Good Case Study On Pathophysiology
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The possible causes for the symptoms described in this case are urethral stricture, prostatic enlargement and partial outflow obstruction of urinary bladder.
According to Huether and McCance (746), diagnosis in such a case is based on good clinical history, thorough examination and laboratory investigations. Uroflowmetry and multi-channel urodynamic testing is used to assess the urinary tract for obstruction. Digital Rectal Examination (DRE) should be done along with laboratory levels of Prostate Specific Antigen (PSA). For specific testing, Ultrasound Prostate with post-voidal volume, pressure flow study, serum creatinine and Blood Urea Nitrogen (BUN) should be preferred.
Complete obstruction of the urethra causes bladder outflow obstruction representing a single entity of an umbrella term, Lower urinary tract symptoms (LUTS). The obstruction prevents the bladder for emptying and resulting into retention of urine in the bladder. This causes incontinence due to increased intra-abdominal pressure or repeated urinary tract infections (UTIs) and kidney stones.
The likely cause of symptoms in this patient is Over Active Bladder (OAB) or neurogenic bladder.
The age of the patient and an increase in intra-abdominal pressure and leaking on staining conditions like sneezing, laughing or coughing determines the probable most etiology of condition in this case.
In an untreated case of incontinence, a condition is developed known as low bladder wall compliance. The condition prevents the bladder from stretching and accommodating urine. Simultaneously, the detrusor muscle loses its capacity to contact promoting urinary stasis inside the bladder. Urinary stasis can give rise to bladder stone and repeated bouts of UTIs. Intra-vesicular pressure rises which can predispose to the development of hydroureter and hydronephrosis ultimately leading to impaired renal function in a case of low bladder wall compliance.
The possible diagnoses in this case are rapidly progressive glomerulonephritis (RPGN) nephritic syndrome or acute kidney injury (AKI).
Glomerulonephritis is an immune mediated diseased process. It is done by two pathways; deposition of antigen-antibody complexes in the glomerular basement membrane also called as type III hypersensitivity reaction and secondly by activation of antibodies against the antigens already present in the glomerulus which is also called as type II hypersensitivity reaction. Toxins, ischemic injury, drugs and vasculitides are non-immune causes of glomerulonephritis. The complexes activate pro-inflammatory cytokines and inflammatory mediators which damages the glomerular structures. This injury hampers effective membrane filtration and decreases the glomerular filtration rate (GFR). There is also change of polarity in membrane that promotes filtration of proteins causing proteinuria.
The nephritic glomerulopathy exacerbates with time and even with treatment. Most patients require dialysis due to renal failure. Pharmacotherapy delays the need for invasive treatment modalities.
The likely cause of infertility in this patient is endometriosis.
The exact mechanism that leads to infertility in patients having endometriosis is very unclear but few theories have been postulated explaining its pathogenesis. Infertility in endometriosis can occur if there is any mechanical obstruction in the process of ovulation or passage of ovum. It could also be the result of pro-inflammatory mediators and cytotoxins which are responsible to cause inflammation and cell killing. Impaired or faulty phagocytosis of spermatozoa by phagocytes and macrophages, defective development and maturation of follicles, implantation defects and magnitude of oxidative stress are also implicated in the pathogenesis of infertility in a case of endometriosis.
Endometriosis can occur due to attachment of endometrial cells during backward menstruation into the pelvic cavity, vascular or lymphatic spread of endometrial cells, immune mediated response via T cell, conversion of epithelial cells into endometrial cells, genetic predisposition and use of digoxin or similar compounds.
Treatment includes ovulation suppression by using combined hormonal contraceptives, gonadotropin releasing hormone (GnRH) agonists and Intrauterine device (IUD) containing levonorgestrel. Endometrial implants can surgically be removed by laparoscopic or laser techniques.
The likely cause of the manifestations in this patient is kidney stones.
The chemicals that should be measured for prevention of recurrence of kidney stones are calcium, oxalate, uric acid, citrate, cysteine, xanthine and pH of the urine. Their concentrations should be measured in the serum, blood or urine to ascertain the underlying cause of stone formation so that same event can be prevented from occurring again.
There are three different kinds of kidney stones and they include; calcium stones, struvite stones and uric acid stones. Risk factors for calcium stones are hypercalciuria, hyperuricosuria, hypercitraturia, hyperoxaluria, alkaline urine, renal tubular acidosis, hyperparathyroidism and crystal growth inhibitor deficiency.
Risk factors predisposing an individual to get struvite stones are alkaline urine, bacterial infection with urease producing bacteria like Proteus, Pseudomonas or Klebsiella.
Uric acid stones occur in individuals with high uric acid levels in serum and urine, both. High purine diet, gout, acidic urine, cystinuria and xanthinuria are all linked to the development of uric acid kidney stones.
Huether, Sue E., and Kathryn McCance. Understanding Pathophysiology. 5th ed. St. Louis, Misouri: Elsevier / Mosby, 2012. Print.
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