Urinary System Flashcards
What is the predominant cation and anion in the extracellular fluid?
cation is sodium and anion is chloride
How do the kidneys affect the intra-cellular composition of ions?
By directly affecting the concentration of ions and small molecules in the ECF
How is ultra-filtrate different to plasma?
Ultra-fitrate doesn’t contain cells and large organic molecules that are found in plasma
What are the 5 main functions of the urinary system?
Control the concentration of substances in the ECF and therefore control the osmolarity of the ECF. Also, to control pH, excrete waste products and control the volume of ECF.
These then impact on blood pressure, cell function and cell size
From what type of mesoderm does the urinary system originate?
Intermediate mesoderm
What are the 3 embryological types of kidney systems and how are they different?
Pronephros is initial one, in cervical region. Never functions in humans but does involve nephrotomes and develops alongside a duct which runs from cervical region to cloaca.
Next is Mesonephros which develops caudally to pronephros. This is the embryonic kidney. It’s duct is functional but can’t conserve water so can’t concentrate urine. It also sprouts the ureteric bud which drives the development of the final stage.
Metanephros is last one, which starts off as metanephric blastema. This develops into the true kidney. The ureteric bud makes conact with the blastema and eventually develops into calyces and the renal pelvis
Through what developmental error, can there by duplication of the ureter?
By complete splitting of the ureteric bud
What are the three parts of the urogenital sinus?
Bladder part, pelvic and phallic sections
What are the four parts of the male urethra?
pre prostatic, prostatic, membranous and spongy
How many litres, roughly, of ECF are there?
About 15 litres
Roughly at which vertebral level, are the kidneys located?
T12-L3
Which are the three most common sites of blockage caused by kidney stones?
Junction of renal pelvis and ureter
Where ureter crosses pelvic brim
Where ureter enters bladder wall
What are supernumerary renal arteries?
Where there’s more than one renal artery going to one kidney
What parts of the nephron are located in the medulla?
Loop of Henle and collecting duct
What is the average GFR?
Roughly 125 ml/min
What are the two main sections of the renal corpuscle and what are they made up of?
Vascular pole - afferent and efferent arterioles and the glomerulus
Urinary pole - Bowman’s capsule
What makes up the filtration barrier of the renal corpuscle?
The visceral layer of bowman’s capsule (podocytes) and capillary endothelium (v leaky + fenestrated)
Where in the nephron is lined by simple squamous epithelium?
Glomerulus parietal layer and endothelium
Thin descending and ascending limb on loop of Henle
Everywhere else is simple cuboidal
Where in the loop of Henle does active transport not take place?
Thin limbs
What makes up the juxtaglomerular apparatus?
Macula densa
Juxtaglomerular cells of afferent arteriole
Extraglomerular mesangial cells
Compare the appearance of the collecting duct to the thick ascending limb
Both have simple cuboidal but collecting duct lumen is larger and less regular
Describe the path that collecting ducts take through the renal medulla
Ducts merge to form larger ducts. First form ducts of bellini, then renal papillae and then exit into calyx
What layers of smooth muscle are there in the urinary bladder?
2 Circular layers and 1 longitudinal
How does the diameter of glomerular arterioles contribute to filtration?
Diameter of afferent arteriole is always slightly bigger than the efferent arteriole so pressure of blood inside the glomerulus is increased so there’s increased hydrostatic pressure so filtration is promoted
What are the 3 forces involved in plasma filtration?
Hydrostatic pressure in cappilary
Hydrostatic pressure in capsule
Osmotic gradient between capillary and tubule
What types of sodium channels are found on apical membranes in different parts of the tubule?
PCT - Na-H antiporter and Na-GLucose symporter
Loop of Henle - Na-K-2Cl symporter
Early DCT - Na-Cl symporter
Late DCT and collecting tubule - ENaC
What is the Transport maximum?
Renal threshold for glucose = 200mg/ml
Point at which further increases in concentration do not result in increased filtration/excretion
How is clearance calculated?
(urine flow rate x amount in urine)/ arterial plasma concentration
What is the reference range for GFR in men and women?
Men = 115-125 ml/min Women = 90-100ml/min
How is renal plasma flow calculated?
Plasma makes up about 55% of renal blood flow. = 0.55 x rbf = 0.55 x 1.1 = 605ml/min
How is filtration fraction calculated?
= gfr divided by renal plasma flow
What is the autoregulatory response to decreased BP?
Dilation of afferent arteriole to increase hydrostatic pressure in capillary
What is the tubular glomerular feedback response to increased NaCl concentration?
GFR needs to decrease so juxtaglomerular apparatus is stimulated to release adenosine to cause vasoconstriction of afferent arteriole
What happens to ECF volume if sodium excretion is less than sodium uptake?
Sodium is retained, primarily in ECF so water leaves the nephron which increases ECF volume. There is therefore an increase in blood volume and arterial pressure and there may subsequently be oedema
What channels are there apically in Section 1 of the PCT?
Sodium/glucose co transporter
Na/H exchanger
Contransport of sodium with amino acids/ carboxylic acids/ phosphate
also aquaporin channels
What electrolyte transport occurs apically in S2/S3 of PCT?
Na/H exchange
paracellular and transcellular chloride transport
What are the driving forces behind water reabsorption of PCT?
Oncotic force of peritubular capillary
Osmotic gradient between tubule and interstitium
Hydrostatc force in intersitium
Describe sodium reabsorption in descending limb of loop of Henle
Doesn’t absorb sodium but instead has no tight gap junctions so there’s paracellular uptake of water
Describe sodium reabsorption of ascending limb
Descending limb concentrated filtrate so there’s reabsorption of sodium through NaKCC2 channel and secretion of potassium via ROMK channel.
Describe sodium reabsorption of DCT
Early DCT isn’t very permeable to water to is very diluting. Sodium is reabsorbed via Na/Cl- symporter. There’s also calcium reabsorption
Describe action of principle cells of collecting duct
70% of cells in CD are principal cells.
Reabsorb sodium through ENaC but this sets up electrical gradient in lumen for paracellular chloride uptake. Also variable uptake of water through aquaporin 2 channels, sensitive to ADH
What are the four neurohormonal factors that control blood pressure?
RAAS
Natriuretic peptide hormone
ADH
sympathetic nervous system
How does the sympathetic nervous system act to increase blood pressure?
Acts on alpha1 receptors to cause vasoconstriction of afferent and efferent arterioles to decrease renal blood flow and so GFR. This stimulate reabsorption of sodium via NHE of PCT. Also stimulates renin release
Also acts on beta1 receptors to increase rate and force of heart contraction
How does atrial natriuretic peptide act to control blood pressure?
Release from atrial myocytes in response to stretch (increased BP) cause vasodilation of afferent arteriole of glomerulus to increase sodium excretion by increasing GFR
When is renin released?
Due to reduced perfusion pressure at baroreceptors in afferent arteriole of kidney.
Also due to reduced NaCl concentration at macula densa. Granular cells of juxtaglomerular apparatus is sympathetically stimulated to release renin
How does renin lead to angiotensin 2 production?
Renin cleaves angiotensinogen into angiotensin 1. this is cleaved into angiotensin 2 by ACE
What actions does angiotensin 2 have?
Breaks down bradykinin to reduce vasodilation
Acts on vascular smooth muscle to cause vasoconstriction of arterioles
Acts on PCT to increase sodium reabsorption.
Acts of principal cells of collecting duct to stimulate sodium reabsorption via ENaC channels
Stimulates release of noradrenaline
Stimulates release of ADH from hypothalamus
What action does ADH have?
Inserts aquaporins into apical membrane of principal cells in collecting duct to increase water retention
Stimulates NaK2Cl in thick ascending limb to increase sodium reabsorption
Why are prostaglandins important in blood pressure control?
Have vasodilation action and locally act to enhance glomerular filtration and decrease sodium reabsorption. Act as a buffer to excessive vasoconstriction caused by SNS and RAAS
Why are NSAIDs dangerous to give to patients with renal/cardiovascular disease?
Inhibit formation of prostaglandins so in renal disease, cause further vasoconstriction so further reduction of GFR and can cause acute renal failure.
Can exacerbate heart failure and hypertension by increasing sodium and so water retention.
What are some adrenal causes of secondary hypertension?
Conn’s syndrome - aldosterone secreting adenoma
Cushing’s syndrome
Phaeochromocytoma - tumour of adrenal medulla
How does renovascular disease cause hypertension?
Occlusion of renal artery decreases perfusion pressure in that kidney so renin is stimulated to be released from JGA cells causing vasoconstriction and increased sodium reabsorption in other kidney
How can hypertension be treated?
ACE inhibitors
Thiazide diuretics - inhibit Na/Cl cotransporter in DCT but can cause hypokalaemia
Beta blockers to decrease heart rate and contractility
vasodilators - alpha1 blockers reduce sympathetic tone
calcium channel blockers reduce entry into smooth muscle cells
What is the steady osmolality of body fluid?
275-295 mOsm/kg
Where are changes in osmolarity detected?
By osmoreceptors in Organum Vasuloum of the Laminae Terminalis in the hypothalamus
What maintains the concentration gradient set up by the loop of Henle and counter current multiplication?
Counter current exchange by Vasa Recta
Where is ADH released from?
Posterior pituitary gland
What effects does ADH have on different parts of the nephron?
Vasoconstriction of afferent arteriole
Increased Na, K and Cl reabsorption in TAL
Increased water reabsorption in late DCT and CD
Increased K+ secretion in cortical CD
Increased urea reabsorption in Medullary CD
How does ADH increase water reabsorption?
Causes insertion of Aquaporin 2 channel on apical membrane, via a GPCR. There are always aquaporin 3 and 4 present so water enters cell and leaves across basolateral membrane. AQP2 is then retrieved by endocytosis in absence of ADH
What happens in SIADH syndrome?
Loss of negative feedback of ADH secretion so there’s massive water retention, causing big drop in blood osmolarity and so causes hyponatraemia
In plasma, in what forms does calcium exist?
45% as free ionised calcium
45% protein bound (80% of which bound to albumin)
10% complexed to citrates/phosphates etc
How is intestinal absorption of calcium controlled?
By vitamin D.
Where in the nephron is calcium reabsorbed?
65% in PCT
25% in loop of Henle
10% in DCT
Where is vitamin D produced?
D2 is absorbed in the gut and D3 is synthesised in the skin in the presence of UV light
How is vitamin D activated?
Hydroxylated in liver to calciferol then it travels to the kidneys where it’s hydroxylated to calcitriol, it’s activa form
What actions do calcitriol and PTH have on calcium?
Calcitriol binds to calcium in the gut, increasing its absorption
PTH Increases conversion of calciferol to calcitriol. It also increases reabsorption of calcium from kidney and increases its release from bone and decreases reabsoprtion of phsophate and bicarbonate
What are the main causes of hypercalcaemia?
Primary hyperparathyroidism
Hypercalcaemia of malignancy, either haematologcial or non-haematological
How is hypercalcaemia managed?
Loops diuretics and hydration to increase excretion
Bisphosphonates to inhibit bone breakdown and calcitonin to oppose pTH
Treat underlying condition
What factors can lead to renal stone formation?
Low urine volume
hypercalcuria
Low urine pH <5.47
How are renal stones managed?
Increasing fluid intakes and restricting intake of oxalate, sodium, calcium and animal protein
How much HCO3- is filtered by the kidneys each day?
4500 mmol
What is the average excretion of H+ by the kidneys, per day?
50-100mmol
What are the effects of alkalaemia?
decreased Ca2+ solubility so nerve excitability. If pH is more than 7.45 there’s paresthesia and tetany
Above 7.55 there’s a 45% mortality rate and above 7.65 there’s an 80% mortality rate
What are the effects of acidaemia?
Increases plasma potassium (hyperkalaemia) by increased activity of H+/K+ exchanger. There’s decreased cardia and skeletal muscle contractility, decreased glycolysis and decreased hepatic function. If pH is less than 7.1 there are severe effects. If it’s lower than 7.0 effects are life-threatening
What can cause metabolic acidosis?
Tissues producing acid or decreased kidney function meaning decreased HCO3-
How can the two different causes of metabolic acidosis be distinguished between?
By calculating the anion gap. If there’s decreased kidney function, HCO3- will be replaced by Cl- but if it’s due to acid production then when H+ is produced, there will also be another anion produced.
Do calculation of concentrations of (Na+ + K+) - (Cl- + HCO3-) should be around 10-15 mmol/l
If more than this then HCO3- has been replaced by a different anion and acidosis is due to tissues producing acid, rather than decreased kidney function
How can more HCO3- be made by the kidneys?
Kidneys are highly metabolically active so produce a lot of CO2 + H20. these react to give H+ + HCO3- the H+ is secreted into lumen and HCO3- enters the ECF
Also, can be made from amino acids. eg glutamin goes to alpha ketoglutarate which breaks down into HCO3- + NH3
HCO3- enters ECF and NH3 reacts with H+ to give ammonium (NH4+) which is excreted in urine
How can H+ be excreted in the DCT?
By combining with ammonia to give ammonium
By combining with HPO4^2- to give H2PO4-
Why does persistent, severe vomiting cause metabolic alkalosis?
Increased alkaline tide so increased HCO3- in plasma. Also, there’s decreased volume so kidneys try to take up more Na+ and Cl- so increased action of NHE so more H+ excreted and more HCO3- excreted.
Can be solved by rehydration
What are the levels of K+ in the ECF and ICF?
ICF - 120-150mmol/l
ECF - 3.5 - 5 mmol/l
What are the ECG changes seen in hyperkalaemia?
Raised T wave, increased PR interval and depressed ST segment
Then widened QRS complex (atrial standstill)
Eventually ventricular fibrillation
What are the ECG changes seen in hypokalaemia?
Low T wave and high U wave and depressed AT segment
How is K+ handled in different parts of the nephron?
67% of K+ is reabsorbed in PCT, irrespective of intake
20% is reabsorbed in TAL, irrespective of intake, driven by Na/K/ATPase and NKCL2
Also some secreted by principle cells of Collecting duct if there are high dietary levels
Intercalated cells of collecting duct reabsorb 10-12% of dietary intake
What drives the secretion of K+ from principle cells?
Na/K/ATPase sets up gradient of high intracelular K+ and low Na+. Na+ then moves into cell from lumen, down it’s concentration gradient through ENaC. As there’s no accompanying anion, this sets up a negative potential in lumen, which K+ is attracted to so leaves the cell
What is meant by external balance of potassium?
Balance between GI absoprtion and loss, renal excretion, ECF intake
What external balance factors promote secretion of K+ by principal cells?
Increased aldosterone, acts by increased protein transcription for ENac and Na+/K+/ATPase channels
Increased ECF K+ concentration as it increases Na+K+ATPase activity
Alkalosis
What is meant by internal balance of potassium?
Balance between K+ content in ECF and ICF
What internal balance factors promote uptake of K+ into ICF?
Hormones such as insulin, aldosterone and catecholamines
Alkalosis
Increased ECF potassium concentration
What internal balance factors promote shift of K+ into ECF?
Low ECF K+ concentration
Exercise in recovery phase of action potential
Cell lysis such as in crush injury (rhabdomyolysis), intravascular haemolysis such as in incompatible blood transfusion or cell lysis in chemotherapy
Plasma tonicity - increased ECF osmolarity draws water out of cells. This increases ICF K+ concentration so it moves out down its concentration gradient
What are are the common external balance causes of hyperkalaemia?
Increased uptake with decreased renal function
Inadequate renal function due to kidney injury or reduced aldosterone (ACEi, K+ sparing diuretics)
What are the common internal balance causes of hyperkalaemia?
Diabetic ketoacidosis (no insulin decreased K+ uptake) Metabolic acidosis Cell lysis
What is the common external balance cause of hypokalaemia?
Excessive loss ie in diarrhoea/vomiting or due to diuretics/high aldosterone levels
What’s the common internal balance cause of hypokalaemia?
Metabolic alkalosis
How should hyperkalaemia be treated?
Initially with IV calcium gluconate to decrease its effect on the heart and IV insulin with glucose to promote uptake. Also nebulised beta agonists eg salbutamol.
Depending on severity, maybe dialysis to remove excess
How should hypokalaemia be treated?
Treat cause
IV or oral K+ replacement
K+ sparing diuretics if due to aldosterone
How does COPD lead to type 1 respiratory failure?
There’s airway narrowing so increased resistance to ventilation. Therefore there’s a ventialtion perfusion mismatch. Resp rate increases but as there’s decreased elasticity, there’s decreased recoil and it’s harder to force air out. Decreased ventilation means there’s decreased pO2 but pCO2 is still normal
How does COPD lead to type 2 respiratory failure?
Low pO2 of type 1 resp failure increases respiratory drive. Eventually, ventilation decreases so much that pCO2 is affected and is now main respiratory drive
What is shown in spirometry of a patient with COPD?
Reduced FEV1:FVC If over 80%, mild COPD If between 50 and 79%, it's moderated If between 30 and 49% it's severe and if it's lower than 30, it's very severe
How is COPD managed?
No cure, only aims to improve health status, mobility, symptoms and number of exacerbations. First advice is to stop smoking as it reduces rate of deterioration.
Can be given steroid/beta agonist inhalers for frequent exacerbations
Activity programmes also used as they improve MRC score
What is an exacerbation of COPD?
Classed as increase wheeze and dyspnoea also increased sputum and worsening chest tightness and fluid retention
How are COPD exacerbations treated?
Bronchodilators, antibiotics if indicated by sputum, corticosteroids, oxygen and assisted ventilation
What are the common types of normal flora of the respiratory tract?
Viridans streptococci Neisseria Anaerobes Candida Streptococcus pneumoniae Streptococcus pyogenes Haemophilus influenzae Psuedomonas E coli
What are the specific immune defences in respiratory tract, protecting it from infection?
Muco-ciliary clearance mechanism
Coughing and sneezing reflexes
Mucosa - lymphoid follicles in pharynx and tonsils. Mucosa secrete IgA and IgG. Macrophages in alveoli
What is hospital acquired pneumonia?
Pneumonia that develops at least 48 hours after admission, with no previous signs on admission.
What are the organisms that most commonly cause hospital acquired pneumonia?
Enteric gram negatives
Pseudomonas
Anaerobes
Staph. aureus
What are the most common symptoms of pneumonia?
Malaise Fever Productive cough with either clear/purulent or rust coloured sputum Dyspnoea Pleuritic chest pain
What chest signs are found in pneumonia?
Bronchial breath sounds crackles wheeze dullness on percussion Increased vocal resonance
How is the severity of pneumonia assessed?
CURB 65
C - confusion with AMT 7
R - Resp rate over 30
B - Blood pressure 3 signs - consider ITU referral
In an immunocompromised host, what oppurtunistic pathogens can cause pneumonia?
Can be normal pathogen that's particularly virulent or an oppurtunistic pathogen: Cytomegalovirus Pneumocystis jiroveci Candida Aspergillus Mycobacterium Cryptosporidia Toxoplasma
What antimicrobials are given in pneumonia?
If hosptial acquired, more likely to be gram -ve so IV co-amoxiclav
If community, most common is pneumococcal so give a penicilli.
What are some host factors that promote development of a UTI?
Shorter urethra, ie in females
Obstruction
Neurological problems leading to residual urine
Ureteric reflex problems
What are some bacterial factors that promote the development of a UTI?
Faecal flora colonising the perineum
Adhesion by fimbriae and adhesins
K antigens that allow formation of polysaccharide capsule, protecting bacteria against host defences
Haemolysins that cause damage to membranes of urinary tract
Urease, produced by some bacteria that forms ammonia for a favourable environment for survival
When might white cells be present in urine but without bacterial growth?
Appendicitis Previous antibiotic use Urethritis caused by STI Vaginal infection or inflammation Tuberculosis Chemical inflammation
What are the 3 most common causative agents of UTIs?
Coliforms such as E coli
Coagulase negative staphylococcus
Proteus
How is an uncomplicated UTI treated?
Increased fluid intake
3 day course of trimethoprim or nitrofurantoin
How is treatment of complicated UTI different to that of an uncomplicated one?
Increase antibiotic course from 3 to 5 days.
Follow up with culture to check infection has cleared
Can also use cephalexin as well as trimethoprim and nitrofurantoin
How is pyelonephritis treated?
14 day course of systemic, broad spectrum antibiotic such as co-amoxiclav or ciprofloxacin
What are the symptoms of bacterial cystits?
Dysuria Frequency Haematuria Urgency \+/- low grade fever
What action to loop diuretics have on the nephron?
Block Na-K-2Cl in the loop of Henle so decreased Na and K reabsorption.
What action do Thiazide duretics have on the nephron?
Block Na-Cl symporter in early DCT so also increases calcium reabsorption.
What action do Potassium sparing/aldosterone antagonists have on the nephron?
Block aldosterone receptors in late DCT and early collecting duct so decreased transcription of ENac and Na/K/ATPase channels so decreased Sodium reabsoprtion and so decreased K excretion
What diseases cause diuresis?
Diabetes mellitus
Nephrogenic and cranial diabetes insipidus
Psychogenic polydipsia
What adverse effects can arise from diuretic use?
Hypo- and Hyperkalaemia Hyponatraemia Hypovolaemia Increased risk of gout attacks Glucose intolerance Increased LDL levels Erectile dysfunction with thiazides
What stimulates urination?
Afferent fibres in detrusor muscle sense when bladder is filled with roughly 400mls. These travel through S2-S4 to micturition centre in cerebral cortex. This increases parasympathetic stimulation through pelvic nerve (S2-S4) which releases ACh to contract detrusor muscle. Micturition centre and Pons make conscious decision to urinate which transmits through somatic pudendal nerve to external urethral sphincter to relax - urination
What occurs in the continence phase of urination?
When bladder is filling, continence centres make conscious decision to retain urine so send signals via pudendal nerve to contract external urethral sphincter. Sympathetic nervous system also transmits via hypogastric nerve (T10-L2) so relax detrusor muscle and contract internal urethral sphincter
What is the stress-relaxation phenomenon of the bladder?
Bladder walls have many rugae so when bladder distends, these folds disappear but intra-vesicular pressure remains the same
What are the 4 main types of urinary incontinence?
Stress
Urgency
Mixed
Overflow
How is urinary incontinence managed conservatively?
Modified fluid intake Weight loss Cessation of smoking Avoid constipation Decreased caffeine intake Timed voiding with fixed schedule
How can stress urinary incontinence be surgically managed?
Intramural bulking agents Fascial sling to support urethra Low tension vaginal tapes Open retropubic suspension to correct anatomical position of urethra in males: Male sling Artificial urinary sphincter
How can Urge urinary incontinence be pharmacologically managed?
Antichlinergics
Botox
How can urge urinary incontinence be managed surgically?
Sacral nerve neuromodulation
Autoaugmentation to increase functional capacity and decrease pressure
Augmentation cystoplasty
Ileal conduit
Where are the main sites of glomerular injury?
Subepithelial (podocytes)
Within GBM
Mesangial/paramesangial
Subendothelial
What is nephrotic syndrome?
More than 3.5 grams of protein lost in urine per day (torrential) most often due to podocyte injury. There’s normally generalised oedema due to decrease in oncotic pressure
What are the 3 main primary causes of nephrotic syndrome?
Minimal change glomerulonephritis (in children. flatted foot processes) Focal segmental glomerulosclerosis (circulating factor. Scarring of podocytes) Membranous glomerulonephritis ( IgG immune deposits at podocytes)
What’s a secondary cause of nephrotic syndrome?
Diabetes mellitus (microvascular damage in glomerulus and scarring of basement membrane)
What are 2 inherited causes of nephritic syndrome?
Alport syndrome (x - linked) associated with deafness and type 4 collagen in GBM so GBM is thickened and split Thin glomerular basement membrane syndrome which is benign with isolated haematuria
What are 3 non-inherited causes of nephritic syndrome?
IgA nephropathy - IgA deposits in mesangium so mesangial proliferation and scarring. Associated with mucosal infections.
Vasculitis - ANCA causes vessel inflammation and glomerulus gets blocked with thrombi. Neutrophils are hyperactivated and so attack endothelium. Causes segmental necrosis and cresents
Goodpasture syndrome - IgG deposits abnormally due to autoantibody against Type 4 collagen in GBM (as well as in pulmonary basement membrane so associated with pulmonary haemorrhage)
Extremely rapidly progressing with hypertension haematuria and general feeling of unwell
What’s the difference between focal and diffuse glomerular damage?
Focal - affects less than 50% of glomeruli
Diffuse affects more than 50% of glomeruli
What is meant by glomerulosclerosis and glomerulonephritis?
Glomerulosclerosis is collapse of capillary and scarrin
Glomerulonephritis is inflammation in glomerular tuft
How is prostate cancer treated?
If localised, with surveillance at first and potentially radiotherapy or a radical prostatectomy
If locally advanced, surveillance and maybe hormones and/or radiotherapy
If metastasised then surgical castration or medical castration where LHRH agonists are given to decrease testosterone. Palliative treatment includes single dose radiotherapy, bisposphonates and chemotherapy
What are the symptoms or renal cell carcinoma?
Haematuria
Loin pain
Swelling
Hypertension
What are some common sites of metastases in renal cell carcinoma?
Right atrium
Lymph nodes
Subcapsular fat
How can renal cell carcinoma be treated?
Surveillance
radical or partial nephrectomy
Removal of kidney, adrenal gland, fat and upper ureter
How is upper tract transitional cell carcinoma investigated?
Ultrasound
CT urogram
Retrograde pyelogram
Uretoscopy
How is bladder carcinoma treated?
If low risk and non muscle invasive then consider intravesical chemotherapy
If higher risk and non muscle invasive, give intravesical chemotherapy
If muscle invasive, give neoadjuvant chemotherapy and a radical cystectomy or radiotherapy
How does upper tract transitional cell carcinoma present?
Haematuria and flank pain
How does bladder carcinoma present?
haematuria
frequency
dysuria
What is oliguria?
Abnormally low urine production. Defined as less than 500ml a day or less than 20ml an hour.
What is the pre-renal cause of AKI?
Reduced renal perfusion. May be due to reduced effective extracellular fluid volume or impaired renal autoregulation.
What are some post-renal causes of AKI?
Due to obstruction of urine outflow, distal to the renal pelvis. If in pelvis or ureter, needs to be bilateral or for other kidney to be non-functioning.
Cause can be from within the lumen, e.g. clot, calculi, tumour, papillary necrosis
Can be from within wall eg ureteric stricture or congential problem but these normally cause CKD (eg neurogenic bladder)
Can be due to external pressure, eg AAA, malignancy, diverticulitis, prostatic hypertrophy
What are some intrinsic causes of AKI?
Acute tubular necrosis due to acute ishaemia or due to nephrotoxins.
Glomerular arteriolar disease, often due to immune acute glomerulonephritis
Acute tubular nephritis - inflammation of interstitium due to toxins or infection
What are some nephrotoxins?
Can be endogenous eg bilirubin, urate of myoglobin from rhabdomyolysis
or exogenous eg drugs such as NSAIDs or ACE inhibitors, CT contrast or antifreeze and weedkiller
How is AKI treated?
If pre-renal cause, correct volume problem to restore perfusion
If intrinsic acute tubular necrosis, treatment is supportive so avoid further nephrotoxins and maintain perfusion
If post-renal, reestablish flow with urological intervention
When is dialysis indicated for AKI?
If there’s hypercalcaemia, uraemic symptoms, volume overload, metabolic acidosis, pericardial rub, presence of dialyzable nephrotoxin
How can microscopy be used to investigate AKI?
If hyaline casts, may be pre-renal cause although they can be present normally
If muddy brown casts, may be acute tubular necrosis
If red blood cells cast, may be Rapidly Progressive glomerulonephritis
How is fractional Na excretion used to evaluate Acute Tubular Necrosis?
(Urine Na x Plasma creatinine) / (Plasma Na x urine creatinine) x 100
If less than 1, pre-renal AKI
If more than 1, ATN
What are some differential diagnoses and what other signs can help confirm diagnosis of glomerular disease?
Polycystic kidney disease Renal stones Renal tumour Arteriovenous malformation Glomerular disease
If there’s also proteinuria and/or hypertension, more likely to be a glomerular problem
What type of macroscopic haematuria is found in glomerular disease?
Episodic brown smokey urine with out blood clots
What kind of infection can cause nephritic syndrome in children?
Streptococcal infection such as impetigo or pharyngitis causing post-streptococcal glomerulonephritis
What are some symptoms of chronic kidney disease?
Breathlessness Lethargy/tiredness itching Nausea/vomiting Sleep reversal Nocturia Restless legs Aches and pains
What can chronic kidney disease be caused by?
Immune system Infection Vascula problems Hypertension Genetic Obstruction Systemic disease Unknown cause
What changes are seen in chronic kidney disease?
Functioning renal tissue is replaced by extracellular matrix and there’s glomerulosclerosis and tubular interstitial fibrosis. Progressive loss of excretory and hormonal functions
What effect can CKD have on haemopoiesis?
Kidneys secrete erythropoietin so when damaged erythropoietin levels fall, there’s decreased red blood cell formation and survival so there are symptoms of anaemia
How can serum creatinine levels be used to assess GFR?
Calculate eGFR using serum creatinine, age and ethnicity
= 186 x ([serum creatinine] x 88.4) ^-1.154 x age ^-0.203 x 0.742 if female x 1.21 if black
What are the differences between acute and chronic transplant rejection?
Acute rejection happens within 6 months. There’s increased serum creatinine levels and fever and pain at graft. There’s immune cell infiltrate and tubular damage but responds to further immunosuppression
Chronic rejection happens over 6 months after transplant. There’s progressively increasing creatinine levels and proteinuria. There are vascular changes, fibrosis and tubular atrophy. Doesn’t respond to further immunosuppression
How often must haemodialysis be carried out?
3 times a week, 4 hours at a time
How can the cause of CKD be assessed?
Auto-antibody screen
Measure levels of complement, ANCA and CRP
Carry out imaging
