Gastrointestinal and Renal Diseases’ Pathophysiology

Intra-abdominal pathologies can affect various systems, including hepatobiliary, gastrointestinal, renal, genitourinary, and endocrine systems. The gastrointestinal and hepatobiliary systems are interconnected and may share certain pathophysiological processes. The purpose of this paper is to describe the pathophysiology of certain GIT, hepatobiliary, and renal conditions.


The gastrointestinal tract (GIT) maintains a balance between acid secretion and mucosal defense to prevent damage to the mucosa, especially in the upper GI. Ulcers arise when there is a discrete erosion of the GI mucosa, especially by acids from the GIT or pathogens. Peptic ulcers arise from elevated acid secretion that is also facilitated by infections such as Helicobacter pylori. These ulcers expose underlying mural layers to the actions of the gastric acids. The ulcers also cause inflammation that presents with pain through the production of pain meditators such as prostaglandins and bradykinins. When left untreated, these ulcers can perforate the GIT wall and lead to peritonitis with severe outcomes.

Hepatitis Markers After Hepatitis Vaccine

Hepatitis is simply the inflammation of the liver parenchyma, especially involving the liver cells and hepatocytes. The most common causes of hepatitis are hepatitis viruses (McCance & Huether, 2019). However, toxins and exogenous substances such as acetaminophen and alcohol can cause hepatitis. The triple serological markers for hepatitis B, such as hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (HBsAb), hepatitis Be antigen (HBeAg), hepatitis Be antibody (HBeAb), hepatitis B core antibody (HBcAb) are detected in blood in hepatitis B infection (Jia et al., 2020). Hepatitis B vaccination is a preventive strategy that prevents worse outcomes of hepatitis B virus infection in the future. These markers indicate an active infection, recent infection, chronic infection, or recurrent hepatitis infection. However, after hepatitis B vaccine shots, these markers can stay elevated for as long as two weeks later. Rise anti-HBs or HBsAb can suggest a recent hepatitis B vaccine or recent infection (Guvenir & Arikan, 2020). Therefore, a history of recent vaccination is important in building the patient’s health history and evaluating hepatitis.

Gastroesophageal Reflux Disease

Gastroesophageal Reflux Disease (GERD) results from the movement of gastric content containing gastric acid into the esophagus leading to symptoms in the presence or absence of esophageal injury. Alteration in the competency of the lower esophageal sphincter (LES), decreased esophageal motility, and decreased gastric emptying have been described as the pathophysiologic mechanisms of GERD. Irritation of the esophagus by the gastric acid causes a burning retrosternal pain that most patients describe as ‘heartburn.’ Esophageal erosion and ulcers can result from corrosion by the refluxate, and repeated attempts to regenerate risk neoplastic transformation of the injured lower esophagus (Hammer & McPhee, 2018). Sometimes the refluxate can rise higher up to the proximal third of the esophagus leading to aspiration and laryngitis.


Pancreatitis is an inflammation of the pancreas, an endocrine and exocrine gland that empties exocrine contents into the duodenum. Exocrine contents are digestive enzymes that have a crucial role in pancreatitis (Hammer & McPhee, 2018). Pancreatitis results when the outflow of these enzymes is obstructed by mechanical or functional causes (McCance & Huether, 2019). Infections such as viruses also play a part in the impedance of the flow of digestive enzymes from the pancreas; stagnation of these enzymes leads to their activation and, thus, proteolysis and lipolysis of the pancreatic parenchyma and ducts. In acute pancreatitis, this condition can be self-limiting but can also complicate into severe cases leading to leakage of these lytic contents into the abdomen, thus peritonitis. In chronic pancreatitis, the bouts of acute pancreatitis are repeated, and the pancreas attempt to health through fibrosis that worsens the obstruction. Acute presentation in upper abdominal pain that radiates to the back, but the chronic presentation is seen in malabsorption and digestive insufficiency of the gut. Abscesses and cysts in the pancreas are some of the long-term complications.

Liver Failure – Acute and Chronic

Liver failure can be part of multiple organ dysfunction syndromes (MODS) or occur independently. Acute liver failure is associated with overwhelming toxins such as acetaminophen. Acute liver failure, sometimes referred to as fulminant liver failure, is rare but results from hepatic necrosis. Infections such as hepatitis B virus (HBV) and hepatitis C virus (HCV) can also cause fulminate liver failure due to overwhelming hepatic inflammation and resultant apoptosis and necrosis (McCance & Huether, 2019). In cases of toxic injury from acetaminophen, fulminant liver failure can occur as early as five days. Anorexia and vomiting accompany jaundice because the failing liver cannot metabolize bilirubin and participate fully in the hepatobiliary functions to enhance fat metabolism. On the other hand, chronic liver failure results from a preexisting liver condition such as cirrhosis, chronic hepatitis, and autoimmune hepatitis. In these settings, the liver fails because the regenerative potential is overwhelmed by parenchymal fibrosis. The liver becomes smaller and harder and loses its metabolic and synthetic functions. Jaundice, malabsorption, ascites, and hepato-renal syndrome follow this end-stage liver disease.

Gall bladder disease

The gall bladder is known for its storage and concentration functions in the bile metabolism pathway. The most common pathophysiology leading to gallbladder disease arises from obstruction of bile flow and inflammation of the gallbladder. Gallstones and cholecystitis are the most common gall bladder disease. In gallstone disease, also known as cholelithiasis, supersaturation of one of the components of bile at the expense of the other leads to the crystallization of small stones. Aggregation of these stones leads to the formation of large stones that eventually block the flow of bile from the bladder (McCance & Huether, 2019). This causes pain when the gall bladder is contracting to expel contents after meals. The pain is usually colicky and located in the right upper quadrant. These gallstones, when pushed downwards from the bladder, causes more stasis that leads to inflammation and distension of the gall bladder, a disease called cholecystitis. Pain is also a common outcome of this disease process.

Inflammatory bowel disease

Inflammatory bowel diseases (IBD) are chronic, relapsing, and idiopathic conditions characterized by inflammation of the gastrointestinal tract. Ulcerative colitis (UC) and Crohn’s disease (CD) are the two main forms of IBD. Race and genetics have been identified as risk factors for IBD. The exact cause of these diseases is not fully understood, but it is thought that environmental factors may play a role in their development. These elements may change the mucosal epithelium’s ability to act as a barrier, increasing the uptake of luminal antigens and decreasing immunological tolerance to typical intestinal antigens. As a result, pro-inflammatory cytokines and other inflammatory mediators are produced to further ran inflammation, invading the mucosa and deeper layers to produce persistent, recurring symptoms. In UC, these lesions are limited to the mucosa and lower gastrointestinal tract, while in CD, they can involve the foregut and midgut structures (McCance & Huether, 2019). The loss of absorptive function of the mucosa can lead to nutritional problems in affected individuals. Both UC and CD can present with similar symptoms, making the diagnosis a challenge.


Outpouching from the large bowel results in herniation that, when inflamed, is called diverticulitis. The cause of diverticulitis is unknown, but abnormal colonic motility and alteration in the microbiota of the colon have been implicated in this disease. Diverticula develop where the tunica muscularis of the colon is breached by arteries that feed the mucosal layer. Diverticula frequently result in the muscles around them becoming thicker, which can raise intraluminal pressure and cause a herniation. Diverticula’s specific cause is unknown, although it’s believed that routinely eating a low-residue diet, which minimizes fecal volume, may be a factor in their development (McCance & Huether, 2019). Diverticulitis can present with vague lower abdominal pain, diarrhea, or constipation. However, fever usually accompanies the infection in diverticulitis.

Jaundice and Hyperbilirubinemia

Jaundice is defined as the yellowish, sometimes green, discoloration of the skin and sclera. It results from elevated bilirubin levels above 2.5 mg/dL, especially for adults, a condition called hyperbilirubinemia. Hyperbilirubinemia can result from excess bilirubin production (pre-hepatic jaundice), diminished metabolism (intrahepatic jaundice), or blocked outflow from the liver canaliculi and the biliary system (obstructive jaundice or surgical jaundice) (McCance & Huether, 2019). Therefore, the bilirubin builds up in the system and gets deposited in the skin, sclera, and in the worst cases, the brain. Bilirubin deposition in the skin can cause itchiness and xanthomas (Hammer & McPhee, 2018). Depending on the cause of jaundice, symptoms may vary. In obstructive jaundice, pale stool and darkened urine can occur. In intrahepatic jaundice, mostly due to hepatitis, fever and right upper quadrant pain can occur.

Gastrointestinal Bleeding – Upper and Lower

Gastrointestinal bleeding is a manifestation of various underlying disease processes. Upper GI bleeding occurs from the esophagus to the point of ligament of Treitz. Lower GI bleeding starts from the ligament of Treitz to the rectum (Awadie et al., 2022). Causes include ulcers, trauma, tumors, varices, neoplasia, medications, and tears. Bleeding in the upper GI tract can cause hematemesis and black tarry stools, also called melena. Lower GI bleeding will more likely cause frank blood in stool, a condition also known as hematochezia. Nevertheless, this bleeding will cause some degree of anemia, depending on its severity. Shock and fatigue are also possible complications.

Hepatic Encephalopathy

Hepatic encephalopathy results from advanced liver function because this liver cannot perform deamination efficiently to eliminate nitrogen compounds such as ammonia. The buildup of ammonia in the bloodstream cause neuropsychiatric symptoms such as confusion, decreased consciousness levels, tremors, and altered cognition. In advanced cases, coma can result and this signifies severe liver dysfunction. Therefore, precipitants such as infections, inflammation, hemorrhage, and electrolyte imbalances should be prevented in liver disease patients.

Intra-Abdominal Infections (e.g., Appendicitis)

Intra-abdominal infections can arise from the visceral organs or the peritoneal space. Appendicitis is one of the commonest intra-abdominal infections. Appendicitis results from inflammation that results from parasites, fecal impaction, or foreign materials in the appendix (McCance & Huether, 2019). These causes obstruct the appendiceal lumen leading to the buildup of mucous and an increase in the intraluminal pressure. This pressure increase leads to reduced perfusion and ulceration that promotes bacterial invasion that causes appendicitis (Guvenir & Arikan, 2020). Gangrene and perforation can complicate appendicitis, and this worsens the pain felt at McBurney’s point. Anorexia, constipation, and diarrhea are other common symptoms that result from this inflammation and peritoneal irritation.

Renal Blood Flow and Glomerular filtration rate

Glomerular filtration rate (GFR) is the fluid volume that both kidneys filter per minute. On average, both kidneys filter about 180L of fluid per day, thus 125ml in one minute. This is the standard rate in men. Usually, the kidneys receive about 20-25% of cardiac output, which is about 1.1L per minute. This forms the renal blood flow. Blood from the heart is pumped into renal arteries that reach the Bowman capsules in the renal cortex through afferent arterioles (McCance & Huether, 2019). And after filtration leaves through the efferent arterials into the medulla and back into circulation through the renal veins.

Kidney Stones

Kidney stones result from the supersaturation of urine. Supersaturation can result from high calcium salts, high oxalate salts, or low urine volume. Therefore, crystals of these slats nucleate, grow and aggregate within the kidney collecting ducts leading to stein formation. These stones obstruct the flow of urine from the kidney to the ureters, and this can result in nephrocalcinosis and hydronephrosis, which can cause kidney failure, among other complications. Flank pain can result from this condition.

Infections – urinary tract infections, pyelonephritis

Urinary tract infections (UTIs) can involve the lower urinary tract, which includes the urethra and urinary bladder, or the upper urinary tract, which involves the ureters and the kidneys. Sources of infection can be iatrogenic, hematogeneous, sexually transmitted infections, or due to normal microbiota imbalance. Escherichia coli is the most common cause of UTI in females (McCance & Huether, 2019). However, the role of gonococcal causes cannot be overlooked in men. Obstructive causes such as prostate enlargement, pregnancy, and urinary stones are the most common causes. However, immune incompetence also plays a part in the proliferation of these pathogens. The inflammation due to the infection causes pain whose location is important in determining the region of the urinary tract involved. An ascending pattern of these infections is also possible from the urethra to the bladder.

Acute Kidney Injury

A key pathophysiology in acute kidney injury is the reduction in renal blood flow. This can be caused by systemic and local cases. Renal artery stenosis is responsible for a local reduction in renal blood flow. Systemic causes such as shock and reduced cardiac output also cause a reduction in blood flow. This hypoperfusion leads to a reduction in GFR and an increase in reabsorption of sodium and water, increased aldosterone and vasopressin secretion, and thus reduced urinary output. Renal tubular injury from infections, toxins, and ischemia leads to cell death through apoptosis and necrosis, causing cast formation in the tubules causing further obstruction, back-leak, and reduction in GFR, thus oliguria (McCance & Huether, 2019). Post-renal obstruction from stones and tumors causes an increase in intraluminal pressure and inflammation that cause renal vasoconstriction and decreased filtration pressure. The result is the production of little urine and the retention of toxic wastes.

Renal Failure – Acute and Chronic

Glomerular and tubular dysfunctions are the key processes in renal failure that leads to a reduction in GFR. These dysfunctions cause compensatory adaptive proliferation of the remaining healthy nephrons leading to loss of excretory and non-excretory function that is implicated in chronic renal failure (McCance & Huether, 2019). In acute renal failure, there is a sudden buildup of urea and creatinine that leads to uremia and other systemic complications. Retention of fluid in both cases leads to edema in the lower limbs and orbits, ascites, and anasarca. Activation of the renin aldosterone angiotensinogen system leads to hypertension. In chronic cases, the kidney loses synthetic function and cannot process vitamin D or produce erythropoietin. Therefore, rickets, osteoporosis, and anemia result from chronic cases.


Awadie, H., Zoabi, A., & Gralnek, I. M. (2022). Obscure-overt gastrointestinal bleeding: a review. Polish Archives of Internal Medicine132(5).

Guvenir, M., & Arikan, A. (2020). Hepatitis B virus: From diagnosis to treatment. Polish Journal of Microbiology69(4), 391–399.

Hammer, G. D., & McPhee, S. J. (2018). Pathophysiology of disease: An introduction to clinical medicine 8E (8th ed.). McGraw-Hill Education.

Jia, Q., Yu, F., Zhou, Q., Chen, X., Gu, Z., & Ma, C. (2020). The predictive effect of five hepatitis B virus markers on re-vaccination time of hepatitis B vaccine. Experimental and Therapeutic Medicine20(2), 1709–1715.

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.

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