Urinary System Flashcards
Describe the alterations to the filtrate as it travels along the nephron:
Filtration occurs at glomerulus, pressure is maintained by specialised circulation. In PCT reabsorption occurs via peri tubular capillaries but filtrate remains isotonic. Further reabsorption and countercurrent multiplication occurs in the loop of Henle allowing the formation of concentrated urine. DCT continues reabsorption of water and electrolytes to produce a hypotonic secretion. In the collecting duct water can be further reabsorbed by inserting Aquaporins using ADH.
Describe the development of the kidney from the intermediate mesoderm of the trilaminar disc:
Pronephros develops pronephric duct which drives development.
Mesonephros develops caudally and mesonephric duct sprouts ureteric bud to induce development = embryonic kidney.
Metanephros develops in caudal region (definitive kidney), differentiation driven by ureteric buds action on metanephric blastema.
Ascent of metanephric kidney from pelvic region crossing arterial fork formed by vessels returning blood to placenta.
What is the urogenital ridge?
Region of intermediate mesoderm gives rise to the embryonic kidney and the gonad
What causes renal agenesis?
Ureteric bud fails to interact with the metanephric blastema causing oligohydramnios.
What is a Wilm’s tumour?
Nephroblastoma, malignant tumour containing metanephric blastema, stroma and epithelial derivatives.
What is the cloaca?
Single structure where GI, urinary and reproductive tracts end in region of the hind gut.
What is the urachus?
Fibrous remnant of canal that drains foetal bladder (allentois) that becomes median umbilical ligament.
How is the male urethra formed?
The mesonephric ducts make independent openings in the urogenital sinus and the prostate and prostatic urethra are formed.
What are the functions of the kidneys?
Regulation and control of concentrations of substances in extracellular fluid
Excretion of waste products
Endocrine- synthesis of renin, erythropoietin, prostaglandins
Metabolism- activation of vitamin D, catabolism Of insulin, PTH and calcitonin
Regulation of acid-base balance
Describe the alterations to the filtrate as it travels along the nephron:
Filtration occurs at glomerulus, pressure is maintained by specialised circulation. In PCT reabsorption occurs via peri tubular capillaries but filtrate remains isotonic. Further reabsorption and countercurrent multiplication occurs in the loop of Henle allowing the formation of concentrated urine. DCT continues reabsorption of water and electrolytes to produce a hypotonic secretion. In the collecting duct water can be further reabsorbed by inserting Aquaporins using ADH.
Describe the development of the kidney from the intermediate mesoderm of the trilaminar disc:
Pronephros develops pronephric duct which drives development.
Mesonephros develops caudally and mesonephric duct sprouts ureteric bud to induce development = embryonic kidney.
Metanephros develops in caudal region (definitive kidney), differentiation driven by ureteric buds action on metanephric blastema.
Ascent of metanephric kidney from pelvic region crossing arterial fork formed by vessels returning blood to placenta.
What is the urogenital ridge?
Region of intermediate mesoderm gives rise to the embryonic kidney and the gonad
What causes renal agenesis?
Ureteric bud fails to interact with the metanephric blastema causing oligohydramnios.
What is a Wilm’s tumour?
Nephroblastoma, malignant tumour containing metanephric blastema, stroma and epithelial derivatives.
What is the cloaca?
Single structure where GI, urinary and reproductive tracts end in region of the hind gut.
What is the urachus?
Fibrous remnant of canal that drains foetal bladder (allentois) that becomes median umbilical ligament.
How is the male urethra formed?
The mesonephric ducts make independent openings in the urogenital sinus and the prostate and prostatic urethra are formed.
What are the functions of the kidneys?
Regulation and control of concentrations of substances in extracellular fluid
Excretion of waste products
Endocrine- synthesis of renin, erythropoietin, prostaglandins
Metabolism- activation of vitamin D, catabolism Of insulin, PTH and calcitonin
Regulation of acid-base balance
How is the female urethra formed?
The mesonephric ducts regress and the ureteric bud opens into the urogenital sinus, the female urethera is formed by the pelvic part of the urogenital sinus.
How are external genitalia formed?
By the genital tubercle, folds and swellings. In males the GT elongates and the folds fuse to form the spongy urethra, in females there is no fusion and the urethra opens into the vestibule.
What is a fistula?
Abnormal connection between two hollow spaces e.g. Urorectal fistulae.
What causes hypospadias?
Direct fusion of urethral folds so urethra opens onto ventral surface rather than the end of the glans
What is meant by a renal corpuscle?
Primitive renal tubule derived from ureteric bud grows into primordium of true kidney and envelops the glomerulus.
What makes up the bowman’s capsule?
Simple squamous parietal and visceral layers and pod oxygen with food processes and filtration slits that share a basement membrane with the capillary endothelium.
What epithelium is used in each part of the nephron?
PCT- simple cuboidal with brush border Descending Loop of Henle- simple squamous Thick ascending limb-simple cuboidal DCT- simple cuboidal Collecting duct- simple cuboidal
What makes up the juxtoglomerular apparatus?
Macula densa, juxtaglomerular cells of afferent arteriole, extra glomerular mesangial cells
What are the differences between cortical and juxtamedullary nephrons?
The loop of Henle in juxtamedullary nephrons is longer and these nephrons have vasa recta instead of peri tubular capillaries.
Explain the pressures acting on the filtrate at the glomerular tuft:
Hydrostatic pressure in capillary forcing filtrate out
Hydrostatic pressure of bowman’s capsule forcing filtrate back in
Oncotic pressure difference forcing filtrate back in
Explain what is meant by autoregulation?
Keeps GFR normal limits (80-180mmHg).
Myogenic- smooth muscle reacts to being stretched by constricting
Tubular glomerular feedback- macula densa acts as a sensor, concentration-dependent salt uptake through NaK2Cl cotransporters. Increased GFR leads to increased sodium and chloride delivery which stimulates the JGA to release adenosine for vasoconstriction and prostaglandins for vasodilatation.
How are solutes and water reabsorbed in the PCT:
Sodium moves down its concentration gradient into the apical cells using the gradient established by the sodium-potassium-ATPase. Sodium and glucose are also reabsorbed via a cotransporter.
What transporters are used to reabsorb sodium in the nephron?
PCT- Na-H antiporter, Na-glucose symporter
Loop of Henle- NaK2Cl symporter
DCT- NaCl symporter and ENaC
How does secretion occur in the nephron?
By transepithelial transport using an Na-H antiporter driving the cation exchanger and passive carrier-mediated diffusion down favourable gradients.
What is the filtration fraction?
Proportion of the substance that is actually filtered
What is meant by renal clearance?
The volume of plasma that is completely cleared of a substance by the kidneys per minute
How is renal clearance calculated?
(Substance concentration in urine X volume of urine) / concentration of urine in plasma
What features must a substance have to be used to determine GFR?
Freely filtered
Detectable
Unable to be secreted/reabsorbed
How would you calculate eGFR?
(140-age) X mass(kg) X constant // serum creatinine
What is the filtered load?
Amount of substance that is freely filtered that enters the renal tubule. Calculated as plasma conc X GFR
What is the renal threshold?
Plasma concentration of a substance at which transport maximum (Tm) is reached and the substance spills into urine
What is glomerulotubular balance?
Blunting of Na+ excretion in response to GFR changes so if GFR spontaneously increases the rate of sodium and water reabsorption increases proportionally.
How are solutes reabsorbed along the loop of Henle?
Paracellular uptake of water in descending limb leading to high concentration of solutes in filtrate at loop. Sodium is reabsorbed passively paracellularly in the thin ascending limb. In the thick ascending limb there is active sodium and chloride uptake through the NaK2Cl channel but it is impermeable to water so fluid leaving the loop is hypo-osmotic.
What cotransporters are in the DCT that allow reabsorption of sodium and therefore water?
NCC transporter on apical membrane
NCX exchanger on basolateral membrane
Gradient established by sodium-potassium ATPase
What are the effectors of change in volume control?
Changes in osmotic pressure and hydrostatic pressure causing changes in GFR.
Sodium reabsorption in PCT stimulated by RAAS
Principle cells of CD and DCT affected by aldosterone
What is the RAAS?
RAAS is responsible for long term regulation of blood pressure.
Renin released from granular cells of JGA, stimulated by NaCl delivery, reduced perfusion pressure or sympathetic stimulation.
Renin converts angiotensin to angiotensin I which is then converted to angiotensin II by ACE present on epithelial cells.
Angiotensin II stimulates aldosterone release.
What are the actions of angiotensin II?
Vasoconstrictor, causes ADH, aldosterone and noradrenaline release, stimulates sodium reabsorption via Na-H exchanger.
What is the action of aldosterone?
Acts on principal cells to stimulate sodium and water reabsorption via ENaC channels and stimulates sodium-potassium-ATPase
What is the effect of sympathetic stimulation on the kidney?
Causes vasoconstriction thus decreasing GFR and sodium excretion. Activates the Na/H exchanger and basolateral sodium-potassium-ATPase. Stimulates release of renin from JGA.
What are natriuretic peptides?
Synthesised and stored in atrial myocytes released in response to stretch and low pressure volume sensors in the atria.
Decreased ECV inhibits release of ANP to increase BP.
How do NSAIDs affect the kidney?
Inhibit cyclo-oxygenase pathway that results in prostaglandin formation (vasodilators).
How does dopamine affect the kidney?
Formed locally in kidney from circulating L-DOPA causing vasodilation and increased renal blood flow thus reducing sodium chloride reabsorption by inhibiting NH exchanger in principal cell membranes
How does renovascular disease lead to hypertension?
Renal artery stenosis causes decreased perfusion so increased renin.
How does renal parenchymal disease lead to hypertension?
Early loss of vasodilator substances and later sodium and water retention due to inadequate glomerular filtration
What is Conn’s syndrome?
Aldosterone secreting adenoma
How would you manage a patient with chronic hypertension?
ACE inhibitors, angiotensin II receptor antagonists, thiazides/spironolactone, vasodilators and potentially beta-blockers
Where are osmoreceptors located exactly?
The organum vasculoum of the lamina terminalis (OVLT) anterior and ventral to the third ventricle in the hypothalamus
What is the effect of ADH on plasma osmolarity?
ADH receptors when activated cause the change of ATP to cAMP by adenylyl cyclase which then activates PKA to insert AQP2 channels into the apical membrane of the collecting duct thus increasing retention of water.
What are the consequences of ADH?
Vasoconstriction that reduces GFR
Increased solute reabsorption in thick ascending limb
Increased water reabsorption and potassium secretion
Increased water and urea reabsorption in the medulla
What is diabetes insipidus?
Pituitary gland does not produce enough ADH/acquired ADH insensitivity
What is syndrome of inappropriate ADH secretion?
Excessive ADH release from posterior pituitary or ectopically leading to dilutional hyponatraemia and increased total body fluid
How is the corticopapillary osmotic gradient established?
Urea acts as an effective osmole. Vasa recta act as a countercurrent exchanger in a hair pin configuration. Urea moves out of the collecting duct with water and then diffuses back into the thick ascending limb thus increasing the osmolarity of interstitium. This creates the hyper osmotic medullary interstitium.
How is active vitamin D produced?
Cholecalciferol produced in the skin using UVB, hydroxylated in the liver to produce 25-(OH) vitamin D (calcidiol) and then again in the kidney to produce calictriol. (Kidney hydroxylation stimulated by PTH).
What are the actions of calcitriol?
Increases intestinal uptake, promotes osteoblasts activity and maturation of osteoclasts, promotes conversion to inert vitamin D and inhibits use of absorbed phosphate
What does calcitonin do?
Stimulated by rise in plasma calcium concentration, and causes a rapid fall in calcium by inhibition of reabsorption and renal tubular cell reabsorption.
What are causes of hypercalcaemia?
Malignancy, primary hyperparathyroidism, sarcoidosis, lithium etc.
What are the clinical manifestations of hypercalcaemia?
Anorexia, nausea, vomiting, constipation, pancreatitis, hypertension, sensitivity to digoxin, polyuria, polydipsia, nephrocalcinosis, cognitive difficulties, depression
What can cause hypercalcaemia of malignancy?
Parathyroid hormone-related peptides (PTHrP)
Ectopic PTH
Cytokines
1,25-dihydroxyvitamin D granuloma
How would you manage acute hypercalcaemia?
Saline (sodium causes calcium loss)
Loop diuretics
Bisphosphonates
Calcitonin
What types of renal stones are there?
Calcium oxalate/phosphate Magnesium ammonium phosphate Urate Cysteine Xanthine
Explain the pathogenesis of renal stone formation:
Supersaturation of urine with solutes, product of free ion activities of stone components. Solubility is affected by urine pH, volume and excretion.
What investigations would you perform for renal stones?
History, blood screens, urinalysis, urine culture, radio graphic, non-contrast CT, ultrasound
How do you manage renal stones?
Small stones pass spontaneously
Larger stones treated by extra corporeal shockwave lithotripsy, ureteroscopy, per cutaneous nephrolithotomy or open surgery
Dietary restrictions and increase of fluid intake
How are changes in plasma pH detected?
Peripheral chemoreceptors in aortic sinuses detect changes in pH
How does the kidney compensate for changes in pH?
Varying excretion/production of bicarbonate (from CO2 and amino acids such as glutamine).
Bicarbonate is ordinarily recovered in the PCT; NHE moves H+ into the lumen where it combines with bicarbonate to produce water and CO2 which enters the cell effectively removing bicarbonate from the lumen.
What is the response of tubular cells to acidosis?
Decreased pH enhances activity of NHE and ammonium production in proximal tubule and increases activity of proton pump in DCT so there is an increased capacity to export HCO3- into the ECF
What is the significance of maintaining a high intracellular potassium and low extracellular potassium concentration?
Generates a gradient for the resting membrane potential, thus increasing outside potassium decreases the gradient leading to depolarisation and decreasing the extracellular potassium leads to hyperpolarisation
What happens to potassium levels following a meal?
The intestines absorb dietary potassium which quickly moves into cells, after a delay kidneys excrete potassium. Intracellular buffering is necessary as potassium is later released from cells so it can be excreted by the kidney.
What can drive potassium into cells?
Insulin, aldosterone and catecholamines
Increased potassium in the ECF
Alkalosis causes a reciprocal shift of H+ to K+
What can cause potassium to move out of cells via ROMKs?
Exercise- skeletal muscle contraction releases K+
Cell lysis e.g. Rhabdomyolysis and chemotherapy
Increased plasma tonic its e.g. DKA causes water to move into ECF so conc of potassium intracellularly increases thus generating a gradient
Acidosis causes reciprocal shift
How do kidneys adjust K+ excretion and secretion?
K+ is freely filtered then reabsorbed at PCT and Loop of Henle
K+ reabsorbed paracellularly in PCT actively by NaKCC2 in thick ascending limb.
K+ is secreted by DCT principal cells. Movement of sodium via ENaC channels creates a favourable electrochemical gradient for K+ secretions via apical potassium channels.
What factors affect potassium secretion?
Concentration of potassium on ECF stimulates sodium-potassium-ATPase and increases permeability of potassium channels on apical membrane.
Aldosterone increases transcription of above channels.
Acid-base status
Increased distal tubular flow rate washes away luminal K+ so increases potassium loss.
Increased sodium delivery to distal tubule causes increased sodium reabsorption thus promoting potassium secretion
What are the effects of hyperkalaemia?
Arrhythmia, heart block, paralytic ileus, acidosis, high T waves, prolonged PR interval, widening QRS complex, VF
What causes hyperkalaemia?
Increased intake Decreased excretion e.g. AKI, ACEi, low aldosterone DKA Cell lysis Metabolic acidosis
How would you manage a hyperkalaemic patient?
IV insulin and glucose
Calcium gluconate
Nebulised beta agonists
What causes hypokalaemia?
Diarrhoea, vomiting, diuretics, high aldosterone promoting excessive loss
Metabolic alkalosis
What are the clinical features of hypokalaemia?
Arrhythmia, paralytic ileus, muscle weakness, nephrogenic DI, low T wave
How do you treat hypokalaemia?
IV potassium replacement and potassium-sparing diuretics that block aldosterone on principal cells
What factors may predispose a patent to a UTI?
Shorter urethra in females, obstruction (e.g. Prostate, pregnancy, stones, tumours), neurological, ureteric reflux
What features of a bacteria may allow it to successfully invade the urinary system?
Fimbrae for attachment
K antigen permits polysaccharide capsule
Urease creates favourable environment
Haemolysins
What clinical syndromes are associated with urinary tract infection?
Frequency and dysuria
Acute pyelonephritis
Chronic nephritis
Septicaemia and shock
How would you investigate a suspected UTI?
Nitrites, leucocyte esterases and urine culture (mid stream urine sample best to eliminate contaminants)
What are the sensitivity and specificity of nitrite and leucocyte esterases tests?
Nitrite testing is very specific but not sensitive
Leucocyte esterase testing is very sensitive but less specific
How would you treat a UTI?
3 day course of trimethoprim for uncomplicated
7 day course for complicated
Pyelonephritis is a 14 day course of Ciprofloxacin or Cefuroxime
Give an example of a loop diuretic and explain its mechanism of action:
Furosemide
Blocks NaK2Cl transporter in loop of Henle
Give an example of a thiazide and explain its mechanism of action:
Bendroflumethiazide
Blocks the NaCl transporter in early DCT
Give an example of a potassium sparing sodium channel inhibitor and explain its mechanism of action:
Amiloride
Blocks ENaC
What is spironolactone?
A competitive aldosterone inhibitor. It is potassium sparing
Give an example of an osmotic diuretic and its action:
Mannitol
Increases osmolarity of filtrate so reduces sodium and water reabsorption throughout the tubule
What are the muscles of the bladder and its sphincters and their innervation?
Destructor urinae muscle supplied by the pelvic nerve (S2-4)
Internal urethral sphincter is physiological and sympathetic supplied by the hypogastric nerve (T10-L2)
External urethral sphincter is under somatic control of the muscles of the pelvic floor (levator anni) and is supplied by the pudendal nerve (S2-4)
What occurs during the continence phase of micturition?
Receptive relaxation- intravesicular pressure doesn’t increase with filling due to increasing sympathetic innervation that further relaxes the bladder. Rugae flatten and bladder capacity increases, throughout the external urethral sphincter is closed.
What occurs during the voiding phase of micturition?
Parasympathetic innervation to the detrusor muscle causes it to contract increasing intravesicular pressure. The internal urethral sphincter relaxes and there is voluntary relaxation of the external urethral sphincter. This process is controlled by Barrington’s nucleus.
What would the effect of a lower motor neurone lesion be on urinary continence?
Decreased detrusor pressure leading to residual urine and overflow incontinence
What would the effect of an upper motor neurone lesion be on urinary continence?
Dilated ureters, thickening of the detrusor muscle and increased detrusor pressure causing detrusor sphincter dyssynergia
What are the three main types of urinary incontinence?
Stress urinary incontinence
Urge urinary incontinence
Overflow incontinence
Name common symptoms that accompany urinary incontinence:
Frequency Urgency Nocturia Hesitancy/terminal dribble Splitting/spray stream
What examinations would you perform for suspected urinary incontinence?
Abdominal examination, DRE, vaginal exam and external genitalia stress test in females.
What investigations would you use for a patient with urinary incontinence?
Urine dipstick, urodynamics e.g. Frequency-volume chart, pressure-flow studies, pad tests, cytoscopy
How would you manage a patient with urinary incontinence?
Modify fluid intake Decrease caffeine intake Timed voiding on a fixed schedule Indwelling catheter Sheath device Incontinence pads
What specific steps can be used to manage stress incontinence?
Pelvic floor muscle training
Duloxetine- noradrenaline and serotonin uptake inhibitor to increase EUS activity
Surgery e.g. Sling procedures
How would you specifically manage urge urinary incontinence?
Bladder training
Anticholinergics
Beta-3 adrenoceptor agonists to increase capacity to store urine
What is AKI?
Clinical syndrome where there is an abrupt decline in actual GFR leading to upset ECF volume, electrolyte and acid-base homeostasis and accumulation of nitrogenous waste productions.
What are the KDIGO definitions for AKI?
Increased serum creatinine > 26.5 umol/L within 48 hours
Increased serum creatinine > 1.5x baseline within 7 days
Urine volume
Give examples of what can cause AKI:
Pre-renal- volume depletion, heart failure, cirrhosis
Intrinsic renal- glomerulonephritis, ischaemic ATN
Post-renal- obstruction
What happens in pre-renal AKI?
Actual GFR decreased due to decreased renal blood flow
No cell damage
Responds to fluid resuscitation
Intrarenal polycyclins high to decrease afferent tone and circulating vasoconstrictors to increase efferent tone
AKI occurs when compensatory mechanisms (autoregulation) are overwhelmed
What is acute tubular necrosis?
Caused by ischaemia, sepsis and nephrotoxins. Damaged cells cannot resort salt and water efficiently or expel excess water so fluid resuscitation leads to fluid overload.
What causes glomerular arteriolar disease?
Acute glomerulonephritis e.g. IgA nephropathy Haemolytic uraemic syndrome Malignant hypertension Pre-eclampsia Pyelonephritis
What can cause obstruction?
Must block both kidneys, or single functional kidney.
Obstruction with continuous urine production leading to increased intraluminal pressure leading to hydronephrosis.
Stones, clots, tumours, congenital megaureter, enlarged prostate, aortic aneurysm, haematuria, anuria, loin-groin pain.
What potential complications are there of AKI?
Hyperkalaemia
Hyponatraemia
Hypocalcaemia
What investigations would you carry out for suspected AKI?
Urinalysis, urine microscopy, ultrasound, CXR, kidney biopsy
How would you manage a patient with AKI?
Restrict fluids to prevent volume overload
Treat hyperkalaemia with dextrose and insulin
Treat acidosis with sodium bicarbonate
Dialysis is required when high potassium is persisting, if bicarbonate doesn’t resolve acidosis, persisting fluid overload despite diuretics, or if there is a dialysable nephrotoxins e.g. Aspirin
What are the features of nephrotic syndrome?
Proteinuria, hypoalbuminaemia, oedema with insidious onset
What are the features of nephritic syndrome?
Abrupt onset, classically accompanies post-streptococcal glomerulonephritis infection in children
Oliguria, hypertension, generalised oedema, haematuria, normal albumin, renal impairment
What is rapidly progressive glomerulonephritis?
Renal function deteriorates over days, presents as a uraemic emergency
Associated with systemic vasculitis, crescenteric glomerulonephritis
What is minimal change glomerulonephritis?
Common in childhood/adolescence
Heavy proteinuria with no progression to renal failure
Responds to steroids but may recur
What is focal segmental glomerulosclerosis?
Nephrotic syndrome in adults caused by a circulating factor that damages podocytes, may progress to renal failure
What is membranous glomerulonephritis?
Commonest cause of nephrotic syndrome in adults, subepithelial immune complex deposits targeted into phospholipase A2 receptors (IgG)
What is IgA nephropathy?
Has relationship to mucosal infection
May have proteinuria, haematuria, nephritic syndrome
Causes mesangial damage by deposition of circulating IgA immune complexes
What is Alport’s syndrome?
Hereditary nephropathy
X-linked abnormality of collagen IV
What is Goodpasture syndrome?
Rapidly progressive glomerulonephritis with acute onset of severe nephritic syndrome
Classic association with pulmonary haemorrhage in smokers
Auto antibody to collagen IV (IgG)
Treatable with immunosuppression and plasmaphoresis
What is vasculitis?
Group of systemic disorders with no immune complex/antibody deposition
Segmental crescenteric necrosis
Association with anti-neutrophil cytoplasmic antibody which causes neutrophils to attack endothelium
How might a patient present with prostate cancer and what are the risk factors?
Urinary symptoms, bone pain, most patients a symptomatic.
Age, family history, BRCA2, ethnicity
How would you treat prostate cancer?
Surveillance, radical prostatectomy, radiotherapy
Hormones (LHRH agonists), zonedronic acid, chemotherapy
What are the risk factors for bladder cancer?
Smoking, schistosomiasis, occupational exposure e.g. hair dyes, smelting, rubber/plastics
How can you treat bladder cancer?
Transurethral resection, intravesicular installation of mitomyosin C, radical cystectomy, chemotherapy and radiotherapy
How would you diagnose and treat renal cell carcinoma?
Ultrasound, CT-guided biopsy
Surveillance, nephrectomy, ablation or molecular therapies targeting angiogenesis
How would you investigate and treat upper tract transitional cell carcinoma?
Ultrasound, CT urogram, retrograde pyelogram, ureteroscopy
Treated by nephro-ureterectomy
What is chronic kidney disease?
Irreversible and sometimes progressive loss of renal function over a period of months to years. Renal injury causes the replacement of renal tissue by extracellular matrix on response to tissue damage.
What can cause chronic kidney disease?
Obstruction/reflux nephropathy, hypertension, diabetes/myeloma, glomerulonephritis, pyelonephritis, polycystic kidneys, Alport’s syndrome
What investigations would you carry out of you suspected CKD?
Auto antibody/complement/Ig etc
Imaging
What are potential complications of CKD?
Acidosis- may affect muscle, bone and renal function, treated with oral sodium bicarbonate tablets
Anaemia- decreased EPO and RBC survival
Metabolic bone disease- decreased GFR leads to decreased hydroxylation of vitamin D and phosphate retention thus decreasing calcium retention leading to hypocalcaemia
How can you prevent the progression of CKD using management?
Treat existing conditions Reduce smoking and obesity Increase exercise Give ACEi to reduce proteinuria Lower lipids
What are the symptoms of end-stage renal failure?
Fatigue, difficulty sleeping, volume overload, nausea, pruritis, sexual dysfunction
What are the principles of haemodialysis?
Flow in a countercurrent fashion creates a concentration gradient
Uses primary arteriovenous radiocephalic fistula
Contraindicated by heart failure and coagulopathy due to risk of thrombosis and bleeding
Discuss the advantages and disadvantages of haemodialysis?
Adv: less responsibility for care, more days off from treatment
Disadv: travel time and waiting, ‘tied’ to dialysis times, restrictions on fluid intake/diet
Explain the principles of peritoneal dialysis:
Catheter inserted into the peritoneum, highly concentrated dialysate draws water out
CAPD- 4-5 bag changes per day
APD- overnight dialysis
Contraindicated by adhesions, previous abdominal surgery, hernias, large muscle mass or obese (peritoneal surface area too small)
Discuss the advantages and disadvantages of peritoneal dialysis:
Adv: self sufficiency/independence, fewer diet restrictions, easy to travel
Disadv: frequent daily exchanges, patient responsibility
What are the principles of renal transplant?
Reduced mortality and morbidity plus better quality of life
Peri-operative risk, malignancy/infection risk due to immunosuppression, risk of diabetes/hypertension from meds
Tissue match must be ABO and HLA
Donors may be live, deceased after brain death or deceased after circulatory death
