Mr. Newman is a 49 year old male who has hematuria, fever and severe flank pain. He also has bilateral lumbar tenderness, bilateral renal enlargement, liver enlargement, ankle and facial edema, skin pallor, and lung sounds suggest pulmonary edema.
His vital signs are as follows: BP 172/100, heart rate 92 beats per minute, and a temperature of 102.2 F. There have been some labs done. His red blood count is 3.1 million cells, white blood count is 22,000 cells, potassium is 5.4 mEq/L, calcium is 6.8 mg/dL, phosphate is 4.3 mEq/L, urea is 37 mg/dL, creatinine 2.0 mg/dL, albumin is 2.9 mg/dL, and pH is 7.29. With labs like these, more testing was done. A chemistry panel which showed protein 1.7 gm/24 hours, glomerular filtration rate of less than 30 ml/minute, and his urine sediment showed presence of gram negative bacilli, presence of white blood cells, presence of red blood cells, and granular and waxy casts.
Mr. Newman had a genetic screening that showed a mutation on Chromosome 16. This mutation results in the formation of abnormal membrane protein called polycystin. It is inherited from one of his parents. The mutation takes place in 1 to 2 homologous chromosomes. With him only have one copy; it has stayed latent for many years. Now he has two abnormal polycystin genes. Polycystin genes act as receptors for extracellular growth.
Cystic lesion has formed in Mr. Newman’s kidney. Cyst forms when cells in any region of the nephron divide rapidly. Proximal tubule cells have divided. Dilated segment fill with glomerular filtrate. The dilated segments grow until it eventually separates from the nephron; after it separates the cyst forms. A cyst has formed and it continues to grow. Cysts begin to secrete calcium and chloride ions into the lumen.
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"Sickle-cell anemia" Sickle-cell anemia is an inherited disease, in which the red blood cells become crescent shaped. As a result it functions abnormally, and causes small blood clots. Sickle-cell anemia is caused by a genetic, or defective gene that produces an abnormal form of hemoglobin. Hemoglobin distorts red blood cells after they release oxygen in the tissue. Someone who inherits hemoglobin ...
Mr. Newman’s kidney weighs 4 kilograms. It has multiple cysts of varying size and shapes. Some of the cysts are infected causing him to have lumbar tenderness, fever, and urine sediment changes. Other cysts are hemorrhagic. As the cysts rupture, they are excreted in the urine causing him to have blood in his urine. Very little normal renal tissue exists. No obvious regions of renal cortex or renal medulla can be identified. The hilus and entire collecting system are severely disrupted. His is kidney is non-function and needs to be removed.
Cysts exert pressure causing destruction of nearby tissue. Loss of nephrons results in the inability to maintain normal solute balance, excrete wastes such as urea and creatinine, secretes erythropoietin causing severe anemia. The pressure on blood vessels interferes with renal blood flow causing hypertension.
Mr. Newman’s disease has resulted in a number of organ system defects. He has a reduced glomerular filtration, which causes accumulation of water that result in pulmonary edema. He has anemia and reduced platelet function that causes subcutaneous bruising. Also due to anemia, he has an elevated blood urea level that can lead to bleeding disorders. Due to his increased blood urea levels, he may have trouble getting an erection. Cysts destroy normal renal tissue in the kidneys. The cysts could cause hepatic enlargement, abdominal pain, and reduced hepatic function. Increased urea levels may cause pericarditis. Effects of increased urea levels in blood may cause encephalopathy resulting in coma or death. Berry aneurysms may rupture resulting in hemorrhage or even death.
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... with the antiserum Reporting Test Results Positives Blood group A positive (A ... ] BUE creatinine[Blood Urea Erythrocyte Creatinine] FBS[Fasting Blood Sugar] Lipid profile ... 100ml PROCEDURE TO DETERMINE BLOOD GLUCOSE LEVEL. URINE SUGAR TEST The ... ova, larva, trophozoites and cyst of Helminthes and protozoa ... maldigestion, dietary insufficiency), renal and hepatic diseases result in hyperproteinaemia. If ...
The answers to the question are as follows. Polycystic kidney disease is what best explains Mr. Newman’s clinical signs and symptoms. Cysts form in the kidneys as a result of multiple genetic mutations. The normal function of this protein is regulation of cellular differentiation and proliferation. Red blood count is decreased due to decreased erythropoietin secretion. Mr. Newman’s urine sediment analysis results are hematuria due to ruptured cysts. The event illustrated is an apoptosis. Urinary protein concentration, red blood cells count, BUN concentration, and blood creatinine concentration indicate severe renal disease. Image shown describes multiple cysts. Complications result from uremia or excessive urea levels in the blood are pericarditis and encephalopathy. Decreased glomerular filtration rate is most associated with pulmonary edema.