Question 1- According to the case presented, including the clinical manifestations and microscopic examination of the vaginal discharge, what is the most probable diagnosis for Ms. P.C.? Support your answer and explain why you get to that diagnosis.

The most probable diagnosis for Ms. P.C. is an acute pelvic inflammatory disease. This infection is secondary to a gonorrheal infection that has spread to the uterus or the fallopian tubes. Pelvic inflammatory disease is an infection of the female’s reproductive organs caused by a sexually transmitted infection (Ledger,2021). It develops as a result of bacterial flora in the vagina and cervix climbing into the body of the uterus. Since the patient’s gonorrhea has gone untreated for several days, this has contributed to the escalating spread of the bacterium that causes PID. The patient presented with some signs and symptoms consistent with acute pelvic inflammatory disease caused by gonorrhea. These clinical manifestations include lower abdominal pain, nausea and emesis, and heavy and thick, greenish-yellow color, malodorous vaginal discharge.

The pelvic inflammatory disease has a rapid onset with incubation of two to five days, and the start of lower abdominal pain begins a few days after the last day of the menstrual period. The patient experienced nausea and vomiting, which manifested late into the manifestation of the disease. In addition, the patient reported having had unprotected sex eight days ago, which is an indicator of a possible sexually transited infection. On microscopic examination, white blood cells and gram-negative intracellular diplococci were present. These findings are consistent with Neisseria gonorrhoeae infection.

Question 2- Based on the vaginal discharge described and the microscopic examination of the sample, could you suggest which would be the microorganism involved?

The microorganism involved is Neisseria gonorrhoeae. Gram-negative coccus Neisseria gonorrhoeae has a diameter of 0.6 to 1.0 m and is typically seen in pairs with adjacent flattened sides. The organism is frequently discovered intracellularly in the polymorphonuclear leukocytes (neutrophils) of the gonorrhea pustular exudate. Under a microscope, Neisseria gonorrhoeae has the shape of a kidney bean and is an aerobic, non-spore-forming, non-motile, encapsulated, and non-acid-fast bacteria.

Neisseria gonorrhoeae uses a variety of tactics to evade the host immune system, including ongoing modifications to the antigenic structure of its surface, resistance to complement-mediated bacteriolysis, and perhaps the synthesis of IgA1 protease (Ledger, 2021). In addition, it has the ability to be phagocytosed without opsonization by the macrophages and is able to grow among macrophages. It has acquired some antimicrobial resistance over time, such as third-generation cephalosporins and azithromycin.

Question 3- Name the criteria you would use to recommend hospitalization for this patient.

Clinicians may advise hospitalization in some circumstances to manage the pelvic inflammatory disease. The health care provider’s judgment and the application of specified standards from the 2021 STI Treatment Guidelines should be the foundation of this choice. The criteria I would use to recommend hospitalization for this patient include the following. Ms. P.C. is a 19-year-old sexually active female who presented with lower abdominal pain and profuse vaginal discharge, which is thick, greenish-yellow in color, and very smelly. Microscopic examination of the vaginal discharge showed the presence of white blood cells and gram-negative intracellular diplococci microorganism, which is Neisseria gonorrhoeae. From the above clinical manifestations and findings of the microscopy exam, empirical therapy with antibiotics should be begun immediately (Williams, 2018). After clinical improvement with parenteral therapy, transition to oral therapy with doxycycline 100 mg 2 times/day and metronidazole 500 mg 2 times/day is recommended to complete 14 days of antimicrobial treatment.

                                                                                     References

Ledger, W. J. (2021). Pelvic inflammatory disease. Schlossberg’s Clinical Infectious Disease, 419-421. https://doi.org/10.1093/med/9780190888367.003.0064 (Links to an external site.)

Williams, E. (2018). Closing the audit cycle in managing pelvic inflammatory disease (PID): Updating trust guidelines greatly improves PID treatment. https://doi.org/10.26226/morressier.5731a408d462b8028d88c6ac (Links to an external site.)

Question 1-The attending physician thinks that Mr. J.R. has developed an Acute Kidney Injury (AKI). Analyzing the case presented names of the possible types of Acute Kidney Injury. Link the clinical manifestations described to the different kinds of Acute Kidney Injury.

Acute kidney injury (AKI) is described as a sudden decline in kidney function that occurs over a matter of hours and includes both structural kidney damage and a loss of function that impairs the renal system. It is associated with increased serum creatinine levels, a decrease in urine output, and the requirement for renal replacement treatment (Sharples, 2017). In this case, I agree Mr. J.R. had AKI in the process. Acute Kidney Injury (AKI) can be classified into pre-renal, intrinsic renal, and post-renal categories. Mr. J.R. suffered pre-renal acute kidney injury as evidenced by his clinical manifestations and can be accounted for by the patient’s prolonged gastroenteritis. The extrarenal loss from vomiting, diarrhea, sweating, and volume depletion due to the inability to tolerate fluids are the leading causes of pre-renal AKI in Mr. J.R.

The patient is febrile (100.5F) with present nausea and vomiting. The patient experienced diarrhea, as shown by the 5-6 bowel movements. In addition, Mr. J.R. cannot tolerate any solid foods or liquids, which contributes to dehydration. Pre-renal acute kidney injury can occur with a normal kidney function, but decreased renal perfusion linked with intravascular volume depletion brought on by vomiting, inability to tolerate fluids, and diarrhea can result in reduced glomerular filtration rate. On the other hand, non-specific clinical manifestations can be associated with either pre-renal, intra-renal, or post-renal acute kidney injury (Hoste et al., 2018). In this case, they include the bothersome metallic taste in the mouth, paleness, sweating, general body weakness, and dizziness, as reported by the spouse.

Question 2-Create a list of risk factors the patient might have and explain why.

Risk factors are fundamental ideas in epidemiology used to construct theories regarding the causes of diseases and explain their spread. The following are the risk factors the patient might have.

Volume depletion associated with gastroenteritis- the patient, acquired gastroenteritis after eating two burritos for supper. Gastroenteritis is a potential risk factor for acute kidney injury. It is related to excessive fluid losses via the gastrointestinal tract reducing the fluids circulating back to the kidneys (Hoste et al., 2018).

Excessive nausea and vomiting- cause loss of fluids in the body through oral evacuation. In this case, the patient experienced nausea with vomiting for two days. These extrarenal causes may have contributed to the pathogenesis of AKI.

Diarrhea is associated with excessive fluid loss via the gastrointestinal tract with minimal fluid absorption. Mr. J.R. has diarrhea resulting from gastroenteritis.

Inability to tolerate solid foods and liquids- in cases of gastroenteritis, a patient is advised to take large amounts of fluids to replace the lost fluids from the body. Mr. J.R. cannot tolerate liquids which puts him at risk of acute kidney injury as the fluids lost were never compensated.

Fever- the patient had a fever of 100.5F which contributed to insensible water loss due to excessive sweating through the skin and perspiration (Hoste et al., 2018). Although it does not cause significant fluid losses, it has contributed to volume depletion in this patient.

Age- the patient is 73 years old. Old age is a risk factor for acute kidney injury explained by the loss of the autoregulation processes making the kidneys brittle and susceptible to damage.

Question 3- Unfortunately, the damage to J.R.’s kidney became irreversible, and he is now diagnosed with Chronic-kidney-disease. Please describe the complications the patient might have on his Hematologic system (Coagulopathy and Anemia) and the pathophysiologic mechanisms involved.

Chronic Kidney Disease (CKD) is defined as kidney damage or a GFR of 60 mL/min/1.73 m2 or less for three months or longer, regardless of the underlying reason. It may be a complication of acute kidney injury. It is associated with complications of the hematological system, as discussed below.

Coagulopathy of chronic kidney disease

Compared to healthy individuals, CKD patients exhibit a coagulopathy that includes delayed clot formation, higher ultimate clot strength, and decreased clot breakdown. In this population, the elevated clot strength is caused by supra-normal fibrinogen levels. These patients have intrinsic platelet abnormalities where there is impairment of adhesion of platelet glycoprotein receptors to von Willebrand factor (Vwf) (Mukhaerjee, 2018). In this case, platelets have reduced granule serotonin release and ADP, which reduce the number of platelets aggregating, leading to delayed clot formation. In normal conditions, the secreted serotonin and ADP attract more platelets to the site of clot formation. This causes easy bruising and bleeding from the oral and nasal mucosa. In addition, bleeding can occur following invasive procedures.

Anemia of chronic kidney disease

The pathophysiologic mechanism involved in anemia of CKD is multifactorial. It is associated with relative erythropoietin deficiency. Erythropoietin is the hormone that allows the formation of more erythrocytes. Decreased levels of this hormone lead to low red blood cell count resulting in anemia (Mukherjee, 2018). Uremic-induced inhibitors of erythropoiesis can also be implicated in this scenario where there is inhibition of forming more red blood cells leading to low hemoglobin levels. Also, shortened erythrocyte survival and disordered iron homeostasis contribute to anemia.