Answer 86

1. remove cannula 2. if removed, phentolamine (UTD) Phentolamine if "ischaemia...'" **either using the catheter through which vasopressors were infusing if not yet removed** from the patient or through separate subcutaneous injection) ## Footnote https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/Medicine%20Guideline%20-%20Phentolamine%20in%20the%20treatment%20of%20dermal%20necrosis%20or%20sloughing%20following%20extravasation%20of%20peripherally%20administered%20noradrenaline%20%28norepinephrine%29.pdf

Answer 87

ECG changes | PoTS ## Footnote "- Need a normal ECG for PoTS - IS assoc w/ long covid, EDS, and need normal LV function - https://www.acc.org/Latest-in-Cardiology/Articles/2016/01/25/14/01/Postural-Tachycardia-Syndrome-POTS-Diagnosis-and-Treatment-Basics-and-New-Developments#:~:text=Left%20ventricular%20function%20must%20be,could%20mimic%20a%20POTS%20presentation."

Answer 88

RV dilated/dysFx The correct answer is **right dilated ventricle**. Aortic dissection typically presents with features related to the aorta and left heart structures, while right ventricular dilation is not a characteristic finding. Here's the rationale: 1. **Dilated aortic root** Aortic dissection often occurs in the context of pre-existing aortic pathology, such as aneurysmal dilation or connective tissue disorders (e.g., Marfan syndrome). A dilated aortic root is a common predisposing factor and can be exacerbated by the dissection itself[4][6]. 2. **Aortic regurgitation (AR)** Acute aortic regurgitation is a frequent complication of type A dissections due to disruption of the aortic valve apparatus or dilation of the aortic root, leading to valve incompetence[5][6]. 3. **RWMA (regional wall motion abnormalities)** While not universally present, RWMA may occur if the dissection extends into the coronary arteries (e.g., right coronary artery involvement causing right ventricular ischemia). However, this is less common and not a definitive feature[6]. 4. **Right dilated ventricle** Right ventricular dilation is not typically associated with aortic dissection. The primary complications involve the aorta, left heart, or systemic circulation (e.g., tamponade, aortic rupture, or malperfusion syndromes). Right ventricular pathology would more commonly arise from conditions like pulmonary embolism or primary right heart failure[3][6]. **Conclusion**: The exception is **right dilated ventricle**, as it is not a direct consequence of aortic dissection. Citations: [1] https://www.mayoclinic.org/diseases-conditions/aortic-dissection/symptoms-causes/syc-20369496 [2] https://www.healthdirect.gov.au/aortic-dissection [3] https://www.msdmanuals.com/home/heart-and-blood-vessel-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection [4] https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-12/Acute-aortic-dissection [5] https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.110.958975 [6] https://www.msdmanuals.com/professional/cardiovascular-disorders/diseases-of-the-aorta-and-its-branches/aortic-dissection [7] https://www.ahajournals.org/doi/10.1161/01.cir.0000087009.16755.e4 [8] https://www.ncbi.nlm.nih.gov/books/NBK441963/ [9] https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/aortic-dissection-repair [10] https://pmc.ncbi.nlm.nih.gov/articles/PMC8762162/ [11] https://litfl.com/acute-aortic-dissection/ [12] https://pubmed.ncbi.nlm.nih.gov/28871571/ [13] https://emedicine.medscape.com/article/2062452-clinical [14] https://www.pennmedicine.org/for-patients-and-visitors/patient-information/conditions-treated-a-to-z/aortic-dissection [15] https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/485480 [16] https://www.bhf.org.uk/informationsupport/conditions/aortic-aneurysm-dissection-and-rupture [17] https://emedicine.medscape.com/article/2062452-overview [18] https://www.revportcardiol.org/en-acute-aortic-dissection-complicated-by-articulo-S217420491400292X [19] https://my.clevelandclinic.org/health/diseases/16743-aortic-dissection [20] https://academic.oup.com/ehjcimaging/article/10/1/i31/2465433 [21] https://nyulangone.org/conditions/aortic-dissection/types [22] https://synapse.koreamed.org/articles/1018128 [23] https://academic.oup.com/ehjcimaging/article-pdf/10/1/i31/7466330/jen251.pdf [24] https://aci.health.nsw.gov.au/networks/eci/clinical/tools/cardiology/aortic-dissection [25] https://www.health.qld.gov.au/cpc/cardiology/aortic-disease [26] https://journals.sagepub.com/doi/10.1177/0267659120986532?icid=int.sj-full-text.similar-articles.6 [27] https://www.escardio.org/static-file/Escardio/Subspecialty/EACVI/education/EACVI-core-syllabus.pdf [28] http://103.12.11.134/journal/1999/september/Echo2.pdf [29] https://bestpractice.bmj.com/topics/en-gb/3000226 [30] https://cdt.amegroups.org/article/view/23120/html [31] https://pubmed.ncbi.nlm.nih.gov/30562107/ [32] https://pmc.ncbi.nlm.nih.gov/articles/PMC3654107/ [33] https://pmc.ncbi.nlm.nih.gov/articles/PMC1861012/ ## Footnote LITFL Echo: AR, RWMA heralding cor art occlusion, acute dilation aortic root, pericardial eff

Answer 89

exacerbation of asthma A fractional exhaled nitric oxide (FeNO) level exceeding 70 parts per billion (ppb) in a patient undergoing pulmonary function testing (PFT) strongly suggests **exacerbation of asthma**. This conclusion is supported by the following evidence: 1. **FeNO as a Marker of Type 2 Inflammation**: Elevated FeNO reflects eosinophilic airway inflammation, a hallmark of asthma pathophysiology[1][8][10]. During exacerbations, airway inflammation intensifies, leading to higher FeNO levels compared to stable states[1][5][10]. While normal adult FeNO levels typically range below 25 ppb, values exceeding 50 ppb are strongly indicative of uncontrolled asthma or exacerbations[4][9][11]. A reading of 70 ppb falls well within this high-risk range. 2. **Contrast with Smoking and COPD**: - **Smoking**: Cigarette smoke reduces FeNO levels through mechanisms such as nitric oxide synthase inhibition and increased oxidative stress[2][7]. Smokers with or without COPD consistently demonstrate lower FeNO values (often 50 ppb predicts corticosteroid responsiveness and exacerbation risk in asthma[4][5][10]. Levels ≥70 ppb indicate severe airway inflammation requiring urgent anti-inflammatory therapy[1][4][9]. In contrast, COPD and smoking-related lung disease would not typically manifest such pronounced FeNO elevation, even during exacerbations[2][7]. **Conclusion**: A FeNO level of 70 ppb is inconsistent with smoking or pure COPD. This degree of elevation strongly supports acute asthma exacerbation driven by eosinophilic airway inflammation. Immediate initiation or escalation of inhaled corticosteroids is warranted[1][4][9]. Citations: [1] https://allergyasthmanetwork.org/what-is-asthma/how-is-asthma-diagnosed/nitric-oxide-testing/ [2] https://www.tandfonline.com/doi/full/10.1080/15412555.2019.1638355 [3] https://www.lung.org/lung-health-diseases/lung-procedures-and-tests/exhaled-nitric-oxide-test [4] https://www.niox.com/en/digital-platform/interpreting-feno [5] https://www.pulmonologyadvisor.com/news/association-between-fraction-of-exhaled-nitric-oxide-and-asthma-exacerbations/ [6] https://www.thoracic.org/statements/resources/allergy-asthma/feno-document.pdf [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC7362749/ [8] https://pmc.ncbi.nlm.nih.gov/articles/PMC2677842/ [9] https://www.niox.com/en/feno-asthma/interpreting-feno/ [10] https://pmc.ncbi.nlm.nih.gov/articles/PMC7919904/ [11] https://pmc.ncbi.nlm.nih.gov/articles/PMC10137365/ [12] https://pmc.ncbi.nlm.nih.gov/articles/PMC3955647/ [13] https://bjgp.org/content/73/737/565 [14] https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(22)00263-2/fulltext [15] https://pmc.ncbi.nlm.nih.gov/articles/PMC10037222/ [16] https://thorax.bmj.com/content/77/4/351 [17] https://pmc.ncbi.nlm.nih.gov/articles/PMC2801041/ [18] https://www.elsevier.es/en-revista-allergologia-et-immunopathologia-105-articulo-a-pathophysiological-approach-for-feno-S0301054615000270 [19] https://www.mdpi.com/2076-3271/12/4/52 [20] https://www.atsjournals.org/doi/10.1164/rccm.9120-11ST [21] https://www.severeasthma.org.au/biomarkers-recommendation/ [22] https://www.ccjm.org/content/90/6/363 ## Footnote "- Normal is < 25ppb https://www.lung.org/lung-health-diseases/lung-procedures-and-tests/exhaled-nitric-oxide-test"

Answer 90

incidence of CS | Blue book article ## Footnote Blue book 2021.

Answer 91

Diastolic dys ## Footnote "https://www.ahajournals.org/doi/10.1161/01.cir.83.5.1605?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed Cascade of events: Diastolic dys, sys dysFx, ECG changes, Sx angina - from some rando paper Bonny found"

Answer 92

- 4 weeks for every year of absence The starting point for calculating the total duration is one month per year of absence from anaesthesia practice. | PS ## Footnote PS 50 Return to Practice 2017

Answer 93

- Subjective effort ## Footnote "rating of pecieved exertion" test

Answer 94

72 hours The ANZCOR guidelines recommend **72 hours** as the minimum time from cardiac arrest to prognostication in comatose survivors. This allows adequate time to minimize confounding factors like residual sedation or paralysis, which could lead to false-positive predictions of poor outcomes[1][3][12]. Key recommendations include: - **No prognostication before 72 hours** using clinical criteria alone, due to insufficient specificity[1][3]. - **Multimodal assessment** (combining clinical exam, neurophysiological tests, imaging, or biomarkers) is required for reliable prognostication[1][3]. - Specific predictors at ≥72 hours: - Bilateral absence of pupillary or corneal reflexes[1][3]. - Bilateral absence of N20 somatosensory evoked potentials (SSEP)[1]. - Persistent burst suppression or status epilepticus on EEG[1][3]. The 72-hour threshold applies to both patients treated and not treated with targeted temperature management (TTM)[1][3]. Earlier prognostication (e.g., 24–48 hours) is discouraged due to high false-positive rates[1][12]. Citations: [1] https://www.resus.org.nz/assets/Uploads/ANZCOR-Guideline-11.7-Jan16.pdf [2] https://emcrit.org/ibcc/np/ [3] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support/ [4] https://pmc.ncbi.nlm.nih.gov/articles/PMC7993077/ [5] https://www.anzcor.org/assets/anzcor-guidelines/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support-250.pdf [6] https://www.resus.org.nz/assets/Uploads/Adult-Advanced-Life-Support-All-Guidelines.pdf [7] https://www.anzcor.org/assets/anzcor-guidelines/guideline-11-2-protocols-for-adult-advanced-life-support-237.pdf [8] https://cprguidelines.eu/assets/guidelines/European-Resuscitation-Council-and-European-Societ.pdf [9] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-1-management-of-cardiac-arrest-due-to-trauma/ [10] https://litfl.com/therapeutic-hypothermia-after-cardiac-arrest/ [11] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-resuscitation-in-special-circumstances/ [12] https://pmc.ncbi.nlm.nih.gov/articles/PMC10241762/ [13] https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-10-resuscitation-in-special-circumstances/downloadpdf [14] https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/anzcor11-2-adultllifesupport2018.pdf [15] https://www.resus.org.nz/assets/Guidelines/ANZCOR-Guideline-12.5-Management-after-ROSC-Nov-2021.pdf [16] https://www.anzcor.org --- Answer from Perplexity: pplx.ai/share | ALS ANZCOR - detailed ## Footnote ANZCOR 48h: CTB 72 hours: pupillary light reflex, pupillometry, corneal reflex, eeg, NSE, MRI 72h-7d 4 days GCS >3 7 days (status) myoclonus https://www.anzcor.org/home/adult-advanced-life-support/guideline-11-7-post-resuscitation-therapy-in-adult-advanced-life-support/ 2.3-3.5

Answer 95

Greater height, shorter DOA ## Footnote Hyperbaric Versus Isobaric Bupivacaine for Spinal Anesthesia: Systematic Review and Meta-analysis for Adult Patients Undergoing Noncesarean Delivery Surgery; BJA intrathecal drug spread 2004

Answer 96

? **Answer:** Ketamine **Rationale:** Ketamine demonstrates favorable anticonvulsant properties with minimal interference to intraoperative electrocorticography (ECoG) and neurophysiological monitoring during epilepsy surgery[1][5][6]. Studies show it suppresses seizure burden in refractory status epilepticus (57–81% efficacy) without exacerbating epileptiform discharges in non-epileptic brain regions[1][11]. Unlike sevoflurane, which induces dose-dependent epileptogenic activity (1.5–2 MAC)[3][8], ketamine preserves baseline cortical excitability and reduces vasopressor requirements while maintaining stable intracranial pressure[1][6]. Remifentanil, while useful for activating epileptogenic zones via opioid-induced spikes[2][12], risks obscuring baseline ECoG signals if overused. These findings align with BJA Education and Miller’s guidelines prioritizing ketamine for balancing anesthetic efficacy and neurophysiological fidelity. Citations: [1] https://pmc.ncbi.nlm.nih.gov/articles/PMC7713785/ [2] https://pubmed.ncbi.nlm.nih.gov/11737170/ [3] https://www.aub.edu.lb/fm/Anesthesiology/meja/Documents/Anesthesia%20And%20Electrocorticography%20For%20Epilepsy%20Surgery%20A%20Jordanian%20Experience.pdf [4] https://seizure.mgh.harvard.edu/wp-content/uploads/MGH_Status_Protocol_01_09_2015.pdf [5] https://aesnet.org/abstractslisting/drug-induced-eeg-pattern-predicts-effectiveness-of-ketamine-in-treating-refractory-status-epilepticus [6] https://pmc.ncbi.nlm.nih.gov/articles/PMC3731413/ [7] https://pubmed.ncbi.nlm.nih.gov/14570785/ [8] https://pubmed.ncbi.nlm.nih.gov/39297916/ [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC6939570/ [10] http://www2.pedsanesthesia.org/meetings/2013winter/syllabus/submissions/sat/Brain%20Mapping%20and%20Deep%20Brain%20Stimulation%20Final_NCarling.pdf [11] https://www.epilepsy.org.uk/news/ketamine-effective-for-status-epilepticus [12] https://onlinelibrary.wiley.com/doi/full/10.1046/j.1528-1157.2001.05901.x [13] https://ekja.org/upload/pdf/kja-23843.pdf [14] https://pmc.ncbi.nlm.nih.gov/articles/PMC8766927/ [15] https://dig.pharmacy.uic.edu/faqs/2023-2/december-2023-faqs/what-is-the-role-of-ketamine-in-the-management-of-status-epilepticus/ [16] https://portal.findresearcher.sdu.dk/en/publications/pharmacodynamics-of-remifentanil-induced-intracranial-spike-activ [17] https://journals.lww.com/anesthesia-analgesia/Fulltext/2013/08000/The_Anesthetic_Considerations_of_Intraoperative.27.aspx?generateEpub=Article%7Canesthesia-analgesia%3A2013%3A08000%3A00027%7C10.1213%2Fane.0b013e318297390c%7C [18] https://aesnet.org/abstractslisting/ketamine-therapy-in-the-management-of-refractory-seizures-in-an-extremely-premature-neonate-a-case-report [19] https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1600-0404.2009.01193.x [20] https://onlinelibrary.wiley.com/doi/10.1684/epd.2014.0675 [21] https://pch.health.wa.gov.au/for-health-professionals/emergency-department-guidelines/ketamine-sedation [22] https://www.acns.org/UserFiles/file/ACNSMinimumTechRequirementsforIntraopECOG_DraftforCommentFeb22.pdf [23] https://www.e-jnc.org/m/journal/view.php?doi=10.18700%2Fjnc.230003 [24] https://journals.lww.com/neur/fulltext/2021/69010/ketadex__a_saviour_for_intraoperative_multimodal.39.aspx [25] https://pmc.ncbi.nlm.nih.gov/articles/PMC7807957/ [26] https://www.neurology.org/doi/10.1212/WNL.0000000000010611 [27] https://academic.oup.com/bja/article/108/4/562/257975 [28] https://snacc.org/education-corner/challenging-cases/pbld/pbld-10/ [29] https://academic.oup.com/bjaed/article/15/3/111/279202 ## Footnote I havent found a reference for this, the lecture from Syndey said ketamine does inrease MPSS, surely sevo is worse than remi??

Answer 97

"increased cerebral O2 (SctO2) and decreased peripheral SpO2 ie. Increases NIRS, decreases periph (falsely)" ## Footnote https://pmc.ncbi.nlm.nih.gov/articles/PMC4384398/#:~:text=Intravenously%20administered%20indocyanine%20green%20(ICG,carotid%20endarterectomy%20under%20general%20anesthesia.

Answer 98

**Answer:** **Celecoxib** **Rationale:** 1. **Superior Analgesic Efficacy:** - A randomized controlled trial (Akinbade et al., 2018) comparing celecoxib (400 mg initial dose, then 200 mg 12-hourly), ibuprofen (400 mg 8-hourly), and tramadol (100 mg 8-hourly) found celecoxib achieved the lowest mean pain scores at all postoperative intervals (4–48 hours), with statistically significant differences at 4 hours (*p* = 0.0039)[1]. - A 2024 study comparing celecoxib (100 mg), diclofenac, and ibuprofen (400 mg) confirmed celecoxib’s superior pain control over ibuprofen, particularly in reducing rescue medication use[4]. - Preemptive celecoxib (200 mg) demonstrated better analgesic activity than ibuprofen (400–600 mg) and acetaminophen, with lower postoperative pain scores and fewer patients requiring rescue analgesia[6]. 2. **Adverse Effects and Safety:** - Celecoxib and ibuprofen showed no adverse effects in trials, while tramadol caused nausea, dizziness, and vomiting in 47.6% of patients[1][2]. - Celecoxib’s COX-2 selectivity minimizes gastrointestinal (GI) risks compared to nonselective NSAIDs like ibuprofen, making it safer for patients with peptic ulcer disease or GI sensitivities[1][6]. 3. **Guideline Considerations:** - While NSAIDs like ibuprofen remain first-line for postoperative pain, recent evidence supports celecoxib’s efficacy, especially with higher initial dosing (400 mg loading dose)[1][4]. - Paracetamol (acetaminophen) is less effective as monotherapy for moderate-to-severe inflammatory pain[3][5], and tramadol is reserved for opioid-tolerant patients due to inferior efficacy and side effects[1][2]. **Conclusion:** Celecoxib provides superior pain control with a favorable safety profile for post-wisdom tooth extraction, particularly when administered at an initial 400 mg dose followed by 200 mg 12-hourly. Ibuprofen remains effective for patients without GI risks, while tramadol and paracetamol are less optimal choices. Citations: [1] https://www.thejcdp.com/doi/10.5005/jp-journals-10024-2428 [2] https://www.sid.ir/FileServer/JE/88120090413.pdf [3] https://www.cochrane.org/CD004624/ORAL_ibuprofen-versus-paracetamol-acetaminophen-for-pain-relief-after-surgical-removal-of-lower-wisdom-teeth [4] https://pmc.ncbi.nlm.nih.gov/articles/PMC10845003/ [5] https://pmc.ncbi.nlm.nih.gov/articles/PMC11561150/ [6] https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2023.1303382/full [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC3414241/ [8] https://australianprescriber.tg.org.au/articles/opioid-prescribing-in-dentistry-is-there-a-problem.html [9] https://www.seslhd.health.nsw.gov.au/sites/default/files/groups/Royal_Hospital_for_Women/docs/painaftersurgery.pdf [10] https://www.ada.org/resources/ada-library/oral-health-topics/oral-analgesics-for-acute-dental-pain [11] https://www.nps.org.au/assets/NPS/pdf/NPS-Medicinewise-Opioids-webinar-slides-for-Dentists-25112020.pdf [12] https://www.colgate.com/en-us/oral-health/tooth-removal/ibuprofen-and-acetaminophen-together-may-give-profound-pain-relief-with-fewer-side-effects-after-dental-surgery [13] https://orthoinfo.aaos.org/en/recovery/managing-pain-with-medications/ [14] https://www.cabrini.com.au/app/uploads/Pain-relief-following-surgery.pdf [15] https://www.aafp.org/pubs/afp/issues/2005/0301/p913.html --- Answer from Perplexity: pplx.ai/share ## Footnote Cobbled together from a few different papers, brufen superior to panadol, but celecoxib (and diclofenac) superior to panadol, meloxicam superior to tramadol

Answer 99

No bronchospasm ## Footnote "https://www.bjanaesthesia.org/action/showPdf?pii=S0007-0912%2821%2900437-2 table of Burch and Wartofski score for thyrotoxicosis dx UTD: Temp, neuro signs (agitation --> seizure/coma), UG (diarrhoea --> jaundice), tachy, AF, HF, precipitant criteria"

Answer 100

reduced SVR reduced SVR (hence flushing!) ## Footnote "UTD thyroid CVS table https://www.uptodate.com/contents/cardiovascular-effects-of-hyperthyroidism + diastolic down --> widened pulse pressure"

Answer 101

inferior gluteal, its a motor nerve to glute, for stair climbing type movement ## Footnote primary/ KN/ radiopedia

Answer 102

metoprolol (unopposed alpha) represents the contraindicated agent in classical teaching and examination settings due to lingering concerns about beta-blockers in cocaine toxicity. Contemporary evidence supports nuanced use of selective β1-blockers, but guidelines remain cautious. Phentolamine and GTN are appropriate therapies, while propofol requires judicious application Traditional guidelines contraindicate beta-blockers due to concerns about unopposed α-adrenergic activity58. By blocking β2-mediated vasodilation, non-selective agents like propranolol may exacerbate hypertension and coronary vasospasm25. ## Footnote This was on an episode of ER. But also; https://www.bjaed.org/action/showPdf?pii=S1743-1816%2817%2930053-7. LITFL. primary viva, open anaesthesia

Answer 103

least likely hypoglycaemia?? , they can cause all of these things.. ## Footnote "2019 blue book article Initial increase in Cr which normalises over time" "2019 blue book article Initial increase in Cr which normalises over time https://www.tga.gov.au/sites/default/files/auspar-empagliflozin-171026-pi.pdf SGLT2-i monotherapy does not cause hypoglycaemia"

Answer 104

12h The plasma concentration of buprenorphine decreases by approximately **50% within 12 hours** after removal of the transdermal patch, with a reported range of **10–24 hours**[1][2]. This initial decline reflects the gradual depletion of the subcutaneous depot of buprenorphine that persists after patch removal. The pharmacokinetic profile is characterized by a biphasic elimination pattern, where the rapid initial decline (median 12 hours) transitions to a slower terminal elimination phase with a half-life of ~26 hours[1][5][7]. **Rationale:** - Direct evidence from multiple manufacturer studies (NORSPAN® and BuTrans®) demonstrates a 50% plasma reduction within 12 hours post-removal[1][2]. - The 26-hour terminal half-life cited in other sources[3][5] refers to the subsequent elimination phase after the initial 50% drop, not contradicting the rapid initial decline. - Clinical guidelines emphasize withholding subsequent opioids for ≥24 hours after patch removal due to this pharmacokinetic profile[2][5]. **Correct Answer:** 12 hours Citations: [1] https://www.researchreview.com.au/MUND0082PI.pdf [2] https://www.purdue.ca/wp-content/uploads/2021/09/BUTRANS-PM-E-Jul2021.pdf [3] https://www.drugs.com/medical-answers/long-buprenorphine-stay-system-3566034/ [4] https://www.rxfiles.ca/rxfiles/uploads/documents/butrans-qanda.pdf [5] https://www.safercare.vic.gov.au/sites/default/files/2021-02/GUIDANCE_Opioid%20Conversion%20FINAL_0.pdf [6] https://academic.oup.com/painmedicine/article/19/10/1988/4283321 [7] https://www.tga.gov.au/sites/default/files/auspar-buprenorphine-161213.pdf [8] https://reference.medscape.com/drug/butrans-buprenorphine-transdermal-999581 [9] https://pmc.ncbi.nlm.nih.gov/articles/PMC3004620/ [10] https://www.nps.org.au/medicine-finder/norspan-5-transdermal-patch [11] https://www.nps.org.au/medicine-finder/buprenorphine-sandoz [12] https://pmc.ncbi.nlm.nih.gov/articles/PMC1661652/ [13] https://academic.oup.com/painmedicine/article-pdf/19/10/1988/25842049/pnx235.pdf [14] https://pmc.ncbi.nlm.nih.gov/articles/PMC6822392/ [15] https://healthpsychologyresearch.openmedicalpublishing.org/article/27241-buprenorphine-for-chronic-pain-a-safer-alternative-to-traditional-opioids [16] https://www.medicines.org.uk/emc/product/10079/smpc ## Footnote APMSE Steady state reached after 3d Terminal t1/2 12h vs Fent patch onset 12-24h t1/2 17h"

Answer 105

50-70% above T6, and more likely if complete ## Footnote https://www.bjaed.org/article/S2058-5349(17)30152-X/pdf

Answer 106

5 x 7.5= 37.5mmHg ## Footnote its in the blue book article about hyperbaric medicine: 1kpa = 7.5mmHg

Answer 107

Honey ## Footnote "50-150ml 0.25% sterile acetic acid to neutralise residual alkali (LITFL), sulcrafate recommended by USA Poisons centre. RCH: Honey at home, suculfate in ED"

Answer 108

Induction ## Footnote https://www.bjaed.org/article/S2058-5349(18)30060-X/fulltext. "strong evidence that induction of labour by any method increases the risk of AFE"

Answer 109

BMJ says needle decompression first, then definitive rx with ICC to follow ## Footnote "https://qualitysafety.bmj.com/content/qhc/14/3/e18.full.pdf. Crisis management during anaesthesia: pneumothorax "

Answer 110

TAVI: reduced 1. all cause mortality, 2. stroke, 3. AKI 4. **new onset AF (arrhythmias)**, 5. major bleed 6. anticoag requirement 7. LOS reocvery time TAVI higher 1. major vascular complication (haematoma, dissection, retroperitoneal bleeding) 2. PPM (LBBB and PPM dependency) 3. Paravalvular leak (PVL) No difference = mean gradient TAVI: >80yo or life expectancy < 10 years ## Footnote 2019 European heart journal https://www.escardio.org/Sub-specialty-communities/European-Association-of-Percutaneous-Cardiovascular-Interventions-(EAPCI)/Research-and-Publications/Commented-articles/transcatheter-aortic-valve-implantation-vs-surgical-aortic-valve-replacement-fo

Answer 111

"four bronchopulmonary segments: superior segment anteromedial segment lateral segment posterior segment" ## Footnote radiopedia

Answer 112

CF 1h, Br milk 3 hours < 12 mo: 1:3:4 > 12 mo: 1:3:6 CF:BF:Formula CF 3mL/kg/hr ## Footnote PG07 https://www.anzca.edu.au/resources/professional-documents/guidelines/ps07-guidelines-on-pre-anaesthesia-consultation-an

Answer 113

RV contraction from these options ## Footnote "LITFL https://litfl.com/right-ventricular-function-and-haemodynamic-assessment-echocardiography/. measure of RV Systolic function: TAPSE (Tricuspid Annular Plane Systolic Excursion) normal is >1.7cm (less useful post some cardiac surgery) [measured in AP4C w/ M Mode]"

Answer 114

**Answer:** a) Less transfusion, same thrombosis I think this was remembered incorrectly, BJA says decreased transfusion in cardac and ortho patients, and INCREASED mortality and thrombotic complications therefore dont give to surgical patients , as per NICE guidelines Impact of Preoperative Erythropoietin on Transfusion Requirements and Thrombotic Risk in Major Surgery The administration of erythropoietin-stimulating agents (ESAs) prior to major surgery has emerged as a critical component of patient blood management strategies. A synthesis of evidence from randomized controlled trials and meta-analyses demonstrates that preoperative erythropoietin significantly reduces the need for allogeneic blood transfusions without increasing the risk of thromboembolic complications. This conclusion holds across diverse surgical contexts, including cardiac, orthopedic, and general elective procedures. Mechanisms of Erythropoietin in Preoperative Optimization Erythropoiesis Stimulation and Hemoglobin Augmentation Erythropoietin functions by binding to receptors on erythroid progenitor cells in the bone marrow, stimulating red blood cell production and increasing hemoglobin concentrations[1][6]. In surgical patients with preoperative anemia, this mechanism directly addresses the oxygen-carrying capacity deficit, reducing reliance on transfusions. Meta-analyses report that ESA administration elevates preoperative hemoglobin by 1.2–1.8 g/dL compared to placebo, with sustained effects into the postoperative period[3][7]. Synergy with Iron Supplementation The efficacy of erythropoietin is enhanced when combined with intravenous iron, which addresses underlying iron deficiency present in 40–60% of anemic surgical patients[6]. This combination therapy corrects both erythropoietic drive and substrate availability, achieving hemoglobin optimization in 75–90% of cases[7]. Transfusion Reduction Across Surgical Specialties Cardiac Surgery In coronary artery bypass grafting and valve replacement procedures, preoperative erythropoietin reduces transfusion rates by 45% (risk ratio [RR] 0.55, 95% CI 0.37–0.81)[1]. This effect persists despite the high baseline transfusion risk in cardiac operations, where 50–60% of patients typically require blood products[4]. Orthopedic Surgery Total hip and knee arthroplasty data demonstrate even greater benefit, with a 64% reduction in transfusion requirements (RR 0.36, 95% CI 0.28–0.46)[1]. Erythropoietin-treated patients maintain higher hemoglobin levels at all perioperative time points—preoperative (12.1 vs 11.3 g/dL), postoperative day 1 (10.4 vs 9.1 g/dL), and discharge (11.2 vs 10.1 g/dL)[3]. General Surgery For non-cardiac procedures, ESA therapy decreases transfusion risk by 17% (RR 0.83, p=0.049) while reducing mean units transfused per patient from 1.8 to 1.2[7]. These outcomes are particularly significant in cancer resections, where anemia prevalence exceeds 30%[8]. Thrombotic Safety Profile Venous Thromboembolism Risk Analysis Pooled data from 28 randomized trials (n=4,750 patients) show no increased risk of deep vein thrombosis or pulmonary embolism with erythropoietin use (RR 1.02, 95% CI 0.78–1.33)[1][4]. This finding contradicts earlier concerns derived from oncology studies, where ESAs increase thrombosis risk by 93% (OR 1.93, p500 mL - Contraindications to autologous donation - Iron deficiency (ferritin <100 ng/mL or transferrin saturation <20%)[7] Economic and Logistical Considerations Cost-Benefit Analysis While ESA therapy adds $800–$1,200 per patient, this is offset by: - 56% reduction in transfusion costs ($320 saved per unit avoided) - $2,100 average savings from shorter hospitalization - $4,800–$7,500 per quality-adjusted life year gained through complication avoidance[6] Blood Supply Implications Widespread ESA adoption could decrease perioperative transfusion demand by 18–22%, enhancing blood bank sustainability during shortages[1][4]. Conclusion Preoperative erythropoietin administration safely reduces allogeneic blood transfusion requirements across surgical specialties without increasing thrombotic risk. This dual benefit—achieved through physiological erythropoiesis stimulation and adherence to standardized thromboprophylaxis—positions ESAs as a cornerstone of modern blood management programs. Future research should focus on protocol standardization and long-term outcomes in high-risk subgroups. **Answer:** a) Less transfusion, same thrombosis Citations: [1] https://pubmed.ncbi.nlm.nih.gov/30649068/ [2] https://pubmed.ncbi.nlm.nih.gov/39168487/ [3] https://www.dovepress.com/a-meta-analysis-and-systematic-review-evaluating-the-use-of-erythropoi-peer-reviewed-fulltext-article-TCRM [4] https://journals.lww.com/anesthesia-analgesia/fulltext/2019/05000/preoperative_erythropoietin_vs_placebo__what_does.1.aspx [5] https://ashpublications.org/ashclinicalnews/news/2547/Erythropoiesis-Stimulating-Agents-and-the-Risk-of [6] https://www.cochrane.org/CD012451/ANAESTH_use-erythropoietin-plus-iron-correct-anaemia-surgery-reduce-risk-blood-transfusion [7] https://pmc.ncbi.nlm.nih.gov/articles/PMC8885371/ [8] https://cco.amegroups.org/article/view/1347/html ## Footnote https://watermark.silverchair.com/mkw061.pdf

Answer 115

? TT - most sensitive Ecarin Clotting Time aPTT - qualitative Perplexity

2024.2 MCQ Flashcards

(143 cards)