Urinary Function and Reproductive Function
Urinary Function
Possible Types of Acute Kidney Injury
According to the clinical presentation in Mr. J.R.’s case, prerenal acute kidney injury (AKI) is due to decreased renal perfusion, and most likely for Mr. J.R. The condition is usually caused by situations such as dehydration, hypovolemia or hypotension (Dlugasch & Story, 2021). Such a condition is likely in this case due to severe fluid loss from vomiting and diarrhea, leading to hypovolemia and decreased renal perfusion. His symptoms, weakness, dizziness upon standing, and pale, sweaty skin, suggest hypotension and shock, further reducing blood flow to the kidneys. In this situation, as in prerenal AKI, the kidneys are structurally intact but under perfused, and the absence of previous kidney disease and history of sudden onset following gastroenteritis point to it. Hypoperfusion can progress to ischemic acute tubular necrosis (ATN) and make the condition to transition to intrinsic AKI if t is not treated in a timely manner.
Another possible type for this patient’s case is intrinsic AKI, especially due to acute tubular necrosis (ATN). Such a condition is often the result of direct kidney damage usually due to acute tubular necrosis (ATN) from ischemia or toxins (Turgut et al., 2023). In Mr. J.R.’s case, intrinsic AKI is possible from prolonged hypoperfusion (from dehydration) and concern for nephrotoxicity from Pepto-Bismol. Pepto- Bismol toxicity is very rare, but its metallic taste is a concern because it could mean the presence of uremia, which is a symptom of kidney malfunction. Furthermore, severe dehydration and persistent hypotension may also lead to ischemic injury of renal tubules contributing to development of ATN. The structural damages present in intrinsic AKI distinguish it from prerenal AKI since fluid therapy alone cannot completely restore normal kidney function. From the patient’s symptoms, it is likely that his prerenal AKI was not promptly treated to a point where it may have progressed to intrinsic AKI.
The third type can be post-renal AKI, while Mr. J.R.’s primarily suggests prerenal AKI due to dehydration from vomiting and diarrhea, it is important to consider postrenal acute kidney injury. Patient is elderly and a male, which they are more likely to be considered for this. Postrenal AKI results from obstruction within the urinary tract that blocks urine outflow, causing increased intraluminal pressure, decreased glomerular filtration rate (GFR), and subsequent renal dysfunction (Dlugasch & Story, 2021). Mr. J.R. does not have any hallmark symptoms of urinary retention, decreased urinary output, or flank pain, silent obstruction is still possible, and assessment is necessary. If postrenal AKI is present, rapid intervention is necessary to relieve the obstruction, it can at times reverse renal impairment and prevent progression of chronic kidney disease.
Risk Factors the Patient Might Have
Mr. J.R. (73 years old) is at high risk of developing AKI because of several contributing factors. Due to his advanced age, he has a reduced renal reserve and glomerular filtration rate (GFR), making his kidneys more susceptible to damage from hypovolemia. According to Turgut et al. (2023) the elderly are more likely to suffer from AKI due to decline in their kidney function. Dehydration due to fluid loss due to vomiting and diarrhea has resulted in worsening of renal perfusion. In addition, his fever and excessive sweating have only worsened dehydration, placing him at higher risk of prerenal AKI. Using Pepto-Bismol, which has bismuth subsalicylate in it, can exacerbate his condition further by causing metabolic imbalances. Moreover, it is possible that the patient suffered from food poisoning from contaminated burritos which could introduce nephrotoxins, further affecting the functioning of his kidneys. Possible sepsis can also be present, due to fever, malaise, and Gi symptoms, which all can be early signs of infection. When combined, the factors have likely caused renal hypoperfusion, which, if prolonged, may lead to ischemic acute tubular necrosis and irreversible kidney damage.
Potential Hematologic System Complications (Coagulopathy and Anemia)
Anemia stands as a frequent complication of chronic kidney disease (CKD) because erythropoietin (EPO) production declines in patients with CKD. The kidneys of healthy individuals develop EPO that triggers the bone marrow production of red blood cells. The affected kidneys of CKD patients are unable to produce adequate amounts of EPO which leads to diminished RBC synthesis and subsequent anemia (Portolés et al., 2021). The buildup of uremic toxins cuts down the life expectancy of red blood cells which intensifies anemia in patients. Patients with CKD are prone to iron deficiency from two factors including intestinal absorption issues and chronic inflammatory processes that decrease iron intake. Chronic blood loss from gastrointestinal bleeding further contributes to anemia. CKD patients have symptoms such as fatigue, pallor, shortness of breath, tachycardia, all of which significantly impair their daily activity and have harmful effects on overall quality of life.
Another potential serious hematologic complication in patients with CKD is coagulopathy. Uremic toxins that impair platelet aggregation and adhesion are mainly responsible for coagulopathy (Baaten et al., 2022). Low platelet dysfunction normally leads to bleeding, causing bruising, prolonged bleeding time, and GI hemorrhage. CKD also affects the balance of coagulation factors, which in turn increases bleeding and thrombotic risks. Later stages of CKD have calcium and phosphate imbalances that promote vascular calcification, which is a risk factor for prothrombotic events like deep vein thrombosis and stroke. Such coagulation abnormalities create a inconsistent state where patients are at risk for both excessive bleeding and dangerous clot formation. For CKD patients, anemia and coagulopathy cause major health issues. Monitoring and treatment involve erythropoiesis-stimulating agents, iron supplements, and careful anticoagulation to avoid severe complications.
Reproductive Function
Most Probable Diagnosis for Ms. P.C
The most probable diagnosis for Ms. P.C. is “acute pelvic inflammatory disease (PID) caused by Neisseria gonorrhoeae.” Her symptoms, “lower abdominal pain, nausea, vomiting, and a heavy, malodorous, greenish-yellow vaginal discharge,” along with the presence of gram- negative intracellular diplococci and white cells on microscopic examination are classic for PID. PID a rising infection often triggered by sexually transmitted bacteria (Yusuf & Trent, 2023). The timing of her symptoms, occurring shortly after her menstrual period, is significant because it can facilitate bacterial migration from the lower to the upper reproductive tract. Additionally, her young age (19 years) and history of unprotected sex with a single partner increase her risk for STIs like gonorrhea. Such clinical findings, combined with her lack of prior STI screening, strongly suggest gonococcal PID as the underlying cause of her current condition.
Furthermore, the analysis of Ms. P.C.’s vaginal discharge reveals “gram-negative intracellular diplococci, a hallmark of Neisseria gonorrhoeae infection” (Meyer & Buder, 2020). The absence of yeast or trichomonads effectively rules out candidiasis and trichomoniasis, while the presence of white blood cells (WBCs) confirms an active inflammatory response. Gonorrhea is a leading cause of PID, and its identification in this context strongly supports the diagnosis. However, because Chlamydia trachomatis frequently coexists with gonorrhea but does not appear on Gram stain, additional testing is necessary. Gonococcal PID as the most likely diagnosis, needs treatment to prevent complications.
PID is the primary diagnosis by ruling out other potential diagnosis with consideration of the patient’s clinical presentation and lab findings. Bacterial vaginosis (BV) is not possible because Ms. P.C.’s discharge differs from the typical grayish-white, fishy-smelling discharge seen in BV (Khedkar & Pajai, 2022). Microscopy for BV would show clue cells without elevated WBCs or intracellular diplococci. Trichomoniasis, caused by Trichomonas vaginalis, would present with motile flagellated parasites on wet mount, which were absent in her case. Similarly, candidiasis, characterized by a thick, white, “cottage cheese” discharge, would reveal yeast or hyphae on KOH prep, with minimal WBCs. Ms. P.C.’s symptoms and lab results align poorly with these conditions, further reinforcing gonorrhea-associated PID as the primary diagnosis. The distinction is critical for guiding appropriate antibiotic therapy and preventing long-term reproductive complications.
Microorganism Involved
The most likely microorganism involved in Ms. P.C.’s infection is Neisseria gonorrhoeae, a gram-negative intracellular diplococcus commonly associated with sexually transmitted infections. The presence of “gram-negative intracellular diplococci” on microscopic examination strongly suggests the presence of the bacteria, which is leading cause of PID in young, sexually active women (Meyer & Buder, 2020, p. 8). Such a bacteria infects the cervix, leading to inflammation and purulent discharge, which aligns with the patient’s complaint of “thick, greenish-yellow, malodorous vaginal discharge.” Additionally, her history of unprotected intercourse and recent symptoms of lower abdominal pain, nausea, and emesis further support the diagnosis. Left untreated, gonorrhea can lead to severe complications, including infertility, ectopic pregnancy, and chronic pelvic pain, making early identification and treatment critical to preventing long-term reproductive health consequences.
Criteria for Recommending Hospitalization for this Patient
Ms. P.C.’s clinical presentation strongly warrants hospitalization for pelvic inflammatory disease (PID) management. Her persistent nausea and vomiting indicate systemic illness and a potential inability to maintain hydration or tolerate oral medications (CDC, 2022). The severity of her pelvic pain raises concern for complicated PID, including possible tubo-ovarian abscess formation. The malodorous, purulent vaginal discharge with confirmed gram-negative intracellular diplococci on microscopic examination is highly suggestive of Neisseria gonorrhoeae infection, a common cause of PID in young, sexually active women (Meyer & Buder, 2020). The absence of yeast or flagellated organisms helps rule out other infections such as bacterial vaginosis or trichomoniasis (Khedkar & Pajai, 2022). Such findings, combined with her young age and recent history of unprotected sexual activity, place her at high risk for disease progression. Hospitalization will be recommended for Ms. P.C. by following the CDC recommendations. The CDC (2022) advises hospitalization for PID when surgical emergencies (e.g., appendicitis) cannot be excluded, in cases of tubo-ovarian abscess, during pregnancy, or in patients experiencing severe illness, nausea, vomiting, or fever above 38.5°C (101°F). Hospitalization is also warranted when patients cannot adhere to or tolerate an outpatient oral treatment regimen. Admission would allow for intravenous antibiotic administration, adequate pain management, and timely imaging or surgical intervention should her condition deteriorate, or complications arise (Dlugasch & Story, 2021).
References
Baaten, C. C., Schröer, J. R., Floege, J., Marx, N., Jankowski, J., Berger, M., & Noels, H. (2022). Platelet abnormalities in CKD and their implications for antiplatelet therapy. Clinical Journal of the American Society of Nephrology, 17(1), 155-170. https://doi.org/10.2215/CJN.04100321Links to an external site.
CDC (2022). Sexually transmitted infections treatment guidelines, 2021: Pelvic inflammatory disease (PID). https://www.cdc.gov/std/treatment-guidelines/pid.htmLinks to an external site.
Dlugasch, L., & Story, L. (2021). Applied pathophysiology for the advanced practice nurse. Jones & Bartlett Learning.
Khedkar, R., & Pajai, S. (2022). Bacterial vaginosis: a Comprehensive Narrative on the etiology, clinical features, and Management Approach. Cureus, 14(11), 1-6. https://doi.org/10.7759/cureus.31314Links to an external site.
Meyer, T., & Buder, S. (2020). The laboratory diagnosis of Neisseria gonorrhoeae: Current testing and future demands.
Pathogens, 9(2), 1-19. http://dx.doi.org/10.3390/pathogens9020091Links to an external site.
Portolés, J., Martín, L., Broseta, J. J., & Cases, A. (2021). Anemia in chronic kidney disease: From pathophysiology and current treatments, to future agents. Frontiers in Medicine, 8, 1-14. https://doi.org/10.3389/fmed.2021.642296Links to an external site.
Turgut, F., Awad, A. S., & Abdel-Rahman, E. M. (2023). Acute kidney injury: Medical causes and pathogenesis. Journal of Clinical Medicine, 12(1), 1-11. https://doi.org/10.3390/jcm12010375Links to an external site.
Yusuf, H., & Trent, M. (2023). Management of pelvic inflammatory disease in clinical practice. Therapeutics and Clinical Risk Management, 183-192. https://doi.org/10.2147/TCRM.S350750Links to an external site.