Definitions Of Health Quiz

Explanation
Ischemic bowel disease applies to the structural changes in the colon that occur due to deprivation of blood supply The causes for deprivation of blood could be arterial occlusion, venous occlusion and non-occlusive ischernia. The causes of non-occlusive ischemia include cardiac failure, shock, dehydration, and vasoconstrictive drugs. Depending on the severity and the presentation, it is classified into transmural, mural and mucosal infarction, and chronic ischemic colitis.
In transmural infarction, there is hemorrhagic infarction of the bowel with gangrenous changes, and a risk of perforation. In the mucosal and mural type, the mucosa is hemorrhagic and oedematosus but the remaining layers will remain intact. In chronic ischemia, nnucosal ulceration and inflammation develops, and sub-mucosal chronic inflammation and fibrosis may lead to stricture formation. In the setting of transmural infarction, patients generally present with acute abdominal pain, vomiting, fever, and bloody diarrhea and the patient may progress to shock and vascular collapse within hours.
In the case of mucosal and mural infarctions, the patient presents with an array of non-specific abdominal complaints and intermittent bloody diarrhea. Chronic ischemic colitis may present as an insidious inflammatory disease with intermittent episodes of bloody diarrhea mimicking inflammatory bowel disease. The diagnosis is based on the natural history of the disease, endoscopic findings with supportive biopsy.
Crohn's disease
is a chronic relapsing inflammatory disorder of obscure origin. It is a granulomatous disease and most often involves the small intestine and colon and is characterized by transmural inflammation affecting all layers, presence of non-caseating granulomas, fissuring with formation of fistulas, and skip lesions.
Ulcerative colitis
is an ulcera-inflammatory disease limited to the colon and affecting only the mucosa and submucosa except in the most severe cases. Ulcerative colitis extends in a continuous fashion proximally from the rectum in contrast to the skip lesions in Crohn's disease. Histologically, there is mononuclear inflammatory cell infiltration of the lamina propria collection of neutrophils in the crypts, called crypt abscesses and epithelial cell necrosis. However, there are no well-formed granulomas.
Shigellosis
is a bacterial enterocolitis caused by shigella. It involves primarily distal colon with acute mucosal inflammation and erosion with purulent exudates. Stool culture is diagnostic.
Amebic colitis
is caused by Entamoeba histolytica, a protozoan parasite that spreads by faeco-oral route. They form flask shaped ulcers with a narrow neck and broad base. A stool examination for ova and cyst shows trophozoites and cysts of ameba. These parasites penetrate portal vessels, embolize to the liver to produce solitary discrete hepatic abscess, some exceeding 10 cms

Explanation
Ischemic bowel disease applies to the structural changes in the colon that occur due to deprivation of blood supply The causes for deprivation of blood could be arterial occlusion, venous occlusion and non-occlusive ischernia. The causes of non-occlusive ischemia include cardiac failure, shock, dehydration, and vasoconstrictive drugs. Depending on the severity and the presentation, it is classified into transmural, mural and mucosal infarction, and chronic ischemic colitis.
In transmural infarction, there is hemorrhagic infarction of the bowel with gangrenous changes, and a risk of perforation. In the mucosal and mural type, the mucosa is hemorrhagic and oedematosus but the remaining layers will remain intact. In chronic ischemia, nnucosal ulceration and inflammation develops, and sub-mucosal chronic inflammation and fibrosis may lead to stricture formation. In the setting of transmural infarction, patients generally present with acute abdominal pain, vomiting, fever, and bloody diarrhea and the patient may progress to shock and vascular collapse within hours.
In the case of mucosal and mural infarctions, the patient presents with an array of non-specific abdominal complaints and intermittent bloody diarrhea. Chronic ischemic colitis may present as an insidious inflammatory disease with intermittent episodes of bloody diarrhea mimicking inflammatory bowel disease. The diagnosis is based on the natural history of the disease, endoscopic findings with supportive biopsy.
Crohn's disease
is a chronic relapsing inflammatory disorder of obscure origin. It is a granulomatous disease and most often involves the small intestine and colon and is characterized by transmural inflammation affecting all layers, presence of non-caseating granulomas, fissuring with formation of fistulas, and skip lesions.
Ulcerative colitis
is an ulcera-inflammatory disease limited to the colon and affecting only the mucosa and submucosa except in the most severe cases. Ulcerative colitis extends in a continuous fashion proximally from the rectum in contrast to the skip lesions in Crohn's disease. Histologically, there is mononuclear inflammatory cell infiltration of the lamina propria collection of neutrophils in the crypts, called crypt abscesses and epithelial cell necrosis. However, there are no well-formed granulomas.
Shigellosis
is a bacterial enterocolitis caused by shigella. It involves primarily distal colon with acute mucosal inflammation and erosion with purulent exudates. Stool culture is diagnostic.
Amebic colitis
is caused by Entamoeba histolytica, a protozoan parasite that spreads by faeco-oral route. They form flask shaped ulcers with a narrow neck and broad base. A stool examination for ova and cyst shows trophozoites and cysts of ameba. These parasites penetrate portal vessels, embolize to the liver to produce solitary discrete hepatic abscess, some exceeding 10 cms

Explanation
This patient presents with chronic cough. One of the differentials for chronic cough is gastroesophageal reflux disease (GERD). GastroesophageaL reflux disease typically presents with heartburn, described as burning sensation in the retrosternal area usually after eating food. Other common symptoms include regurgitation and dysphagia. One of the atypical presentations of gastroesophageal reflux disease is chronic cough. Other atypical presentations of gastroesophageal reflux disease could be noncardiac chest pain, sore throat, or asthma. In this patient, evidence in favor of gastroesophageal reflux disease includes longstanding cough, not on any cough inducing medication like ACE inhibitors, dry cough without expectoration, more in the daytime, not associated with fever, weight loss, or other systemic symptoms. Patients with atypical symptoms usually do not report any heartburn. These patients should be started on proton pump inhibitors like pantoprazole, without any diagnostic testing. This is usually diagnostic and therapeutic. Further diagnostic testing like endoscopy is indicated for patients with symptoms despite therapy, with warning signs (like bleeding), or in those with long standing gastroesophageal reflux disease.
Thus the correct diagnosis in this patient is Gastroesophageal reflux disease.
This patient is not immunocompromised and there is no evidence of high risk behavior in this patient, though sometimes HIV patients can present with symptoms of esophagitis.
Esophageal candidiasis is usually seen in HIV infections and hematological malignancies. Patients usually localize their pain to the retrosternal area. The diagnosis is usually confirmed on endoscopy. In this case vignette there is no evidence for either HIV or a hematologic malignancy. There are also no complaints of any retrosternal pain.
Pneumonia is also not a possibility as there is no evidence of fever, elevated white count, elevated CRP, and the chest X-ray has no evidence of infiltrates.
Chronic bronchitis is associated with cough with sputum for most days in a 3 month period for 2 years. This is mostly seen in smokers, but sometimes also occurs in association with exposure to other inflammatory dust and fumes. This patient has had cough for less than a year, is a non smoker, cough is without sputum production, and there is no evidence of exposure to other dust and fumes. Thus chronic bronchitis is not the answer

Explanation
The correct answer choice is low serum Calcium, low serum phosphate, low Vitamin D. This patient most likely has Crohn's disease. This diagnosis is supported with the clinical picture of chronic, intermittent, non bloody diarrhea, as well as the biopsy revealing non-caseating granulomas. The patient's complaints of generalized bone pains are likely to be secondary to Vitamin D deficiency due to her chronic Crohn's disease. Therefore, this patient has osteomalacia.
The Vitamin D deficiency leads to decreased Calcium reabsorption, leading to hypocalcernia. Negative feedback on the parathyroid results lead to increased PTH levels. This results in increased urinary excretion of phosphate.
Primary hyperparathyroidisnn leads to increased Calcium, increased PTH, and low serum phosphate.

Explanation
Entamoeba histolytica is the most common cause of this patient's bloody diarrhea and subsequent development of a hepatic abscess. Amebiasis is caused by Entamoeba histolytica, with the highest prevalence of amebiasis in developing countries where barriers between human feces and food and water supplies are inadequate. Entamoeba histolytica are transmitted via ingestion of the cystic form (infective stage) of the protozoa. Excystation then occurs in the terminal ileum or colon, resulting in trophozoites (invasive form). The trophozoites can penetrate and invade the colonic mucosal barrier, leading to tissue destruction, secretory bloody diarrhea, and colitis. Then, the trophozoites can spread hematogenously via the portal circulation to the liver. However, amebic liver abscess is an uncommon complication of infection with Entamoeba histolytica. The organism invades through the colonic mucosa to reach the liver through the portal system and then can cause associated hepatic parenchymal necrosis and subsequent abscess formation.
Giardia is caused by an intestinal protozoan that produces voluminous diarrhea (look for campers in the mountains developing foul-smelling, frothy diarrhea after drinking from a mountain stream).
Typhoid fever, caused by Salmonella typhip is a systemic illness that produces spleenmegaly, usually in the absence of significant hepatomegaly or hepatic abscesses. Both Shigella (Shigella dysenteriae) and Escherichia coli 0157: H7 are verotoxin-producing strains of bacteria that commonly cause diarrhea, especially in the warmer months. The most serious consequence of these 2 vero-toxin producing gastroenteritis infections is the hemolytic-uremic syndrome (HUS), a leading cause of acute renal failure in childhood. Undercooked ground meat and other foods of bovine origin are important sources of infection of both Shigefla and Escherichia coil 0157: H7, but person-to¬person transmission is a frequent means of acquiring infection as well.

Explanation
The most likely means of transmission of hepatitis C virus (HCV) is by exposure to infected blood, and IV drug abuse is the most common source. In the United States, intravenous drug abuse is the most common mode of transmission of hepatitis C.
Other modes of transmission include receiving blood or blood products, organs, need lestick injuries in healthcare, and vertical transmission from infected mother.
Other less frequent modes include sexual transmission from an infected partner, sharing personal items such as razors (which may have blood on them), and from health care procedures such as dental procedures or injections. There is limited information on whether cocaine snorting carries additional risk of hepatitis C transmission.
Hepatitis A, not hepatitis C, is transmitted by contaminated food from regions endemic for hepatitis A, such as South America, Asia, Africa, etc.
Tick bite is not known to transmit HCV.

Explanation
The patient has acute hepatitis B infection. Hepatitis B surface antigen or HBsAg is a protein on the surface of the hepatitis B virus, and the presence of this antigen indicates acute or chronic infection and that the person is infectious. The presence of IgM antibodies to hepatitis B core antigen (IgM, Anti-HBc) indicates recent HBV infection within the past 6 months. The presence of total hepatitis B core antibody (Anti-HBc) indicates previous or ongoing HBV infection. Recovery or immunity from H BV is indicated by appearance of anti-HBs. Therefore, the interpretation of serology in HBV is as above table

Explanation
Cirrhosis of the liver is characterized by disruption of the normal hepatic architecture by fibrous septa and presence of regenerative nodules of hepatocytes. This occurs as a consequence of persistent liver cell necrosis. Early pathological changes seen in alcoholic liver disease (ALD) include presence of fat and Mallory bodies. The causes of cirrhosis include ALD, chronic viral hepatitis, primary biliary cirrhosis, as well as autoimmune hepatitis, sclerosing chalangitis, hernochromatosis, Wilson's disease, and type IV glycogen storage disease. Progressive liver cell injury and damage due to infection, effects of alcohol, and metals like copper and iron, leads to cirrhosis.
Cirrhosis is normally associated with alcohol abuse; however, the term cirrhosis refers to the replacement of the normal hepatic architecture by non-functioning, fibrous tissues and shrinkage of the liver. There is also formation of regenerative nodules, all of which occur when liver cells stop functioning. Chronic liver damage and subsequent progression to cirrhosis is common in prolonged alcohol abuse.
Acute viral hepatitis
is characterized by mononuclear inflammatory cell infiltration, presence of focal hepatocyte dropout, and ballooning degeneration. The necrotic hepatocytes that are extruded from the sinusoids appear as acidophilic aggregation called Councilman bodies.
Chronic hepatitis
is characterized by mononuclear inflammatory cell infiltration of the portal areas and disruption of the limiting plates of portal tracts to extend into the liver lobules. Periportal fibrosis or bridging necrosis is also present.
Hemochromatosis
is characterized by the presence of hemosiclerin in hepatocytes demonstrated using Prussian blue staining. Glycogen storage disorders
are characterized by the presence of excess glycogen in the hepatocytes, which is demonstrated using Periodic Acid Schiff (PAS) stain.

Explanation
Hepatitis E virus is a naked (+) strand, ssRNA virus. It has clinical and biochemical features that are very similar to Hepatitis A, except that it seems to be more severe in pregnant women. Therefore, Hepatitis E is the virus that is most likely the cause of disease in this case, if serology indicated the absence of Hepatitis A.
Hepatitis C is enveloped and does not cause gastrointestinal symptoms. Rhinovirus causes common cold.
Rotavirus does not present with jaundice as do hepatitis-causing viruses.
Yellow fever can be associated with hepatitis, but it is a lot more severe in presentation than Hepatitis A and is transmitted by mosquitoes, not fecal-orally.

Explanation
Adenovirus is a very common cause of diarrhea and vomiting in children and since it is a DNA virus, it does not encode an RNA dependent RNA polymerase.
Although rotavirus is the most common cause of diarrhea and vomiting in children, it is a dsRNA virus and therefore encodes RNA dependent RNA polymerase.
Influenza A is mainly a respiratory disease, and although it can be associated with abdominal discomfort in children, it usually does not cause such severe abdominal pain that it serves as a reason for an ER visit.
Poliovirus, the etiological agent of polio, causes flu-like symptoms which car progress to cause paralysis; its main manifestation is not diarrhea and vomiting.
B19V is a DNA virus and therefore does not encode RNA dependent RNA polymerase. Additionally it causes destruction of red blood cells, rather than diarrhea and vomiting.

Explanation
Cryptosporidiosis is a protozoan infection caused by Cryptosporidium parvum which replicates intracellularly in the brush border of the small intestine. Infective aocysts are released into the lumen and excreted in the feces. After being ingested by through contaminated water, the oocyst releases sporozoites that transform into trophozoites in the brush border, replicate and produce more oocysts.
Patients present with profuse watery diarrhea and abdominal pain. They may also have nausea and low-grade fever. Diagnosis is confirmed by visualizing the oocysts in acid fast stained stool. Conventional techniques of examining the stool for ova and cysts are not reliable. A stool culture would not yield protozoa. A gastro-esophageal endoscopy would not aid in making a diagnosis as these intracellular organisms reside in the small intestine. Small intestine biopsy for histological examination is not initially required to confirm the diagnosis. It is a last resort.
Management includes supportive measure such as rehydration and hyperalimentation. Nitazoxanide, paromonnycin, and azithromycin may offer some relief. Prevention is by boiling drinking water and using water filters.

Explanation
The infant has necrotizing enterocolitis, which can affect infants any time in the first few months of life, but is most common around the time an infant is started on oral foods. The functional immaturity of the neonatal gut apparently leaves it particularly vulnerable to a combination of ischemic injury and colonization by pathogenic organisms. Formula-fed infants appear to be more vulnerable than breast-fed infants, possibly due to the absence of maternal antibodies or other immunoprotective features in formula. Premature and low-birth-weight infants are also more likely to develop this condition. Affected infants may have either mild gastrointestinal illness or develop frank, life-threatening gangrene of the terminal ileum and ascending colon.
Thickening of the pylorus is a feature of congenital hypertrophic pyloric stenosis, which typically presents with vomiting and regurgitation in an older infant.
A massively dilated colon suggests Hirschsprung's disease, which may present in a similar fashion to necrotizing enterocolitis. The two conditions can usually be distinguished by noting that meconium is usually not passed prior to feeding of the neonate in Hirschsprung's disease.
Bowel loops in the chest cavity are a feature of congenital diaphragmatic hernia, which causes respiratory distress and often death in neonates.
The gastrointestinal tract would be unlikely to appear normal in a case such as this.

Explanation
Mallory-Weiss syndrome is a non-penetrating, mucosal tear at the gastroesophageal junction. The syndrome is brought on from events that suddenly raise trans-abdominal pressure, such as lifting, retching, or vomiting, ulcers, malrotation, volvulus, or inflammatory conditions of the stomach and intestine. Any disorder that brings on vomiting may result in the development of a Mallory-Weiss. The disorder develops as a linear laceration at the gastroesophageal junction. The round shape makes longitudinal tears occur more easily. Alcoholism is a strong predisposing factor for Mallory-Weiss. Hiatus hernia is seen in 35-100% of the patients. Mallory-Weiss tears appear most often in the fifty to sixty-year-old client. The tears can occur also in children. Of note, is that Mallory-Weiss tears occur equally in men and women, however, in women of child bearing age, pregnancy should always be ruled out as the cause, clue to hyperemesis gravidarum in the first trimester.
Other conditions to rule out are: esophageal varices, gastric varices, and hemoptysis.
Esophageal neoplasm is 60%< squamous cell, carcinomas arising from the surface epithelium, most commonly in the middle and lower esophagus. Adenocarcinornas, which constitute 35%, arise from the gastric fundus and develop in the lower third of the esophageal tract. This cancer is most common in older adults, with African Americans affected three times as often as Caucasians, and men three times as often as women.
Risks factors:
• Smoking and tobacco use (chewing)
• Alcohol abuse
• Drug abuse (e.g., morphine, opium)
• Malnutrition
• Environmental carcinogens (e.g., Nitrosamines, silica, fungi)
• History of cancer of the larynx or pharynx
• History of chronic inflammation of the esophagus, achalasia (failure of esophageal sphincter to relax), tylosis, or caustic burns to the esophagus.
Dysphagia is the most common presenting symptom. Regurgitation and weight loss may also occur. The etiology is not well defined but is associated with chronic esophageal irritation.
Esophageal Varices can be caused by portal hypertension (elevated portal pressure beyond 10 mm Hg) in association with cirrhosis, liver parenchymal disease, duodenal ulcer, or acute pancreatitis, Budd Chiari syndrome, schistosomiasis etc. Bleeding esophageal varices eventually develop in about SO% of individuals with cirrhosis.
Portal veins narrow and become obstructed as a result of the underlying disease process. As the lumen narrows, the venous blood returning to the right atrium from the intestine and spleen seeks new routes through collateral vessels. These collateral vessels enlarge and become tortuous, and the mucosa ulcerates.
Complications can include esophageal rupture, with massive hemorrhage and death being the most common.. With acute bleeding, the mortality rate is about 50%. Approximately 60% of individuals die within a year of the first episode of bleeding.
Esophageal stricture formation occurs in about 10% of clients with esophagitis. It is manifested by the gradual development of solid food dysphagia, progressive over months to years. Often there is a reduction in heartburn because the stricture acts as a barrier to reflux. Most strictures are located at the gastroesophageal junction.
In Gastroesophageal Reflux Disease the essential features are:
• Heartburn; may be exacerbated by meals, bending, or recumbency.
• Clinical diagnosis; typical uncomplicated cases do not require diagnostic studies.
• Endoscopy demonstrates abnormalities, such as erythema and friability of the squamocolumnar junction in

Explanation
Mallory-Weiss syndrome is a non-penetrating, mucosal tear at the gastroesophageal junction. The syndrome is brought on from events that suddenly raise trans-abdominal pressure, such as lifting, retching, or vomiting, ulcers, malrotation, volvulus, or inflammatory conditions of the stomach and intestine. Any disorder that brings on vomiting may result in the development of a Mallory-Weiss. The disorder develops as a linear laceration at the gastroesophageal junction. The round shape makes longitudinal tears occur more easily. Alcoholism is a strong predisposing factor for Mallory-Weiss. Hiatus hernia is seen in 35-100% of the patients. Mallory-Weiss tears appear most often in the fifty to sixty-year-old client. The tears can occur also in children. Of note, is that Mallory-Weiss tears occur equally in men and women, however, in women of child bearing age, pregnancy should always be ruled out as the cause, clue to hyperemesis gravidarum in the first trimester.
Other conditions to rule out are: esophageal varices, gastric varices, and hemoptysis.
Esophageal neoplasm is 60%< squamous cell, carcinomas arising from the surface epithelium, most commonly in the middle and lower esophagus. Adenocarcinornas, which constitute 35%, arise from the gastric fundus and develop in the lower third of the esophageal tract. This cancer is most common in older adults, with African Americans affected three times as often as Caucasians, and men three times as often as women.
Risks factors:
• Smoking and tobacco use (chewing)
• Alcohol abuse
• Drug abuse (e.g., morphine, opium)
• Malnutrition
• Environmental carcinogens (e.g., Nitrosamines, silica, fungi)
• History of cancer of the larynx or pharynx
• History of chronic inflammation of the esophagus, achalasia (failure of esophageal sphincter to relax), tylosis, or caustic burns to the esophagus.
Dysphagia is the most common presenting symptom. Regurgitation and weight loss may also occur. The etiology is not well defined but is associated with chronic esophageal irritation.
Esophageal Varices can be caused by portal hypertension (elevated portal pressure beyond 10 mm Hg) in association with cirrhosis, liver parenchymal disease, duodenal ulcer, or acute pancreatitis, Budd Chiari syndrome, schistosomiasis etc. Bleeding esophageal varices eventually develop in about SO% of individuals with cirrhosis.
Portal veins narrow and become obstructed as a result of the underlying disease process. As the lumen narrows, the venous blood returning to the right atrium from the intestine and spleen seeks new routes through collateral vessels. These collateral vessels enlarge and become tortuous, and the mucosa ulcerates.
Complications can include esophageal rupture, with massive hemorrhage and death being the most common.. With acute bleeding, the mortality rate is about 50%. Approximately 60% of individuals die within a year of the first episode of bleeding.
Esophageal stricture formation occurs in about 10% of clients with esophagitis. It is manifested by the gradual development of solid food dysphagia, progressive over months to years. Often there is a reduction in heartburn because the stricture acts as a barrier to reflux. Most strictures are located at the gastroesophageal junction.
In Gastroesophageal Reflux Disease the essential features are:
• Heartburn; may be exacerbated by meals, bending, or recumbency.
• Clinical diagnosis; typical uncomplicated cases do not require diagnostic studies.
• Endoscopy demonstrates abnormalities, such as erythema and friability of the squamocolumnar junction in

Explanation
Mallory-Weiss syndrome is a non-penetrating, mucosal tear at the gastroesophageal junction. The syndrome is brought on from events that suddenly raise trans-abdominal pressure, such as lifting, retching, or vomiting, ulcers, malrotation, volvulus, or inflammatory conditions of the stomach and intestine. Any disorder that brings on vomiting may result in the development of a Mallory-Weiss. The disorder develops as a linear laceration at the gastroesophageal junction. The round shape makes longitudinal tears occur more easily. Alcoholism is a strong predisposing factor for Mallory-Weiss. Hiatus hernia is seen in 35-100% of the patients. Mallory-Weiss tears appear most often in the fifty to sixty-year-old client. The tears can occur also in children. Of note, is that Mallory-Weiss tears occur equally in men and women, however, in women of child bearing age, pregnancy should always be ruled out as the cause, clue to hyperemesis gravidarum in the first trimester.
Other conditions to rule out are: esophageal varices, gastric varices, and hemoptysis.
Esophageal neoplasm is 60%< squamous cell, carcinomas arising from the surface epithelium, most commonly in the middle and lower esophagus. Adenocarcinornas, which constitute 35%, arise from the gastric fundus and develop in the lower third of the esophageal tract. This cancer is most common in older adults, with African Americans affected three times as often as Caucasians, and men three times as often as women.
Risks factors:
• Smoking and tobacco use (chewing)
• Alcohol abuse
• Drug abuse (e.g., morphine, opium)
• Malnutrition
• Environmental carcinogens (e.g., Nitrosamines, silica, fungi)
• History of cancer of the larynx or pharynx
• History of chronic inflammation of the esophagus, achalasia (failure of esophageal sphincter to relax), tylosis, or caustic burns to the esophagus.
Dysphagia is the most common presenting symptom. Regurgitation and weight loss may also occur. The etiology is not well defined but is associated with chronic esophageal irritation.
Esophageal Varices can be caused by portal hypertension (elevated portal pressure beyond 10 mm Hg) in association with cirrhosis, liver parenchymal disease, duodenal ulcer, or acute pancreatitis, Budd Chiari syndrome, schistosomiasis etc. Bleeding esophageal varices eventually develop in about SO% of individuals with cirrhosis.
Portal veins narrow and become obstructed as a result of the underlying disease process. As the lumen narrows, the venous blood returning to the right atrium from the intestine and spleen seeks new routes through collateral vessels. These collateral vessels enlarge and become tortuous, and the mucosa ulcerates.
Complications can include esophageal rupture, with massive hemorrhage and death being the most common.. With acute bleeding, the mortality rate is about 50%. Approximately 60% of individuals die within a year of the first episode of bleeding.
Esophageal stricture formation occurs in about 10% of clients with esophagitis. It is manifested by the gradual development of solid food dysphagia, progressive over months to years. Often there is a reduction in heartburn because the stricture acts as a barrier to reflux. Most strictures are located at the gastroesophageal junction.
In Gastroesophageal Reflux Disease the essential features are:
• Heartburn; may be exacerbated by meals, bending, or recumbency.
• Clinical diagnosis; typical uncomplicated cases do not require diagnostic studies.
• Endoscopy demonstrates abnormalities, such as erythema and friability of the squamocolumnar junction in

Explanation
This patient has renal cell carcinoma.
Smoking is a risk factor for many neoplasms, including renal cell carcinoma.
There is a classic triad associated with renal cell carcinoma: hematuria, flank pain, and a palpable abdominal mass. However, the classic triad is not seen in most patients. Other presenting symptoms include a fever and vveight loss, as the case here. Cells from the proximal convoluted tubule are the most common cells that renal carcinoma arises from. There is an increase incidence of renal cell carcinoma with Von Hippel¬Lindau disease.
Schistosoma haernatobium infection is associated with bladder tumors.
Escherichia coil infection, urolithiasis, and interstitial nephritis are not known risk factors.

Explanation
This patient is most likely to have oxalate stones as patients with Crohn's disease are susceptible to them.
Excessive enteric reabsorption of oxalate is seen in patients with Crohn's disease, which causes hyperoxaluria and consequent oxalate stone formation. Hyperoxaluria, in turn, causes oxalate nephrocalcinosis. IHyperoxaluria is defined as oxalate urinary excretion in excess of 45 mg/day (normal upper limit of urinary oxalate excretion is 40 mg/day). It is observed that patients with Crohn's disease have significantly higher urinary oxalate concentration, which promotes oxalate stone formation and a lower urinary concentration of magnesium and citrate that act as inhibitory factors for nephrolithiasis. Hyperoxaluria is also seen in other conditions such as steatorrhea, ileal resection, dietary excess oxalate intake (vegetarian), and ethylene glycol intoxication. Plain X-ray of the abdomen can be used to demonstrate the presence of calcium oxalate stones. Oxalate stone formation can be reduced by administration of calcium, iron, aluminum, or magnesium supplements to reduce the enteric oxalate absorption by forming complexes with it.
Struvite stones are also called infection stones, as they develop when urinary tract infection (UT') affects the chemical balance of urine. LJTI with urea splitting organisms, such as Proteus, Klebsiella, Serratia, and Mycoplasrna, promotes the formation of struvite stones by creating an alkaline environment.
Calcium phosphate stones are typically seen in patients with metabolic or hormonal disturbances such as renal tubular acidosis and hyperparathyroidism.
Cystine stones develop in a condition called cystinuria, which is an autosomal recessive inborn error in the transport of dicarboxylic acids, namely cystine, ornithine, lysine, and arginine. These patients have large amounts of cystine in the urine, which does not dissolve well and in turn results in its precipitation and stone formation.
Uric acid stones occur when there is hyperuricosuria either due to excessive cell turnover (endogenous) or due to metabolism of excessive dietary (exogenous) intake. Pure uric acid stones are rare and require a low urinary pH (pH < 5.5).

Explanation
Minimal change disease is characterized by no change in the glomeruli as seen by light microscopy. Minimal change disease is also called lipoid nephrosis or nil disease.
There would be inflammatory cells in the parenchyma with acute interstitial nephritis. There would also be interstital edema.
With the light microscope, visible changes would be seen with chronic interstitial nephropathy. Among other visible changes, interstitial fibrosis would be present.
There would be inflammatory cells in the parenchyma with pyelonephritis.
Amyloidosis can cause nephrotic syndrome. However, Congo red stain of the biopsy sample would show green birefringence due to the deposition of amyloid protein.

Explanation
Correct answer is A
The components of nephrotic syndrome are edema, proteinuria, hypoalbuminemia and hyperlipidemia.
Oliguria, decreased glomerular filtration rate, hematuria,
and hypertension all are characteristics that can be seer with the nephritic syndrome.

Explanation
Membranous glomerulopathy is the most common cause of primary nephrotic syndrome in adults, peak age incidence being between 30-50 years. Males are affected twice as commonly as females. Proteinuria, in mernbranous glornerulopathy, is non-selective. Microscopic hematuria is present in about 50% of cases, but red cell casts, macroscopic hematuria, and leucocytes in urine are extremely rare.
Light microscopy of renal biopsy shows diffuse thickening of the GBM (glomerular basement membrane) which is best appreciated with PAS (periodic acid-Schiff) stain. Methenamine silver stain reveals characteristic "spikes" along the GBM. Immunofluorescence reveals granular deposits of IgG, C3 and the terminal components of (C5b-C9).
Focal segmental glomerulonephritis (FSGS) is most commonly present as proteinuria, which can range from minor levels to nephrotic levels. F5GS account for

Explanation
The primary renal neoplasm constitute the fifth most common group of pediatric cancers. The most common in this group are Wilms tumor or Nephroblastoma -80% Clear cell sarcoma - 6% Rhabdoid tumor - Mesoblastic nephronna < 3% Ossifying renal tumor of infancy - very rare Wilms tumor is the most common primary renal tumor of childhood, but its characteristic histological features are missing in this case. It is associated with congenital anomalies exhibiting aberrations in at least two distinct chromosomal loci. Wilms tumor associated gene WT-1 is located on chromosome 11p13. The patients with WAGR syndrome and Denys-Drash syndrome show high risk of developing Wilms tumor. In these patients either deletion or mutation of the WT-1 gene has been traced. In another group of patients with Beckwith-Wiedemann syndrome a second Wilms tumor gene WT-2 has been located just distal to the WT-1 locus. Most children with Wilms tumor present with a large abdominal mass. The combined use of chemotherapy, radiotherapy, and surgery has increased the long-term survival rates to 90%. Clear cell sarcoma is also called a bone metastasizing tumor of childhood. It is a highly malignant neoplasm. They are ten times more likely to metastasize to bone compared to other pediatric renal cancers. Rhabdoid tumor is a highly malignant tumor and metastasizes widely, generally leading to death within 12 months of diagnosis. Mesoblastic nephroma is a rare tumor, which generally presents with an abdominal mass. It has a very good prognosis Ossifying renal tumor of infancy is a very rare tumor of uncertain histogenesis and clinically has a benign course. Refer to the table for additional information.

Explanation
The correct answer choice is osteoporosis. This patient presents with a history of chronic diarrhea and with a rash that waxes and wanes over time. Given the age and clinical findings, this patient has celiac disease. The rash shown in the figure is dermatitis herpetifornnis, a rash described as herpetifornn (i.e. small, clustered) vesicles, which are classically symmetrically distributed over extensor surfaces, including the elbows, knees, buttocks, and shoulders. The fact that it waxes and wanes is also indicatIve of celiac disease. Celiac disease is a result of sensitivity to gluten in the diet.
The complications of celiac disease are vast and varied. Osteoporosis may result from malabsorption of vitamin D and calcium in the intestine. However, it may be reversed by vitamin D and calcium supplementation in addition to follovving a strict gluten-free diet.
Intussusception is the telescoping of the intestine into the preceding portion, most commonly seen in the pediatric age group, and is not necessarily associated with celiac disease.
Meckel's diverticulum is a common cause of anemia in infants. This is classically found 2 feet behind the ileocecal valve, is 2 inches long, and is not a complication of celiac disease.
Trichotillomania is a primary psychiatric disorder characterized by an urge to pull out one's own hair and is not associated with celiac disease.
Patients with celiac disease do not present with sideroblastic anemia. Sideroblastic anemia is more common in patients who are taking isoniazid.