UTD Health & Medical Question

Using the video from Episode 6 on Mr. Fallbrook, answer two of the following prompts: Please identify each prompt you answer by number and restate the question in bold letters. WITH IN-TEXT CITATION AND REFERENCES

Prompt 1: Explain in detail the pathogenesis on how Mr. Fallbrook’s gastroenteritis leads to sepsis and then ARF.

Prompt 2: Research the medication Enalapril. Explain its uses, dosage, and side effects.


Enalapril is an orally active ACE (Angiotensin-Converting Enzyme) inhibitor that works by blocking the active site of ACE. It is an oral prodrug that is converted by hydrolysis to a converting enzyme inhibitor, enalaprilat primarily in the liver. ACE drugs induce natriuresis and lower systemic vascular resistance without increasing heart rate (Elimination of sodium). They are useful in the treatment of hypertension, lowering morbidity and mortality in heart failure and left ventricular dysfunction following a myocardial infarction, and delaying diabetic nephropathy progression.It is particularly useful in treating patients with chronic kidney disease as they diminish proteinuria and stabilize renal function (even in the absence of lowering of blood pressure levels). This effect is beneficial in diabetes, and these drugs are now recommended in diabetes even in the absence of hypertension. These benefits result from improved intrarenal hemodynamics, with decreased glomerular efferent arteriolar resistance and a resulting reduction of intraglomerular capillary pressure. ACE inhibitors are also useful in the treatment of heart failure and as treatment after myocardial infarction, reduce incidence of diabetes in patients with high cardiovascular risk.

ACE inhibitors impede the breakdown of other compounds such as bradykinin, substance P, and enkephalins as well as the conversion of ANG (Angiotensin) I to ANG II. The action of ACE inhibitors to inhibit bradykinin metabolism contributes significantly to their hypotensive action. Increased bradykinin levels are thought to be more essential than decreasing ANG II levels in this scenario.

Elevated bradykinin is thought to be the cause of several negative side effects, such as cough and angioedema. These medicines are not recommended during pregnancy as fetal hypotension, anuria, renal failure, fetal malformations or death, increased teratogenic risk have been reported. Toxicity can lead to severe hypotension. Other adverse effects such as acute kidney injury, dry cough, hyperkalemia, wheezing are also reported.

Dosage:- 10-20 mg oral once or twice daily.

Reference:- Basic and Clinical Pharmacology 14th edition G. Katzung


1. Type 1 diabetes is a chronic autoimmune disease where beta cell destruction may occur over a number of years before clinical diabetes is diagnosed. Type 2 diabetes is the result of an interplay of relative insulin deficiency or a defect in insulin release together with insulin resistance.

DKA is a complex disease process with multiple hormonal abnormalities that cause various deleterious fluid and electrolyte changes. It includes a relative exess ratio of glucogon to insulin. An increase in ketone production and a decrease in peripheral cell use lead to metabolic acidosis.PLEASE EXAMPLE BASED ON YOUR OWN WORD AND RESEARCHES.

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UTD Health & Medical Question

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Introduction: In this response, we will address Prompt 1, which focuses on explaining in detail the pathogenesis of Mr. Fallbrook’s gastroenteritis leading to sepsis and then acute renal failure (ARF). Please note that all information provided will be based on medical knowledge and research.

Prompt 1: Explain in detail the pathogenesis on how Mr. Fallbrook’s gastroenteritis leads to sepsis and then ARF.

Gastroenteritis is characterized by inflammation of the gastrointestinal tract, commonly caused by viral or bacterial infections. In Mr. Fallbrook’s case, the underlying cause of gastroenteritis could be an infective agent such as a bacteria or virus. When the infective agent enters the gastrointestinal tract, it can cause damage to the mucosal lining, leading to disruption of the intestinal barrier function.

The damaged intestinal barrier allows the microbes and their toxins to translocate into the bloodstream, resulting in bacteremia or sepsis. Sepsis is a life-threatening condition characterized by a systemic inflammatory response to the presence of microorganisms or their products in the bloodstream. The release of microbial products triggers an excessive immune response, leading to an uncontrolled cascade of inflammation.

During sepsis, the immune system releases various pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interleukin-6 (IL-6). These cytokines activate endothelial cells, causing the release of inflammatory mediators such as nitric oxide, prostaglandins, and endothelin. These mediators further promote inflammation and vasodilation, leading to increased vascular permeability and hypotension.

The systemic inflammation associated with sepsis can have detrimental effects on the kidneys. The inflammatory mediators disrupt normal renal blood flow and the functional integrity of the renal tubules. Additionally, the release of inflammatory cytokines affects the glomerular filtration rate (GFR) and renal autoregulation. These pathological changes can result in acute renal failure (ARF) or acute kidney injury (AKI).

ARF is characterized by a sudden decrease in kidney function, resulting in the accumulation of waste products and electrolyte imbalances. The reduction in GFR impairs the kidneys’ ability to excrete waste products, regulate fluid and electrolyte balance, and maintain acid-base homeostasis. It can also lead to decreased production of erythropoietin, resulting in anemia.

In summary, the pathogenesis of Mr. Fallbrook’s gastroenteritis leading to sepsis and ARF involves the initial gastrointestinal damage allowing translocation of microbes and toxins into the bloodstream, resulting in sepsis. The systemic inflammatory response associated with sepsis affects renal blood flow, glomerular filtration rate, and tubular function, ultimately leading to acute renal failure.

1. Vincent JL, Sakr Y, Sprung CL, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34(2):344-353.
2. Chertoff J, Chishti Y, Shalaby C, et al. Acute kidney injury and its management. Clevel Clin J Med. 2017;84(12 Suppl 3):S45-S51.
3. Bagshaw SM, Wald R, Adhikari NKJ, et al. Timing of initiation of renal-replacement therapy in acute kidney injury. New Engl J Med. 2020;383(3):240-251.

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