Answer: Vasopressin – synthetic ADH

Answer: ADH

Answer: There is a loss of both sodium and water from the extracellular space as a result of a renal loss of sodium which takes water with it.

Answer: The two primary causes of osmotic diuresis are glucosuria and the use of osmotic diuretics.

Answer: Cystitis: Bacterial infection of the lower urinary tract

·    Usually result from colonisation of the bladder by bacteria normally found in the lower GI tract

·    Inflammation of the urinary bladder and urethra

o remains superficial affecting the bladder mucosa

o mucosa becomes hyperaemic and may haemorrhage

·    Inflammatory response causes formation of pus

Pyelonephritis: A bacterial infection of the upper urinary tract specifically the parenchyma and renal pelvis

·    Gram-negative bacteria

·    Bacteria may gain access through:

o lower urinary tract (ascending)

o bloodstream (haematogenous)

·    May be acute or chronic

Chronic

·    Progressive process – due to recurring bacterial infections superimposed on obstruction, reflux or both

·    Scarring and deformation of renal calyces and pelvis

·    Atrophy and thinning of renal cortex

·    Leads to loss of tubular function and ability to concentrate urine:

o polyuria

o nocturia

o proteinuria

·    Significant cause of chronic kidney disease

·    Signs and symptoms:

o dysuria, urinary frequency, urgency and nocturia – occur due to urine irritating the inflamed bladder wall

o pyuria and foul odour – cloudy urine caused by the inflammatory response and causes the bladder mucus to suppurate; sloughing of the dead cells occurs and causes cloudy appearance

o haematuria caused by inflammation of the bladder mucosa. Mucosa becomes hyperaemic and may haemorrhage

o suprapubic pain caused primarily by distension and increased pressure within the tract. Severity of pain is related to the rate at which inflammation and develop and not the degree

o systemic signs of infection, e.g. raised temperature, increased CRP, WCC

Answer: 

• Escherichia coli
• Klebsiella
• Pseudomonas
• Staphylococcus

Answer: 

• Urinary tract obstruction: calculi, scarring and stricture, tumours, congenital defects
• Neurogenic bladder: bladder dysfunction that may be either flaccid or spastic. It is caused by neurological damage e.g. stroke, spinal injury, MS, tumours
• Vesicoureteral reflux: normal ureteral insertion into the bladder is a competent one-way valve that prevents retrograde flow of urine, especially during micturition. The ureter usually enters the bladder at a steep angle and courses parallel to the bladder wall forming a mucosal flap, the flap becomes compressed against the wall of bladder during micturition preventing urine being forced into the ureter. However, in vesicoureteal reflux the ureter enters the bladder at a right-angle therefore a flap is not formed so urine is forced into the ureter during micturition. Causes: congenital defect in length, diameter or muscle structure
• Congenital/Acquired: urinary tract obstruction – tumour or calculi, structural abnormalities, impaired bladder innervation, bowel incontinence, chronic diseases, e.g. diabetes
• Sexual intercourse: bacteria enter the bladder through the urethera Some women lack a normally protective mucousal enzyme and have decreased levels of cervicovaginal antibodies to enterobacteria
• Female:
  • short straight ureter
  • proximity of urinary meatus to vagina and anus
  • sexual intercourse
  • pregnancy
• Male:
  • uncircumcised
  • prostatic hypertrophy

Answer: 

• Calcium – formed from calcium and may be due to hypercalcaemia, hyercalcuria, excessive bone resorption caused by hyperparathyroidism, vitamin D intoxication or renal tubule acidosis. Calcium stones are the most common type of kidney stones accounting for 70–80%.
• Magnesium ammonium phosphate (struvite stones) – formed in alkaline urine in the presence of bacteria that possess urase (an enzyme that splits urea in the urine into ammonium and carbon dioxide) (urea-splitting UTI). The ammonia ion picks up a hydrogen ion, now ammonium, thereby increasing the pH and alkalinity of the urine. Magnesium is always present in urine, however, due to increased alkalinity, phosphate levels in the urine increase. Together, magnesium and phosphate combine to form struvite stones. Bacterial growth results in the stone continuing to increase in size and, due to its shape, they can eventually be known as staghorn stones.
• Uric acid – formed due to high concentrations of uric acid in urine and gout. They form most readily when the pH of urine ranges from 5.1–5.9.
• Cystine – due to an inherited disorder of amino acid metabolism called cystinuria (genetic defect in renal transport of cystine). Whilst they cause less than one per cent of all kidney stones, they account for a high proportion of calculi in childhood.

Answer: 

Type of AKI	Causes
Volume-responsive AKI	Resulting from decreased blood supply to the kidneys (glomeruli and renal tubule undamaged)
Intrinsic AKI	Resulting from abnormalities within the kidney, including damage to the blood vessels, glomeruli and tubules
Postrenal AKI	Resulting from an obstruction in the urinary collection system may arise anywhere from renal pelvis to urethra

Answer: 

• Initiation: Initially volume-responsive AKI causes ischaemia, hypoxic damage causes intracellular oedema and, if unreversed, cell death. Oliguria usually occurs within 2 days and may last up to 2 weeks. As renal function declines (decreased GFR) urine output decreases, serum urea and creatinine levels rise.
• Established or maintenance (oliguric): Cell damage releases vasoactive cytokines leading to further intrarenal vasoconstriction. Preglomerular vasoconstriction reduces glomerular perfusion and thus glomerular filtration. Widespread intracellular oedema physically compresses lumens obstructing flow of the filtrate produced. Medullary damage reduces sodium reabsorption in the loop of Henle (Urinary sodium is high). Serum urea and creatinine levels continue to rise. Oliguria and anuria persists throughout the established phase. There is a marked decrease in GFR metabolites eg urea, potassium, creatinine are now retained. Urinary output is at it’s lowest point and results in oedema, water intoxication and pulmonary congestion. If oliguria persists it will result in hypertension and uraemia.
• Recovery or diuretic: Tubular cells readily regenerate and the recovery phase begins as they do. As damaged tubules recover function and new (immature) tubule cells grow, filtration improves but tubular reabsorption and solute exchange remain poor. Large quantities of poor quality urine are produced; serum urea and creatinine remain high although they start to decrease. When tubular cells mature, normal function is recovered; urine volumes return to normal and electrolyte balance is restored. Return to normal renal function can take from 3 to 12 months

Answer: 

• Diabetic nephropathy: in diabetes, microvasculature in the organ systems of the body, including kidney, is damaged. In the kidney afferent and efferent arterioles and glomerular capillaries are affected. Glomerular thickening, deposits of IgG and albumin and diffuse glomerulosclerosis. Late nephropathy tubular atrophy, interstitial fibrosis also occur. Physiological mechanism unclear but hyperglycaemia major contributor. ESDR develops in 7–10 years.
• Hypertensive nephrosclerosis: involves development of sclerotic lesions in the renal arterioles and glomerular capillaries that cause them to become thickened and narrowed and eventually necrotic. Benign – renal impairment occurs over many years, malignant associated with malignant hypertension can lead to permanent renal failure rapidly if B/P is not immediately reduced
• Signs and symptoms: Do not become evident until late because of the kidney’s ability to compensate. As nephrons are destroyed the remaining nephrons undergo structural and functional hypertrophy each increasing its function as a means of compensating for those that have been lost. This hyperfiltration can maintain excretory and homeostatic mechanisms even when up to 70% of nephrons are damaged. However, intact nephrons reach a point of maximal filtration and any additional loss of glomerular mass is accompanied by an incremental loss in GFR and subsequent accumulation of filterable toxins. Mechanisms involved in progressive destruction of nephrons depend upon primary cause of renal failure. Secondary insults can rapidly accelerate the process of nephron loss, e.g. alteration in renal perfusion (CCF, intravascular volume depletion), administration of nephrotoxic drugs, urinary obstruction and infections).
  • polyuria – frequency and nocturia
  • anorexia, unintended weight loss
  • fatigue
  • nausea
  • anaemia
  • hypertension

Answer: 

• Stage 1: evidence of chronic kidney damage – persistent microalbuminuria, persistent proteinuria, persistent haematuria, structural abnormalities, biopsy-proven glomerulonephritis.
• Stage 2: Characterised by 40–50% loss of renal function. Kidneys still able to maintain excretory and regulatory functions, patients typically asymptomatic. Early signs of renal failure, e.g. increased BUN/creatinine levels only evident after 50–60% loss. Proteinuria or haematuria evident.
• Stage 3: Residual function is only 20–40% of normal by this time solute clearance ability to concentrate urine and hormone secretion are compromised. Signs of renal failure start to manifest, e.g. fatigue, polyuria and nocturia.
• Stage 4 and 5: Characterised by residual renal function of <15% of normal. Normal regulatory, excretory and hormonal functions are severely impaired. ESRD/ESKD evidenced by marked increases in BUN creatinine clearance, anaemia electrolyte imbalances and fluid overload.

Answer: 

There are three main types of urinary incontinence:

• stress incontinence

• urge incontinence

• overflow incontinence

Answer: The incidence of urinary Incontinence increases with age and it can lead to social isolation and skin breakdown and infections. Physiological changes in ageing such as diminished detrusor muscle strength and muscle mass, reduced blood flow and alterations in nervous control contribute to the development of incontinence. Added to this reduced mobility and comorbidities such as dementia, constipation and infections and medications can all precipitate incontinence.