Urinary Flashcards
The anatomical position of the prostate
Inferior to bladder, superior to the external urethral sphincter. Anterior to the ampulla of the rectum.
The levator ani muscles lie inferolaterally
The anatomical position of the kidney
Retro peritoneal in the the paravertebral channel
Right T12-L3.
Left T11-L2
The course of the ureters
From kidney pelvic inferiorly along psoas major. They cross the pelvic brim by the bifurcation of the common iliac artery. They run along the lateral pelvic wall. At the level of the Ischeal spine they turn obliquely and enter the bladder posteriolaterally. 2cm above the ischeal spine they pass the ovarian artery. Vas deferens found by the volvoureteric junction.
The renal blood supply
Renal artery - segmental artery (3) - interlobar arteries- arcuate arteries- interlobular arteries (90 deg) - afferent arteries
Anatomical position of the bladde
Anterior of the pelvic cavity. Posterior to the pubic symphysis and bone
Explain the pronephros, Mesonephron and it duct and the metanephros.
Pronephros forms in intermediate mesoderm in cervical regions. It’s duct grows caudally and triggers the growth of the mesonephros. Week 4 then regresses
Mesonephros grows caudally week 4 to pronephros, it’s duct grows caudally and joins to the cloaca. Regresses week 8. Mesonephros forms in the urogenital ridge and contains nephrotomes
Urogenital ridge forms on either side from intermediate mesoderm created by the growth of the mesonephros.
The ureteric bud grows from its ducts and joins the metanephric tissue cap. The ureteric bud then stimulates it’s growth. Metanephros is functional from the first trimester
The positional changes of the kidney and problems that can occur
And the body grows caudally the kidneys rise cranially respectively. The blood supply therefore continually regresses and regrows at different parts of the abdominal aorta known as accessory renal arteries. There is lateral displacement so that the kidneys meet the adrenal glands at a 90 degree angle. The kidneys ascend close to each other and this can result in their fusion and as a result horseshoe kidney which can get trapped under the inferior mesenteric artery. The kidney may also have collateral blood supply.
Grow through arterial fork formed by umbilical arteries but one can fail to do so and so becomes a pelvic kidney
Formation of the bladder and urethra
The urorectal septum (mesoderm) grows and divides the cloaca into the urogenital sinus and the anal canal.
The cranial 2/3rds of the urogenital sinus become the bladder and the bottom parts into the pelvic (urethra) and phalic (spongy urethra).
The primitive bladder grows and absorbs the mesonephric duct so that it enters separately to the ureters (later becomes the vas deferens or regresses.)
Ectopic ureteral orifaces/ duplication defects
Do not join bladder but join vagina or urethra. From splitting of ureteric bud.
Urachal abnormalities
Patent urachus
Uracheal cyst
Presents with BPH
Common fistulae?
Exstrophy of bladder- failed reinforcement of cloacal membrane by mesoderm so opens onto abdominal wall.
Hypospadias- defect in folds of urethra so they open onto ventral surface rather than glans of penis.
Identify histological structures of the kidney nephron
Bowman’s capsule- vascular pole extra glomerular mesangial cells of JA. Urinary pole. Capillaries have fenestrated endotheliums. Podocytes have foot processes making slits. Shared basement membrane
PCT - simple cuboidal with brush boarder
Pars recta (straight part)
Thin AL - simple squamous
Tick AL- cuboidal no bb, with tAL, CD and VR in medulla.
DCT- cuboidal, larger lumen than PCT, more mitochondria
CD- larger lumen
Identify ultra structure of ureters
Urothelium
2 layers - circular and longitudinal. Extra layer for final 1/3
Identify ultra structure of bladder
Urothelium
LP
3 layers: spiral, longitudinal and circular
Adventitia
Describe glomerular filtration
Through glomerulus, around 20% (filtration fraction GFR/ RPF)
Depends on hydrostatic pressure diff and osmotic pressure (proteins).
Describe reabsorption in the PCT including OC
Basso lateral:
Na pump
Apical:
NHX
Symporters (glucose, aas, vitamins)
Secretion of Organic anion/cation exchangers with H+ (TM) they enter cells via facilitated diffusion and electrical gradient from Na pump at Basolateral membrane..
Describe reabsorption in TAL
Apical:
NaKCl2
Rom K (back in)
Basolateral:
NaKATP
Describe reabsorption in DCT
Apical: Thiazide: Na/ Cl symporter Ca? Basolateral: NaKATP
Reabsorption CD
Apical:
ENaC
Basolateral:
Na pump
Aquaporin 2
Describe TGF
Increase in GFR = increase in NaCl in DCT
Detected by Macula densa via Nakcl2
Stimulates juxtaglomerular cell to Secrete adenosine to constrict afferent arteriole or prostaglandins to dilate.
Describe secretion
Secretion of K so NaKCl2 can work and maintain. Charge.
Secretion of H+ for HCO3 reabsorption
Organic cations/ anions via baso OCT and luminal anti porter with H+
Describe and calculate clearance, how is it useful
The volume of plasma from which a substance has been completely removed
=(urine conc x urine flow)/ plasma conc
Glucose is 0
Inulin is 125 (not secreted or reabsorbed) = GFR
PAH all is secreted so clearance (ml/min) = RPF (90%)
How are GFR and clearance related
The higher the GFR then the higher the clearance.
Increased by TM- only so much can be reabsorbed.
How do the kidneys Handel sodium in order to change ECF volume. Absorption of sodium and H2O in kidney
Absorb more to increase ECF Na Vs H20 Proximal tub 67 vs 65 LOH 25 vs ? DCT 5 vs 0 Cd 3 vs 5-24
Handling of sodium in PCT
Na/K ATPase Symporters NHX S2/3 - Cl- 3 driving forces for water, osmotic, oncotic, hydrostatic
Glomerulotubular balance and the effect of ECF volume
GFR increases normally Na maintained - always 67% but less is reabsorbed
Difference between principal cells and intercalated cells
Principle- ENaC, aqua portion 2 variable, K secretion
(More distinct membrane)
Intercalated cells, active reabsorption of Cl-, secrete H+
Describe the regulation of NaCl reabsorption (blood pressure)
1: RAAS
2: sympathetic- increase CO, decrease TPR, increase RAAS and decrease GFR, NHE in PCT stimulated
3: ADH
4: Atrial natriuretic peptide, released with stretch of atrium, dilates afferent arteriole to increase GFR, decreases Na reabsorption all along tubule.
Describe how the renin- angiotensin system regulates sodium uptake in response to changes in blood pressure
Increased by decrease in Na reaching macula densa - sympathetic to juxatoglomerular cells to secrete renin. Reduced perfusion pressure by baroreceptors in afferent arteriole stimulates release.
Increased by sympathetic innervation.
Renin- angiotensin I - angiotensin II.
Increases aldosterone at adrenal cortex (increase ENaC and Na pump)
Constricts afferent and efferent arterioles and other vascular SM.
Increases NHX
Stimulates thirst via ADH release at hypothalamus.
Breaks down bradykinin (vasodilator)
Describe the sympathetic control of ADH secretion and the role of the baroreceptor
Low pressure- atria, pulmonary circulation and high pressure.
Drop in pressure or increase in tonicity increases ADH secretion from posterior pituitary. Baroreceptors to brain stem via vagus nerve which also increases sympathetic nerve activity
Actions of ADH
Addition of aquaporin 2 to CD
Increase in NaKCl2
Discuss prostaglandins and NSAIDS
Prostaglandins dilate afferent arteriole.
NSAIDs inhibit cycloxygenase and prevent prostaglandin production causing more vasoconstriction decreasing GFR and increasing BP.
Describe essential and secondary hypertension including causes.
Essential has no cause
Secondary does
Mild 140-159/90-99
Moderate 160-179/100-109
Severe 180+/110+
Renalvascular disease- low perfusion, baroreceptors increase RAAS.
Chronic renal disease
Conn’s syndrome- aldosterone adenoma
Cushings - high cortisol - stim Na reabsorption
Pheochromocytoma- secretes adrenaline and noradrenaline
Treating hypertension
Diet, smoking, exercise, alcohol, Na intake. ACE inhibitors Ca channel blockers A1 receptor blockers Beta blockers Thiazides diuretics
Regulation of body fluid osmolarity in terms of responses to water deprivation and drinking
Deprivation- more reabsorbed to maintain osmolarity and vice versa.
Water to control osmolarity
Na into control vol.
Distinguish the factors that regulate thirst and cause secretion of ADH
Stim by hyper osmolarity or hypovolaemia/ hypotension
Detected by osmoreceptors in the organum vasculoum of the laminae terminalis (OVLT).
Key factors of ADH/ thirst stimulation
Salt desire opposite of thirst.
Hedanistic appetite and regulatory.
Thirst requires significant change.
Describe the role of ADH and the production of hyper and hypo osmotic urine
Aquaporin 2
NaKCl2
Urea
Describe the syndrome of secretion of inappropriate ADH (SIADH) and it’s inappropriate consequences
Not inhibited by lowering of blood osmolarity
Too much water reabsorbed
Hyponatraemia- nausea, vomiting, lethargy, headache, appetite loss, irritability, seizures, coma, cramps
Treated with ADH receptor antagonists.
Describe the corticopapillary osmotic gradient
Osmolarity increases into medullar due to urea and nakCl2/ TAL.
Means more water is reabsorbed as medulla up is more conc that tdl and less conc than TAL.
Counter current system means that vasa recta is less conc as it descends (next to TAL) so osmolites diffuse into it so it is isoosmotic at the tip of the hairpin, as it ascends it is more conc so h2O that has diffed from tdl diffuses into it.
Discuss how the kidneys regulate Ca and PO4.
Vitamin D - short half life ask converted to 25 Hydroxy/ calciferol. Converted to calcitriol by 1 alpha hydroxylase stim by PTH and inhibited by PO4. Stim osteoblasts to stim osteoclast precursor cells to mature, increases gut absorption and kidney reabsorption (also PO4).
PTH stimulates osteoclasts, kidney reabsorption at DCT of ca and mg amd decreases PO4.
Where is ca reabsorbed in the kidney
65% PCT
20-25 ascending LOH
10 in DCT under PTH
Discuss the causes, symptoms and management of hypercalcaemia
Causes:
Primary hyperparathyroidism- parathyroid tumour
Haematological malignancy or non producing PTrH.
CVS: arrhythmias, shortened QT, enhanced sensitivity to digoxin
General: depression, coma, fatigue
GI: anorexia, poly uria, poly dipsia, constipation
Nephrocalcinosis
General management. Hydrate, loop diuretics to increase Ca excretion.
Specific measures- bisphosphonates, calcitonin
Treat underlying condition
Discuss calcium renal stones and their formation
Factors:
Low urine
Hypercalcuria
High oxalate consumption.
Organic matrix
Formation:
Supersaturation with respect to calcium oxalate
Ionic strength decreases risk e.g. Na, k, Cl
PH affects- lower pH enhances urinary citrate, but It favours uria acid stone formation.
Manifestations of renal stones
Asymptomatic
Haematuria
Pain and complications of a blockage in renal tract
Inhibitors of calcium oxalate and calcium phosphate stone formation
Citrate Pyrophosphate Magnesium Glucosaminoglycans (gag) RNA fragments Acidic glycoproteins
Management
Increase fluids
Restrict oxalate and Na possibly and possibly ca and animal proteins
Referal for surgery
Pathogenesis of UTI
Bacteria travels up urethra in between micturition. E. coli and pseudomonas aeruginosa. Use pili to adhere. Urease for protection from urea. Ecoli has k antigen to protect from host defense. Haemolysins damage cell membranes. May be coag neg staph on hospital Patient factors: Short urethra Blockage e.g. BPH, renal stone Diabetes- glucosuria Incomplete emptying- neurological Ureteric reflux
Appropriate clinical and laboratory investigations to diagnose UTI
Simple- urine dipsitic- nitrates and leukocyte esterase. If both positive give 3 days antibiotics
Complex (not a women or recurrent)- look for cause e.g. Imaging, midstream culture (msc), bacterial count over 105 cfu/ml (colony forming units) then significant. Look at turbidity, Haematuria, proteinuria. Possibly microscopy.
Antibiotic testing. 5 days antibiotics, treat underlying condition. If pyelonephritis or systemic then 10-14 days treatment.
Sterile pyuria- antibiotics, STI, TB, appendicitis
Appropriate anti microbial treatment and prophylaxis
Trimethoprim, nitroflurotoin Severe the co-amoxiclav Most are amoxicillin resistant. Prophylactic take at night Increase fluid intake
Summarise the main classes of diuretics and their mechanism of action
Loop diuretics- nakcc2, inhibit Ca absorption, more volume so less Na absorption distally. Furosemide
Thiazide- Na/Cl symporter, increases ca absorption. K sparing e.g. Bendroflumethiazide.
ENaC blockers - k sparing e.g. Amiloride
Aldosterone inhibiting - not as potent e.g. Spironolactone.
Osmotic diuretics - cannot be reabsorbed, increase osmolarity so less Na reabsorbed and h2O. Also draws h20 out of cells into ECF
Carbonic anhydrase inhibitors, less H+ so less NHX so more Na excreted. PCT. Not potent as other means e.g. Cl.
Theory of rational prescribing of drugs
Spironolactone first as K sparing.
Loop diuretics very potent e.g, heart failure or cirrhosis after spirono.
Hypertension then thiazides as it has vasodilator effects.
Conns syndrome then spironolactone
The adverse effects of diuretic use and abuse
Hyperkalaemia/ hypokalaemia depending if K sparing or not.
Hyperkalaemia particularly dangerous if on m supplements, ace inhibitors or renal impairment.
Stim raas (increase I’m vol) which also leads to hypokalaemia (aldosterone)
Carbonic anhydrase can cause acidosis but good for treatment of glaucoma.
Thiazides and loop diuretics can cause high uric acid levels which leads to gout, glucose intolerance and increased LDLs.
Thiazides cause erectile dysfunction
All can cause hyponatraemia
The object of diuretic therapy
M
What is the normal range for plasma pH?
7.38-7.42
Clinical effects of acidaemia and alkalaemia
Acidaemia- reduced muscle contraction, hyperkalaemia, arrhythmias, reduced glycolysis, reduced hepatic function
Alkaemia- tetany, parasthesia, death
Cellular mechanisms of reabsorption of HCO3 in the proximal tubule
NaKATPase, NHX, carbonic anhydrase, diffusion.
Aas create ammonium and hCO3 in PCT
Cellular mechanisms of H excretion in the distal tubule
H pump
H/K X
Active.
Normally not needed
Mechanism of buffering H in urine, explain the concept of titratable acid and the role of NH4
Minimum pH of urine is 4.5
H+ buffered by PO4 (titratable acid) and ammonia as ammonium
Types of UTI
Lower UTI
Bacterial cystitis- dysuria, polyuria, Haematuria, suprapubic pain
Abacterial cystitis- no bacteruria, honeymoon cystitis, trauma, fastidous organisms, STI, non infective inflammation,
Prostatitis- fever dysuria, perineal and low back pain- prostate
Upper UTI-
acute pyelonephritis, with fever and loin pain
Chronic interstitial nephritis, renal impairment following chronic inflammation.
Asymptomatic covert bacteruria only important in children and pregnancy
Describe the interactions between acid base status and plasma K
Hyperkalaemia acidosis due to favoring extracellular H+ movement so less H+ excretion
Hypokalaemia alkalosis due to intracellular pH acidic favoring HCO3 reuptake and H+ excretion
Describe the interaction between renal control of acid base balance and control of plasma volume
Volume comes first.
E.g. Vomiting- hypovolaemic and alkalosis.
Na uptake increase so NHX and Na/HCO3 adds to alkalosis.
Give fluids and it will sort itself out.
Describe the major causes of metabolic acidosis and the role of the anion gap to distinguish
Lactic/Ketoacidosisis, loss of HCO3 in kidney.
Anion gap = Na+H - (HCO3+ Cl). Larger if different anion e.g. Lactate
Why is the internal balance of K so important?
Intracellular lay- acid/base, DNA replication, cell growth, water, enzymes
Resting membrane potential
Describe how potassium handling occurs in the various segments of the nephron
Pct- passive diffusion 67%
LOH- NaKCC2 20%
DCT cd principle- ENaC K+ secretion 0-20%
DCT CD intercalated - K/H ATPase, 10-12%
Effect of aldosterone, ECF k, acid base status and affect on K+
Aldosterone- increases Na/K ATPase
ECF k - stimulates aldosterone secretion and K secretion in principle cells as higher K intracellularly
Acidaemia decreases K in principles decreasing secretion and vice versa.
Describe potassium balance and regualtion of ECF, icf concs.
External balance- kidneys
Internal balance- K into/ out of ICF.
Long term vs short term
Factors causing K shift inwards
Insulin stim ATPase High K ECF Catecholamines (exercise) stim ATPase Alkalosis K/H X Aldosterone
Factors causing K shift from icf to ECF
Acidosis, Low K ECF Exercise contraction and net release of K- uptake by non contracting cells Trauma / cell lysis Plasma hypersomolarity
Effects of K on RMP and heart excitability
Hyperkalaemia - depolarised RMP, less active fast Na channels, less excitability
Vice versa
Causes of hypokalaemia
External balance, low k intake, vomiting, diarrhoea, diuretic drugs or osmotic diuresis, high aldosterone levels
Internal balance - alkalosis
Clinical features of hypokalaemia
Heart
GI- paralytic ileus
Neuromuscular dysfunction so muscle weakness
Renal- dysfunction of CD, unresponsive to ADH so nephrogenic diabetes
ECG changes in hypokalaemia
(3) Shallow T wave/ inverted at wave Prominent U wave(3.5) ST depression (2) Wide pr possible
Treatment hypokalaemia
Treat cause
Oral/ IV K
K sparing diuretics - spironolactone or amiloride if aldosterone
Causes hyperkalaemia
External
Renal dysfunction e,g. acute/ chronic failure
Mineralcorticoid insufficiency e.g. K sparing or adrenal insufficiency
Internal- cell lysis or acidaemia
ECG changes hyperkalaemia
6.5- 7 tall peaked T
8 prolonged P-R interval, tall T, st segment depression
9 no P wave widened QRS
10 VF.
Treatment of hyperkalaemia
Acute - reduce k effect on heart with IV calcium gluconate
Insulin and glucose
Dialysis
Long term Dialysis Oral k binding resins in the gut Reduce intake Treat cause
The innervation of the bladder
Sympathetic innervation to detrusor muscle (B3) to relax and a1 to the urethra to contract (T10-L2) hypogastric nerve.
Parasympathetic to contract detrusor (M3) via the pelvic nerve S2-4.
Somatic innervation to the external sphincter via the pudendal nerve S2-4 and nicotinic receptor
Also a sensory nerve- bladder, spinal cord, thalamus/pons- cerebral cortex.
Explain how continence occurs. What drug controls this?
Cerebral continence centre - pontine continence centre- sympathetic nuclei in spinal cord- detrusor relaxation
Somatic closes external urethral sphincter
Controlled with B3 agonist Mirabegron
Explain how voiding occurs
When bladder around 400ml
Sensory innervation fires more rapidly.
Micturition regions in cerebral- pons- sacral levels of ps - bladder to contract.
External sphincter opens via somatic nerve
Incidence of urinary incontinence
SUI most common 50%
Then MUI then UUI and other.
Prevalence of UI with age
Increases rapidly with age until 50 and then less so.
Risk factors associated with urinary incontinence
O&G - pregnancy, childbirth, pelvic surgery
Predisposing- race, family predisposition
Promoting- co morbidities, obesity, age high intra abdominal pressure, UTI, drugs, menopause
Types of UI
SUI - leakage on cough
UUI- sudden urge with accompanies leakage
MixedUI
Overflow- under activity of detrusor
Investigation of UI
Urine dipstick- UTI, haem, glycosuria, protein
Non invasive urodynamics- frequency volume chart, drink and void, bladder diary, post micturition residual volume
Invasive urodynamics- flow and pressure, in anal canal and bladder to find bladder pressure
Pad tests - urine weight
Cystoscopy- look for tumour
Initial management of patient with urinary incontinence
Drink less Stop smoking- cough Less caffeine UUI Avoid constipation Bladder training- scheduling Pharmacological Surgical Pelvic floor muscle trainingkndwelling catheter, sheath device or incontinence pads Weight loss
Pharmacological management of patients with urinary incontinence
Anticholinergic - oxybutynin but non specific so side effects
B3 agonist- Mirabegron
Botulism toxin to inhibit ACh release ŵith UUI
Duloxetine- not recommended, noradrenaline and serotonin uptake inhibitor increasing external urethral sphincter
Surgical management of patients with urinary incontinence
Women permanent:
Sling (adds resistance uses fascia lata or Rectus fascia)
Retro public suspension proceedure (improve support and urethral positioning
Low tension vaginal tapes (minimally invasive and supports urethra)
Temporary:
Bulking agents e.g. Collagen and silicone to increase urethral resistance
Male:
Sling
Artificial urinary sphincter
Also for UUI:
Augmentation cystoplasty (bowel)
Urinary divergence
Examination of UI
Height, weight, abdominal exam (palpable bladder), DRE (prostate)- limited neurological examination, female, external genitalia and stress test
Pre renal causes of oliguria and AKI
Hypovolaemia e.g. Sepsis, heart failure
NSAIDs - constriction
Acei- dilation
Renal causes of AKI
Renal artery/ vein occlusion, intra renal vascular/.
Intrarenal obstruction
Glomerulonephritis primary or secondary e.g. Vasculitis, wegners granulomatosis, SLE (systemic lupus erythromatosus)
Ischemic ATN (from prerenal)
Toxin ATN- drugs e.g. Gentamicin,urate, bilirubin, endotoxins, x ray contrast
Interstitial disease- acute pyelonephritis or toxin induced
Rhabdomyolysis
Malignant hypertension
Pre eclampsia
Post renal causes of AKI
Obstruction
Lumen- calculi, blood clot, papillary necrosis, tumour
Wall- congenital e.g. Megaureter, neurogenic bladder, ureteric stricture (CKD)
Pressure- BPH, Diverticulitis, tumour, aortic anneurysm, ligation of ureter
Methods used to investigate AKI
Function Na excretion = (urineNa/ plasmaNa)/(urineCr/plasmaCr) x100
BP
Dehydration- HR, cool extremities, mucous membranes, dry axillae, increased skin turgor.
pH
Electrolytes
Osmolarity
Sepsis?
Abdo exam- obstruction? Rectal exam, blood in catheter?
Urinalysis- blood, protein, leukocytes
Urine microscopy - red cell cast the. Glomerulo nephritis
Imaging
Renal biopsy after post and pre and ruled out
CXR for fluid overload +- infection
Signs of cardiac failure, sepsis or UTI
Management of AKI
Volume overload- give fluids
Hyperkalaemia- calcium gluconate
Acidosis- protein restrict, bicarbonate
Dialysis especially if ureamic- pericarditis, intractable N/V, reduced consciousness
Supportive for ATN
Post renal failure- urological intervention TPR e-establish urine flow
Causes of microscopic Haematuria
Infection Poly cystic kidneys Arteriovenous malformations Kidney/glomerular disease Renal stones Renal/bladder tumours Glomerular disease if microhaematuria with protein or hypertension
Causes of macroscopic Haematuria
Glomerular disease but often brown and smokey (not clots).
Haemoglobinuria, myoglobin urea, food dyes
Usually painless
IgA nephrology most common
Symptoms of proteinuria
Frothy urine
Less immunoglobulins so infection
Less oncotic so oedema
Imbalance of coag cascade so risk of thromboemboli
Symptoms of nephrotic syndrome
Hypoalbuminaemia Oedema Proteinuria >3.5g/24 \+hyperlipidaemia Often muehrche's bands May lead to AKf Caused by focal segment glomerulosclerosis or membranous cause.
Symptoms of nephritic syndrome
Hypertension Haematuria Hypoalbuminaemia Rapid onset Oliguria Often occurs in post streptococcal glomerulonephritis in children Requires renal biopsy for diagnosis Pores in Podocytes
Describe rapidly progressive glomerulonephritis
Renal function deteriorates over days. Ureamic emergency.
Renal biopsy required
Causes of nephrotic syndrome
Minimal change glomerulonephritis, Focal segmental glomerulosclerosis Membranous glomerulonephritis DM Amyloidosis
Describe minimal change glomerulonephritis
Unknown circulating factor leads to Podocyte damage Does not normally lead to renal failure Child/adolescent Responsive to steroids May recur
Describe focal segmental glomerulosclerosis (FSGS)
Other end of spectrum from minimal change. Circulating factor unknown Causes scarring, fibrosis Less responsive to steroids Progressive to renal failure Recur in transplant
Describe membranous glomerulonephritis
IgG immune complexes in BM deposited
Commonest cause of nephrotic
Rule of thirds- third have KF
Autoimmune or secondary to SLE, lymphoma or malaria
How does DM cause nephrotic syndrome?
Thickening of BM
Micro vascular disease
Mesangial sclerosis
Progressive to renal failure
Causes of nephritic syndrome
IgA nephropathy
Hereditary nephropathies
Goodpasture syndrome (anti GBM)
Vasculitis
Describe IgA nephropathy
IgA in mesangium leading to damage and scarring Associated with mucosal infections Commenest GN Often causes renal failure Any age Very variable
Describe hereditary nephropathies
Thin GBM nephropathy Benign familial nephropathy Isolated Haematuria (blood is normal) Alport: X linked Abnormal collagen 4 Deafness Abnormal GBM Progressive to renal failure
Describe goodpasture syndrome (anti-GBM)
Antibody (IgG) targeting collagen IV
Rapidly progressive
Acute onset of severe nephritic syndrome
Treated with immune suppression and plasmapheresis
Rare
Association with smokers and pulmonary haemorrhage
Describe vasculitis
Associated with anti neutrophil cytoplasmic antibody (ANCA) treatable if early
Segmental necrosis
Urgent biopsy needed
Inflammation destroys blood vessels
Risk factors prostate cancer
Age- >80 75%
Fam history
Black>white> Asian
BRCA2 gene mutation
Screening prostate cancer
Not recommended as overdiagnosis
Often PSA raised in other things e.g. BPH, infection, inflammation.
False pos and negs.
Clinical presentation prostate cancer
Asymptomatic
Urinary symptoms e.g. Overactivity
Bone pain from mets
Haematuria (advanced)
Diagnosis/ investigation prostate cancer
DRE
Serum PSA
TRUS- transracial ultrasound - guided biopsy of prostate
Treatment of prostate cancer
Surveillance
Radiotherapy
Radical prostatectomy - open, laparoscopic or robotic.
New:
HIFU (high intensity focused ultrasound)
Primary cryotherapy
High dose rate brachytherapy or external beam
Mets:
Hormones e.g. GnRH agonist or surgical castration
Palliative- single dose radio therapy
Bisphosphonates- zoledronic acid and chemotherapy
If locally advanced then hormones, surveillance and radiotherapy.
BPH via transurethral resection
Risk factors bladder cancer
Age Males 90 TCC Smoking x4 Occupational e.g. Rubbers, plastics, painters, hairdressers Schistosomiasis
Treatment bladder cancer
Transurethral resection bladder tumour
Chemotherapy- intravesical instillation of mitomycin C
Immunotherapy (intra vesicular) for high risk non muscle invasive.
Muscle invasive - chemo and radical cystectomy or radio
Cystectomy them ileal conduit (belly button) or in younger people reconstruction from bowel
Staging and grading of bladder cancer
TNM
Normal stuff e.g. Mitosis, cytoplasm
Renal cell carcinoma aetiology, investigations and treatment
Smoking, obesity dialysis.
May spread peri tubular, IVC/LA, lymphatics
Ultrasound or CT
Radical/partial nephrectomy, surveillance, for mets then molecular therapies against angiogenesis
TCC risk factors, investigation and treatment
Smoking, phenacetin (fever and pain) Ultrasound Ct Retrograde pyelogram Ureteroscopy Treatment nephro-ureterectomy- kidney fat, cuff of bladder, ureter.
Main causes of chronic kidney disease
Infection e.g. Pyelonephritis Immune e.g. Glomerulonephritis Genetic e.g. Poly cystic kidney disease, Alport syndrome Obstruction and reflux nephropathy Hypersension Systemic e.g. Diabetes, myeloma Vascular Risk factors: Proteinuria Hypercalcaemia
Risk factors for chronic kidney failure
N
Define CKD
Progressive and irreversible loss of kidney function from months to years
Classification of CKD
Stages 1-5 based on GFR
1 >90
5 <15
Ways in which CKD can affect the CVD system
Increase in Na and h2O Acidosis Atherosclerosis Cardiomyopathy Pericarditis
Ways in which CKD can affect the haemopoitic system
Anaemia- low erythropoietin
Ways in which CKD can affect the Musculocutaneous system
Bone- renal bone disease
Less VitD- osteomalacia
Less GFT so more po4 so less Ca (complex) so more PTH so osteitis fibrosa cystica
Extra articular calcification
Other effects of CKD
Neuropathy Seizures Coma Tiredness Breathlessness Restless legs Sleep probs Aches and pains NV Itching Chest pain
Investigating CKD
GFR via inulin (in theory too expensive and time) or 24hr creatine clearence.
eGFR ethnicity gender and age
Conservative management of CKD
Lifestyle - smoking, obesity, exercise Treat diabetes Treat BP Ace inhibitors Lower lipids e.g. Statin Monitor
When is dialysis needed
Typically GFR <10
Ureamic, hyperkalaemia, pericarditis, acidosis
Describe haemodyalysis
3x a week for 4 hours
Modified diet low in K and PO4 so no potatoes
Risk of infection
Requires arterial/venous fistula which requires surgery. Lead to ischemia and swelling. Catheter cause stenosis
Home dialyse but need to live with someone
Anti coag and pump needed in machine
Countercurrent system with purified water
Effective but expensive
Describe peritoneal dialysis
Tube into peritoneum 5x a day or overnight High risk of infection High risk of adhesions and GI risk Less cvs risk Most effective initially Leaks may occur
Describe renal transplant
Gold standard From linpvint, cadavas or non heart beating donors or after brain death Placed in iliac fossa Cheap Long term survival Limited supply Op risks Life long immunosuppression Progressive CKD
Sensory innervation of kidneys?
T10-11
Blood supply of the ureters
3 parts:
1 renal arteries
2- common iliac, abdominal aorta and gonadal
3 - internal iliac arteries and everything else
Innervation of ureters
Sensory T12-L2
