I'm attached to the female general ward. I need to present this case in very detail as my preceptor is very strict and I need to have a very good understanding of the case and all the guidelines-based recommendations, like CPG Malaysia, and so on.Ill need a very good understanding of the disease, medication, why what all the 7W questions. The patient is still in the ward, and since I'm on holiday till 14/6, I'll go back to the ward on 15/6 and update the remaining info about the patient's medicine and disease progression, status. For now, this is the information I got about the patient. Usually the flow of presentation goes like: Flow of presentation: 1. Patient, age, gender 2. ⁠what is the chief complaint 3. ⁠what is the diagnosis 4. ⁠on day 1 admitted, wht problem then give what medication, indication for what, then is it appropriate to give the med for this problem, any more better option? (No pci then skip nxt day- same flow summary - until the last day) 5. ⁠next day, some symptoms resolve, dr stop certain medication due to …. Then some other problem arise and dr prescribe ….. the indication for the medication is for …… is it appropriate….. 6. ⁠overall no PCI in this case / u found some pci and need some clarification….. 7. ⁠thank you but rather than solely mentioning if the medications are appropriate or not, it would be better to state the indications. For eg, this pt was started on Tab pantoprazole 40mg BD for (indication) from (duration). Then if anything was found inappropriate/incorrect, it can be mentioned as a PCI & then explain accordingly. Your flow is correct. Just follow the CP2 sections. Ill attach the CP2 form. But some preceptor wants it to b like a story telling like : 1. Patient, age, gender 2. ⁠what is the chief complaint 3. ⁠tell the diagnosis , then the medicines instead of the medicine first then the indication. And carry on with the flow So i want u to generate 2 types of complete script for my presentation Name: Losila Age: 48 Race: Malay Underlying: DM with target organ damage (DKD and diabetic retinopathy), Hypertension, ESKD secondary to DKD (applying zakat for HD centre placement, awaiting approval plan for AVF appointment in June 2026, USCO KUB 6/1/25 CBK renal parenchymal disease Deny taking traditional medicine Was working as a cleaner for 5 years previously Blessed with 4 children Presented to ED on 9/6/2026 2.10 am Patient’s old medicines: Data taken 10/6/26 11 am Medication Dose Frequency Status T. Frusemide 40 mg 80 mg BD Increase to 80 mg TDS T. Metoprolol 100 mg 100 mg BD C T. Felodipine 10 mg 10 mg BD C T. Zincofer 1/1 OD C S/C Insugen R 12 IU TDS C PRN S/C Insugen N 28 IU ON WH T. Vildagliptin 50 mg 50 mg OD WH R. Rosuvastatin 20 mg 20 mg ON WH but planned to continue on 11/6/26 Section Investigation Normal Range 4/10/25 9/6/26 2 am 9/6/26 5 am 9/6/26 11.45 pm 11/6/26 FBC TWBC 4–11 ×10⁹/L — 10.9 — 8.66 8.74 FBC Hb 11.5–16.5 g/100 mL 9.5 8.8 — 6.8 6.6 FBC Platelet 150–400 ×10⁹/L — 193 — 179 187 Renal Profile Urea 1.7–8.3 mmol/L 13.3 33.1 33.5 21.4 22.5 Renal Profile Na⁺ 135–145 mmol/L — 136 138 141 142 Renal Profile K⁺ 3.5–5.0 mmol/L — 6.1 6.1 4.6 4.8 Renal Profile Cl⁻ 96–106 mmol/L — 113 116 110 110 Renal Profile SCr 64–122 µmol/L 399 1408 1415 1052 1127 Renal Profile CrCl 105–150 mL/min — — — — — Renal Profile Ca²⁺ 2.1–2.6 mmol/L — 1.86 — — — Renal Profile Mg²⁺ 0.7–1.3 mmol/L — 0.86 — — — Renal Profile PO₄³⁻ 0.8–1.45 mmol/L — 2.97 — — — LFT Albumin 35–50 g/L — 26 — — — LFT T. Bilirubin <20 µmol/L — — — — — LFT T. Protein 66–87 g/L — — — — — LFT ALP 53–141 U/L — — — — — LFT ALT <32 U/L — — — — — Coagulation PT 10–13.5 sec — — — — — Coagulation APTT 26–42 sec — — — — — Coagulation INR <1.5 — — — — — CE CK 24–195 U/L — — — — — CE LDH 0–248 U/L — — — — — CE AST <37 U/L — — — — — ABG pH 7.35–7.45 — 7.17 7.23 — — ABG pCO₂ 35–45 mmHg — 30 27 — — ABG pO₂ 72–100 mmHg — 246 196 — — ABG HCO₃ 22–29 mmol/L — 10.9 11.3 — — ABG O₂ sat 90–95% — 100% 100% — — Others RBS <11 mmol/L — — — — — Others Lactate 0.5–1.6 mmol/L — 1 1 — — Others Iron 13–27 µmol/L — 9.2 — — — Others Transferrin 2.0–3.6 g/L — 1.5 — — — Others Ferritin 15–205 ng/mL — 231 — — — Others TSAT (%) 15–50% — 21 — — — 9/6/2026 2.30 am Patient came to ED -SOB x 1/12 -Worsening past 2/7 -Requiring for sleeping in sitting position -With orthopnea and Paroxysmal Nocturnal Dyspnea (PND) -Prodcutive cough x 2/52 (yellowish sputum) -Claimed had fever x 2/52 ago -Seek treatment at Hospital Jitra, resolved after given 1 course of antibiotics -Vomiting and loose stool x 2/7 -Vomited fluid content, total 2x -Loose stool around 4x a day, no blood -Associated bilateral lower limb swelling -Non compliant to ROF 500 cc -Still has urine output Otherwise: - no chest pain, no abdominal pain, no sick contact, denied taking outside food recently Upon Arrival to ED, BP: 252/116 mmHg HR: 106 bpm T: 36.3 SPO2: 100% Lungs crepitation bilateral lung CVS: DRNM PA: Soft, non tender Pedal edema up to knee level bilaterally Started on mask CPAP at 2.10 am (9/6/2026) Medicines given in ED: IV lytic cocktail x 2 given at 1 pm 9/6/2026 IV lasix 80 mg STAT given 2.30 am 9/6/2026 and Iv lasix 80 mg TDS given 9.30 am 9/6/2026 IV pantoprazole 40 mg STAT and OD given 2.30 am 9/6/2026 IV GTN titrate accordingly IV Augmentin 1.2 g TDS given 9 am 9/6/2026 9/6/2026 7.30 pm Currently: -Under NPO2 -Done HD today, completed 2H with 10pc transfusion, UF 2C + blood product -On IV GTN -SOB improving -no GI losses -No nausea/vomiting O/E: alert, not tachypneic BP: 180/84 mmHg PR: 92 bpm T: 37 SPO2: 100% under NPO2 DXT: 6.5 Lungs: Bibasal crepts CVS: DRNM Pedal Edema up to the knee CXR: Congested, cardiomegaly Impression: Fluid overload secondary to hypertensive emergency/Advanced CKD Hypochromic macro/micro (I'm not sure) cytic anemia, likely renal anemia Plan: Continue NPO2 KIC off cm Keep SPO2 >95% Keep MAP > 65 Titrate IV GTN accordingly 5) Strict I/O charting ROF 500 cc/day DXT QID Medication: IV Lasix 800 mg TDS, S/C actrapid 6U PRN if DXT> 12, T. Zincofer 1/1 OD, T. CaCO3 500 mg BS Take old medication 9/6/2026 9.25 pm Have done HD 2H today Under NPO2 No fever O/E: Alert, concern BP: 216/110 HR: 105 bpm T: 37 SPO2: 98% Impression: Advanced CKD approaching ESRF with fluid overload, hyperkalemia, metabolic acidosis, and uremia Acute pulmonary edema (APO) secondary to Hypertension emergency Symptomatic anemia secondary to chronic disease and Iron deficiency anemia (IDA) Plan: Continue IV GTN Keep NPO2 IV Lasix 80 mg TDS Take blood Oral Kalimate 15 mg TDS x 3/7 given 9/6 starting 10pm KIV HD if indicated RRT: HD 10/6/2026 8am Diagnosis: Advanced CKD approaching ESRF with fluid overload, hyperkalemia, metabolic acidosis, with uremia Acute pulmonary edema (APO) secondary to Hypertension emergency Symptomatic anemia secondary to chronic disease and Iron deficiency anemia (IDA) *Completed HD yesterday 2H, UF 2.0L + blood product - uneventful Currently: Under NPO2 No fever SOB improving O/E:alert, conscious, not tachpneic BP: 145/83 mmHg PR: 79 T: 37 SPO2: 98% Under NPO2 DXT: 6.7 Lungs: Bibasal Crepitations Pedal edema B/L up to midshin I/O : 227/1600/-1273 Plan: Off IV GTN Trial wean down to RA Keep SPO2> 95% ROF 500 cc/day Strict I/O charting To indent CKD diet To insert IJC once plan for discharge Long term: RRT (To get application from zakat, continue AVF TCA July 2026) DXT QID IV Lasix 80 mg TDS given 6 am, then not given 12 pm, 6pm because oralised T. Zincofer 1/1 OD given 10/6 8 am T. CaCO3 500 mg BD given on 10/6 at 7 am and 5 am 10/6/2026 9.25 am Currently: Under NPO2 No fever SOB improving O/E:alert, not tacypneic, speak in full sentences BP: 169/81 mmHg PR: 79 T:37 SPO2: 100% under NPO2 DXT: 6.7 Lungs: minimal Right lower limb crepitations Pedal Edema B/L lower limbs Impression: Fluid overload secondary to non compliant to ROF with underlying CKD stage 5 U/L diabetic (control) Hypertension Plan: Oralize T. Lasix 80 mg TDS (first dose given 10/6 at 6 pm) ROF 500 cc/day Aim off GTN evening KIV prazosin if BP persistently high KIV HD cm Refer dietitian for reduced salt diet Oral Kalimate 15 mg TDS x 3/7 given 10/6 at 8 am, 4 pm, and 10 pm 10/6/2026 12.49 pm Currently, patient tolerate orally - minimum amount Estimated height: 158 cm Dosing weight: 56 kg EER: 1400-1680 kcal/day EPR:0.6-0.8 g/kg/day Hb: 6.8 Albumin: 26 K+: 6.1 reduced to 4.6 Plan: Educate patient on low sodium , low potassium and low phosphate diet Encourage orally as patient tolerated in ward Ward to indent: Low potassium diet 11/6/2026 8.30 am Diagnosis: Fluid overload secondary to non compliant to ROF with U/L CKD Stage 5 Currently: Under RA No fever Bilateral pedal edema Lungs: right lower zone event O/E: BP: 130/62 mmHg PR:70 bpm T:37 SPO2: 97% DXT: 5.9 I/O: 550/500/+ 50 Plan: To consult nephro for HD today To transfuse 10 pc? During HD Upcoming HD on Sunday To keep over weeword?? For IJC insertion on Sunday (unable to lie flat for IJC today) Off oral kalimate (one dose already guven at 8 am) Off Continuous bladder drainage (CBD) T. Zincofer 1/1 OD given 11/6 8 am T. CaCO3 500 mg BD given on 11/6 at 7 am only and stopped T. CaCO3 1 g TDS is planned but havent given so far T. Lasix 80 mg TDS given at 7 am, 1pm, 6 pm Continue patient own rosuvastatin 20 mg OD 11/6/2026 11.50 am Plan: For 4H HD today QB 250, QD 500 Heparin normal Transfuse 1Q packed cell during HD To insert IJC on Sunday 11/6/2026 12.50 pm Spoken to Dr Hana request 1Q packed cell to tranfuse during HD Not granted i/v/o blood group A+ low in stock To request back if Hb drop post HD So dont forget to generate 2 types of complete scripts

Chapter 2: Use of iron to treat iron deficiency and anemia in people with chronic kidney disease Recommendation 2.1: In people with anemia and CKD G5 receiving hemodialysis (CKD G5HD), we suggest initiating iron therapy if ferritin £500 ng/ml (£500 mg/l) and TSAT £30% (2D). This recommendation places high value on the potential benefits of iron for improving life expectancy and symptoms, reducing the required dose of ESAs, and reducing the need for RBC transfusion, and it places a relatively lower value on the potential side effects of iron. The recommendation applies to both adults and children regardless of treatment with ESAs, hypoxia-inducible factor–prolyl hydroxylase inhibitors (HIFPHIs), or neither. People who are not treated with ESAs or HIF-PHIs and do not have symptoms attributable to anemia may opt for lower ferritin and TSAT initiation thresholds, particularly if they are concerned about potential side effects of iron. The recommendation may not apply to people with active infection. Key information Balance of benefits and harms. Oral or intravenous (i.v.) iron versus no iron. Nineteen studies have compared oral iron (8 randomized controlled trials [RCTs]79–86) or i.v. iron (14 RCTs,79,80,87–98 including 2 RCTs investigating dialysate iron91,92) with placebo in people with CKD G5HD treated with ESAs or HIF-PHIs. Overall, critical outcomes were assessed in a small number of studies with relatively few participants, so the effects of iron on critical outcomes, including all-cause death, cardiovascular events, stroke, myocardial infarction, serious adverse effects, serious gastrointestinal adverse events, serious hypersensitivity reactions, and infections, are very uncertain (Supplementary Table S4). QoL was assessed in a single small RCT including 32 participants. Compared with placebo, iron supplementation agents seem to increase Hb values by an average of w0.5 g/dl (w5 g/l) in people with CKD G5HD (Supplementary Table S5). Iron treatment may result in fewer RBC transfusions and probably also lowers ESA doses; its impact on HIF-PHI dosing has not been assessed. Iron administration also increases TSAT and ferritin levels. Evidence for the effect of iron on cancer outcomes is very uncertain (Supplementary Table S5). Iron status thresholds to initiate iron therapy and treatment targets. Seven RCTs (11 reports) evaluated cutoff values of ferritin and TSAT for initiating iron therapy or for targeting therapy.99–109 However, studies on long-term safety, costeffectiveness, and risk-benefit of using different ferritin and TSAT targets are limited. Healthcare providers selected the dose of ESA that would be sufficient to maintain a Hb of 10–12 g/dl (100–120 g/l), and studies were mostly designed to assess ESA requirements. Only 3 studies assessed outcomes considered critical for decision-making. One small trial randomized 42 participants with CKD G5HD to receive i.v. iron dextran to maintain TSAT either at 30%–50% or at 20%–30%.99 At 24 weeks, 2 of 19 participants died in the low target group versus 1 of 23 participants in the high target group. There was no evidence that the TSAT target influenced the risk of cardiovascular events, hospital admission, or other adverse events. The PIVOTAL trial randomized 2141 participants with CKD G5HD to receive either high-dose iron sucrose, administered intravenously in a proactive fashion (400 mg monthly, unless the ferritin concentration was >700 ng/ml [>700 mg/l] or TSAT $40%), or low-dose iron sucrose, administered intravenously in a reactive fashion (0–400 mg monthly, with a ferritin concentration of <200 ng/ml [<200 mg/l] or TSAT <20% being a trigger for iron administration).105 The rate of the composite outcome of fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, or hospitalization for heart failure after a median of 2.1 years was lower in the group receiving proactive versus reactive treatment (hazard ratio [HR]: 0.80; 95% confidence interval [CI]: 0.64–1.00). Similarly, the rates of the individual components of fatal or nonfatal myocardial infarction and hospitalization for heart failure were lower among people receiving proactive iron than among those receiving reactive iron, as was the risk of death. Rates of stroke, hospitalization, and infection were similar in the 2 treatment groups. Investigators found no apparent differences in either the Euro-QoL-5D QoL health index or the Kidney Disease Quality of Life (KDQOL) score. Adverse events were generally similar in type and number in both groups (risk ratio: 1.01; 95% CI: 0.95–1.08). Fewer (3.5%) people required a blood transfusion, and ESA requirements were generally lower in the group receiving proactive versus reactive treatment. A third study randomized 200 participants with CKD G5HD to receive i.v. iron sucrose to maintain ferritin concentrations between 600–700 ng/ml (600–700 mg/l) or 200– 400 ng/ml (200–400 mg/l) for a period of 6 months.109 The rate of death was similar between the 2 groups. No other critical outcome was reported. Overall, the Work Group felt that available data supported higher rather than lower iron status targets to reduce ESA requirements and improve clinical outcomes. Certainty of evidence. The overall certainty of evidence for iron therapy among people with CKD G5HD is very low (Supplementary Tables S4 and S5). The certainty of evidence was graded to be very low for several critical outcomes due to concerns about risk of bias and very serious or extremely serious concerns regarding imprecision. Values and preferences. Although there has not been a formal assessment of patient values and preferences regarding iron supplementation, the Work Group believes that most people with CKD G5HD would want iron supplementation if it prolonged life, reduced the risk of cardiovascular events, or improved QoL.110 Resource use and costs. Iron supplementation seems to reduce the requirement for ESA therapy. Given the high cost of ESAs, appropriate use of iron in people with CKD would be expected to reduce overall costs. Considerations for implementation. It is difficult to precisely predict the effect iron will have on the status of Hb and iron, which requires repeated testing to assess. This is particularly important given that results will drive dose adjustments and formulation switch in the case of insufficient effect. In the absence of clinical trials that specifically inform the optimal frequency for testing of iron status, and consistent with prior guidelines, it seems reasonable to test iron status every 1–3 months for those with CKD G5HD. Additionally, treatment thresholds and treatment targets may vary across populations (e.g., in Japan, where lower ferritin levels are often targeted). Some dialysis units have developed and/or are using protocols to guide dosing and dosing adjustments based on repeated measures. Such protocols could help implement the above. Rationale Several recent trials evaluated the benefits and harms of various treatment targets. By far the largest of those studies, PIVOTAL, found that compared with a reactive strategy with low-dose i.v. iron, a proactive strategy with high-dose i.v. iron moderately decreased the risk of death and important cardiovascular events without increasing the risk of infection or serious adverse events.105 In addition, there was no evidence for effect modification by vascular access type. Several issues arise when interpreting PIVOTAL.105 First, the trial had 2 arms comparing discrete iron treatment regimens. Compared with a reactive low-dose regimen, the proactive higher-dose regimen resulted in better outcomes. However, this does not imply that the proactive high-dose regimen is the optimal strategy. It is simply better compared with the reactive low-dose regimen. Optimal doses may be somewhere between the 2 regimens, or higher still, although retrospective observational data suggest that more intensive i.v. iron regimens (greater than in PIVOTAL) may be associated with increased risks of mortality and infections.111 Optimal dose finding would require a multiarm trial that includes different ferritin and TSAT targets, using different ESA doses, which may not be feasible in a randomized design. The Kidney Disease: Improving Global Outcomes (KDIGO) 2012 guideline highlighted the difficulty in trying to specify treatment initiation thresholds. PIVOTAL may have indicated that in people with CKD G5HD treated with ESAs, higher iron dosing leads to improved outcomes, but it is not entirely clear what is driving these outcomes. Possibilities include the lower ESA doses required to maintain Hb within the target range, the correction of iron deficiency per se,a combination of these mechanisms, or other mechanisms yet unknown. For any individual, the optimal balance of Hb, ESA, and iron dose at which clinical benefit is maximized is still not known. All this is complicated by the relatively poor diagnostic accuracy of serum ferritin and TSAT to estimate body iron stores or to predict the Hb response to iron supplementation. The Work Group aimed to propose a treatment initiation threshold that would balance the benefits seen with higher iron dosing against the uncertainty about the optimal treatment targets. No studies have evaluated different initiation thresholds using a truly randomized design. The inclusion criteria in terms of ferritin and TSAT have been highly variable, preventing the identification of a clear initiation threshold. Similarly, target studies do not provide a definitive threshold for initiation. The 2012 threshold remains broad, encompassing most of the inclusion thresholds used in various studies. This includes the PIVOTAL study, which included participants with ferritin <400 ng/ml (<400 mg/l) and TSAT <30%. Given that establishing an actual target based on the PIVOTAL data is still problematic, the Work Group felt that it was reasonable to maintain the previous initiation threshold. However, we acknowledge that these numbers are somewhat arbitrary and that future research may lead to revised conclusions. For example, the Dialysis Patients’ Response to IV Iron with Elevated Ferritin (DRIVE) I and II trials investigated the effect of iron administration in people with CKD G5HD with ferritin ranging from 500 to 1200 ng/ml (500 to 1200 mg/l) and TSAT #25%.89 During a 6-week follow-up, people who had received ferric gluconate had achieved a Hb concentration that was 0.5 g/dl (50 g/l) higher than those who did not, without appreciable differences in serious adverse effects. After an additional observation period of 6 weeks, people who had received ferric gluconate required significantly lower ESA doses than those in the control group, with fewer serious adverse events. These data support the use of iron supplementation as an ESA-sparing strategy, even in people with elevated serum ferritin levels, but they would require longer-term confirmation. There are no studies of initiation thresholds in people with CKD G5HD not yet treated with ESAs or HIF-PHIs. For those people, the balance of benefits to harms may be different from that among people treated with ESAs, especially if improved outcomes seen with higher iron dosing strategies primarily stem from reductions in ESA dosage. Concurrently, the threshold for initiating treatment may be lower. There are also no studies in people with CKD G5HD treated with HIF-PHIs, where optimal iron dosing strategies are unknown. It has been postulated that HIF-PHIs may improve iron availability and reduce iron treatment needs compared with ESAs, but this has not yet been demonstrated in RCTs. Additionally, it is possible that higher iron strategies could lower HIF-PHI dosage as seen with ESAs. Since HIF-PHIs have not shown improved safety over ESAs in RCTs (see Chapter 3), lower HIF-PHI dosing could also be beneficial. At present, we found no compelling evidence or rationale to propose an alternative threshold for people not yet treated with ESAs or people treated with HIF-PHIs. We also recognized the advantage of maintaining uniformity for the sake of simplicity. Observational studies in children with CKD G5HD have illustrated that iron reduces the dose of ESA required to maintain target Hb concentrations.112,113 Initiation targets for iron therapy in children with CKD G5HD are unclear; however, 1 RCT showed improved Hb levels with iron therapy in children with CKD G5HD who are iron deplete, defined as TSAT <20% and/or serum ferritin <100 ng/ml (<100 mg/l).114 Another trial on the optimum iron dose conducted in children with CKD G5HD with ferritin #800 ng/ml (#800 mg/l) and TSAT 20%–50% suggested that a broad threshold similar to what is used for adults for initiating iron therapy is appropriate.115 Recommendation 2.2: In people with anemia and CKD G5HD who are initiaing iron therapy, we suggest using intravenous (i.v.) iron rather than oral iron (2D). for the zincofer i would like to know if theres any pci on why the ESA or iron therapy. based on ckd anemia. pls generate a script.