NUR 631 Topic 10 DQ 2

Sample Answer for NUR 631 Topic 10 DQ 2 Included After Question

Answer all of the questions below using the “Discussion Forum Sample” for your discussion response.

Scenario

A.O. is a 28-year-old woman who presents to your clinic with complaints of rectal bleeding and weakness. Five days ago, she noticed bright red blood in her stools. Furthermore, she reports that her daily bowel movements have increased to five or six with significant diarrhea. She has been weak for approximately 3 days. She has not traveled outside of the city, been hospitalized, or received antibiotics recently.

A proctosigmoidoscopy was conducted 3 days after the patient’s discharge from the acute care clinic. A significant pseudopolyps formation could be seen. Biopsies of the colon revealed erosions of the mucosa and ulcerations into the submucosa with mixed acute (i.e., neutrophils) and chronic (lymphocytes and macrophages) inflammatory cells. No dysplastic cells suggesting the development of colon carcinoma were seen. No multinucleated giant cells suggesting Crohn’s disease were seen. Inflammation and ulceration were limited to the rectum and sigmoid colon only. Crypts of Lieberkühn were intensely inflamed. Marked hemorrhaging of capillaries in the mucosa was also observed.

 Laboratory Blood Test Results

  • Na+ = 143 meq/L
  • BUN = 20 mg/dL
  • Plt = 315,000/mm3
  • AST = 33 IU/L
  • K+ = 3.2 meq/L
  • Cr = 1.1 mg/dL
  • PO4-3 = 4.0 mg/dL
  • ESR = 24 mm/hr
  • ALT = 41 IU/L
  • Cl- = 108 meq/L
  • Hb = 10.8 g/dL
  • CRP = 1.5 mg/dL
  • T bilirubin = 0.9 mg/dL
  • Alb = 3.1 g/dL
  • HCO+3 = 18 meq/L
  • Hct = 36%
  • Ca+2 = 8.9 mg/dL
  • PT = 11.3 sec
  • Glu, fasting = 132 mg/dL
  • WBC = 9,400/mm3

Questions

  1. What is the relevance of the last sentence in the first paragraph of the scenario provided above: “She has not traveled outside of the city, been hospitalized, or received antibiotics recently”? Explain your answer in detail.
  2. What is the diagnosis? Explain your answer. Why and how did you come up with this diagnosis?
  3. Identify eight abnormal laboratory blood test values and provide a brief pathophysiological explanation for each of them.

A Sample Answer For the Assignment: NUR 631 Topic 10 DQ 2

Title: NUR 631 Topic 10 DQ 2

What is the relevance of the last sentence in the first paragraph of the scenario provided above: “She has not traveled outside of the city, been hospitalized, or received antibiotics recently”? Explain your answer in detail.

Inquiring about travel assesses the patient’s potential exposure to certain infective agents that may be prevalent in certain geographical locations. Traveler’s diarrhea is the most common travel-associated condition affecting up to 40-60% of travelers. The diarrhea may be the result of bacterial, viral, or parasitic infections although bacterial sources are the most frequent etiology (Dunn, Okafor, Knizel, 2022). It is important to assess for recent hospitalization and antibiotic use as nosocomial diarrhea is a common complication in hospitalized patients. C-diff is usually the focus of physicians when nosocomial diarrhea is present but medications, enteral feedings, and underlying illnesses can also lead to nosocomial diarrhea. Antibiotics also play a role in altering the intestinal microbiome which may play a role in the development of diarrhea in patients (Polage, Solnick, & Cohen, 2012).

What is the diagnosis? Explain your answer. Why and how did you come up with this diagnosis?

The most likely cause of this patient’s symptoms is ulcerative colitis (UC). UC is a chronic inflammatory disease leading to the ulceration of the colonic mucosa. Lesions typically appear in patients between 20-40 years of age. In cases of mild inflammation, the mucosa becomes hemorrhagic and small erosions form eventually turning into ulcers. In chronic disease, polyps develop in the colon form the regenerating epithelium. In this patient’s proctosigmoidoscopy, erosions and ulcers of the mucosa were seen as well as significant pseudopolyps. Another finding in the exam that leads to the diagnosis of UC is the intensely inflamed Crypts of Lieberkuhn. In UC the primary lesion begins with inflammation at the base of the Crypts of Lieberkuhn (McCance & Huether, 2019).

Identify eight abnormal laboratory blood test values and provide a brief pathophysiological explanation for each of them.

K+ 3.2meq/L, normal range is 3.5-5.5 Hypokalemia in this case would be explained by the chronic diarrhea.

ESR 24mm/hr, normal 0-20mm/hr. ESR is elevated in cases of inflammation.

Cl 108 meq/L, normal range 96-106meq/L. This can be elevated due to dehydration from the chronic diarrhea.

Hgb 10.8g/dL, normal range 12-15g/dL. This is due to the bleeding in the GI tract.

CRP 1.5mg/dL, normal range is 0.3-1.0mg/dL. CRP is another biomarker that is elevated in cases of inflammation.

Alb 3.1g/dL, normal 3.4-5.4 g/dL. This could be due to the patient’s malnourished state secondary to the chronic diarrhea.

HCO+3 18meq/L, normal range is 23-29. Shows a metabolic acidosis. Could be in response to the dehydration/inflammatory process form the chronic diarrhea.

Fasting glucose 132mg/dL, normal <100g/dL. This could be elevated as a stress response from the inflammation or due to undiagnosed diabetes.

Dunn, N., Okafor, C., Knize, J. (2022). Travelers Diarrhea (Nursing). StatPearls Internet. Retrieved on July 11, 2023, from https://www.ncbi.nlm.nih.gov/books/NBK568732/

Polage, C., Solnick, J., Cohen, S. (2012). Nosocomial diarrhea: Evaluation and treatment of causes other than Clostridium difficile. Clinical Infectious Diseases, 55(7), 982-989. https://doi.org/10/1093/cid/cis551

McCance, K., Huether, S. (2019). Pathophysiology: The Biological Basis for Disease in Adults and Children. (8th ed.). Elsevier.

A Sample Answer 2 For the Assignment: NUR 631 Topic 10 DQ 2

Title: NUR 631 Topic 10 DQ 2

§  What is the relevance of the last sentence in the first paragraph of the scenario provided above: “She has not traveled outside of the city, been hospitalized, or received antibiotics recently”? Explain your answer in detail.

When the patient said, “Has not traveled outside of the city but has recently been hospitalized and received antibiotics treatment, this as a health provider eliminated the possibility that traveler’s diarrhea was not the cause of excessive diarrhea, rectal bleeding, and weakness experienced by the Mrs. A.O. Traveler’s diarrhoea is primarily disseminated by fecal-oral transmission of the etiologic agent, as reported by Dunn, N., & Okafor, CN. (2022). This occurs most often via ingestion of infected food or drink.  Viruses and bacteria typically have a shorter incubation time (from 6 to 24 hours), but intestinal parasites may take anywhere from 1 to 3 weeks.  Different causes of traveler’s diarrhea have different pathophysiological mechanisms, which may be broadly classified as either non-inflammatory or inflammatory.

Intestinal mucosal absorption is reduced by non-inflammatory drugs, leading to greater gastrointestinal (GI) tract output. However, inflammatory chemicals destroy the intestinal mucosa by the production of cytokines or by invading the mucosa itself. Again, less absorption leads to more frequent bowel movements when mucosal surface area is lost. In addition, the health care provider’s knowledge that the patient had recently been hospitalized and treated with antibiotics aided in the conclusion that the cause of the patient’s excessive diarrhea, rectal bleeding, and feeling of weakness with additional supporting diagnostic procedure, which was proctosigmoidoscopy performed 3 days after the patient’s discharge from the acute care clinic. Significant pseudopolyps development was observed.

Colon biopsies showed both acute (neutrophils) and chronic (lymphocytes and macrophages) inflammatory cell infiltration, with erosions of the mucosa and ulcerations into the submucosa. Colon cancer-causing dysplastic cells were not detected. The presence of large, multinucleated cells, a hallmark of Crohn’s disease, was not seen. Only the sigmoid colon and rectum were affected by the inflammation and ulceration. Lieberkühn’s tombs were on fire like never before. There was also significant bleeding from the mucosal capillaries. All of this evidence led the healthcare provider to the diagnosis of antibiotic-associated diarrhoea, which, according to research by Barbut, F., & Meynard, J. L. (2002), affects between 5 and 30 percent of patients, typically beginning within the first week of treatment with antibiotics and persisting for up to two months afterward.

The use of antibiotics may cause diarrhea because they alter the gut’s usual bacteria. With 1011 bacteria per gram of intestinal material, this microflora creates a balanced ecology that allows for the clearance of pathogens. The excess of microorganisms that cause diarrhea is made possible when antibiotics disrupt the makeup and function of this flora. Antibiotic-induced diarrhea now mostly results from Clostridium difficile. Pseudomembranous colitis and 10–25% of antibiotic-associated diarrhea are both caused by this anaerobic spore-forming bacterium.

3 The colon is damaged and inflamed due to the secretion of two powerful poisons. C perfringens, Staphylococcus aureus, Candida spp, Klebsiella oxytoca, and Salmonella spp. have also been linked to antibiotic-associated diarrhoea. Antibiotic-associated diarrhea may show clinically in a variety of ways, from mild diarrhoea to severe pseudomembranous colitis. Watery diarrhoea, fever, leukocytosis, and the appearance of pseudomembranes on endoscopic inspection are hallmarks of the latter. Toxic megacolon, perforation, and shock are among the most severe consequences (Barbut, F., & Meynard, J. L., 2002).

§  What is the diagnosis? Explain your answer. Why and how did you come up with this diagnosis?

Pseudomembranous colitis, a severe inflammation of the inner lining of the large intestine, manifests as an antibiotic-associated colonic inflammatory complication (Salen P, Stankewicz HA., 2023), was the diagnosis I arrived at after reviewing the patient’s symptoms and diagnostic tests. Ischemic colitis, collagenous colitis, inflammatory bowel disease, cytomegalovirus-induced colitis, vasculitis, bacterial and parasitic organisms, Behcet’s disease, chemotherapeutic medications, and toxins like heavy metal poisoning are all less common causes of pseudomembranous colitis than C. difficile infections. C. difficile is a prevalent cause of diarrhea in people who have recently used antibiotics or been in a healthcare institution, therefore it is often seen as a strictly nosocomial infection.

Colonization by Clostridium difficile occurs when the normal colonic biome has been disrupted by the use of antibiotics, chemotherapeutic medicines, or immunosuppressive medication. The exotoxins toxin A and toxin B are produced by C. difficile and are responsible for inducing colitis. These poisons trigger inflammation, cytoskeleton disruption, and cell death in the colon. These poisons pathologically hyperstimulate the native immune system, invading the intestinal mucosa and causing the pseudomembranes that characterize pseudomembranous colitis (Salen P, Stankewicz HA. 2023) to develop.

§  Identify eight abnormal laboratory blood test values and provide a brief pathophysiological explanation for each of them.

  • ESR = 24 mm/hr – The erythrocyte sedimentation rate (ESR) is a commonly performed hematology test that may indicate and monitor an increase in inflammatory activity within the body due to one or more conditions like autoimmune disease, infections, or tumors. Normal levels for women are 0-15 mm/hr, according to Tishkowski K, Gupta V. (2023). The ESR is not used alone to diagnose a disease, but rather in conjunction with other diagnostic tools to establish the presence or absence of elevated inflammatory activity. A proctosigmoidoscopy was performed in this case 3 days after the patient was released from the emergency room. There was a notable production of pseudopolyps.  Colon biopsies showed a combination of acute (neutrophils) and chronic (lymphocytes and macrophages) inflammatory cells, as well as erosions of the mucosa and ulcerations into the submucosa.
  • CRP = 1.5 mg/dL – C-reactive protein is slightly over the usual range (1.0 mg/dl). Inflammation causes the liver to produce more of a pentameric protein called CRP. C-reactive protein (CRP) may promote or inhibit inflammation depending on the context. By attaching to phosphocholine, phospholipids, histone, chromatin, and fibronectin, it aids in the identification and removal of invading infections and injured cells. It may speed up the elimination of cellular debris, injured or apoptotic cells, and foreign pathogens by activating the traditional complement system and phagocytic cells through Fc receptors (Nehring SM, Goyal A, Patel BC. 2022).
  • K+ = 3.2 meq/L – Potassium concentration below the normal range (-3.5 to 4.5 mg/dl). Losses of potassium in the gastrointestinal tract often result from persistent vomiting, diarrhea, or the use of laxatives. The patient in this instance had severe diarrhea, which caused a loss of potassium in the feces (Castro D, Sharma S. 2023).
  • Cl- = 108 meq/L – Chloride is just marginally higher. Chloride, as stated by Cafasso, J. (2023), is an essential electrolyte that maintains your body’s acid-base (pH) balance, fluid levels, and nerve impulse conduction. In healthy people, the concentration of chloride in the blood should be between 98 and 107 mEq/L. Hyperchloremia may be brought on by extreme diarrhea. Muscle weakness was one of the symptoms this patient was experiencing.
  • Alb = 3.1 g/dL – denotes hypoalbuminemia. The most prevalent plasma protein, albumin, with a concentration between 35 and 50 g/L.  According to Gounden V, Vashisht R, and Jialal I. (2022), albumin accounts for 50% of the total protein composition of plasma. There are several physiological functions for albumin. Maintaining the oncotic pressure within the vascular compartments is one of the most crucial things to do to stop fluid from leaking into the extravascular areas. Around 80% of the colloid osmotic pressure is accounted for by it. In addition to transporting hormones including thyroxine, cortisol, and testosterone, albumin binds at least 40% of the calcium that is circulating in the body.
  • Additionally, albumin serves as the major fatty acid transporter and has strong antioxidant qualities. As a plasma buffer, albumin helps to maintain the proper acid-base balance. In especially in chronic and critically sick patients, albumin is employed as a measure of nutritional status and disease severity (Gounden V, Vashisht R, Jialal I.2022). Hypoalbuminaemia may be caused by reduced albumin synthesis (rarely), increased albumin loss via the kidneys, GI tract, skin, extravascular space, increased albumin catabolism, or a combination of two or more of these processes. In this case, the patient had severe diarrhoea, and protein-losing enteropathy is to blame for the GI tract’s albumin loss.
  • HCO+3 = 18 meq/L – A metabolic acidosis condition defined by an elevated plasma chloride concentration and a reduced plasma bicarbonate concentration results from the loss of bicarbonate reserves due to diarrhea or renal tubular wasting. Bicarbonate is typically released in small amounts into the intestinal lumen in order to neutralize the acidic environment that food enters after gastric emptying. This bicarbonate travels the length of the small intestines and is reabsorbed as bile. However, owing to increased gut motility in diseases with copious watery diarrhea, bicarbonate in the intestines is lost via the stool. As a result, the pancreas and intestinal mucosa secrete more bicarbonate, which causes the blood to become acidic due to bicarbonate loss (Sharma S, Hashmi MF, Aggarwal S.2023). HCO3 level 22-26 mEq/L.
  • Anion Gap = Sodium – (Chloride + HCO3)= 143 –(108+18) = 143-126 =17. The anion gap is an approximation used to establish the amount of ionically active components in the blood that are not normally tested. An anion gap of 8 to 16 mEq/L is considered to be normal for serum. Renal failure, ketoacidosis, lactic acidosis, and consumption of toxins are all linked with a rise in the anion gap, while a normal anion gap acidosis is characterized by a decreased bicarbonate concentration (Sharma S, Hashmi MF, Aggarwal S.2023).
  • Hb = 10.8 g/dL   – Due to the patient’s apparent rectal bleeding in this situation, anemia is detected. Hematochezia, often known as rectal bleeding, manifests as frank red blood emerging from the anus. Pathology from the lower GI tract, which includes the small intestine beyond the duodenum, the colon, the rectum, or the anal canal, is the primary cause of rectal bleeding. Infections like C-diff, which may result in severe hemorrhagic colitis, are one of the reasons (Sabry AO, Sood T. 2023). Normal Hgb level -12-15 g/dl. 

References:

Barbut, F., & Meynard, J. L. (2002). Managing antibiotic associated diarrhoea. BMJ (Clinical research ed.), 324(7350), 1345–1346. https://doi.org/10.1136/bmj.324.7350.1345

Castro D, Sharma S. (2023).  Hypokalemia.  In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482465/

Dunn N, Okafor CN.(2022). Travelers Diarrhea. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459348/

Gounden V, Vashisht R, Jialal I.(2022).  Hypoalbuminemia. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK526080/

Nehring SM, Goyal A, Patel BC. (2022). C Reactive Protein. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK441843/

Sabry AO, Sood T. (2023).  Rectal Bleeding. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK563143/

Salen P, Stankewicz HA.(2023). Pseudomembranous Colitis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK470319/

Sharma S, Hashmi MF, Aggarwal S.(2023). Hyperchloremic Acidosis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482340/

Tishkowski K, Gupta V. (2023). Erythrocyte Sedimentation Rate. In: StatPearls [Internet]. Treasure Island (FL): StatPearls https://www.ncbi.nlm.nih.gov/books/NBK557485/