Card Set Information
Kidney ureter disease
Kidney, ureter disease
Outline the cause of glomerulonephritis
Causes are related to proteinuria, hypertension and primary disease
: Antibodies, immune complexes, complement, cytokines, leukocytes (made outwith kidneys)
: Proteinuria, cytokines, growth factors
Reduced glomerular function puts increased pressure on remaining glomeruli, accelerating renal failure
Describe the role of different cell types in glomerulonepgritis
: Hyperplasia = scarring (glomerulosclerosis) and capillary membrane permeability (leads to haematuria)
: Hyperplasia in bowman's capsule causes 'crescent' formation
: Ig or complex deposition = vasculitis = focal necrosis
: Tubular scarring
Outline the pathophysiology and clinical features of IgA nephropathy
Commonest primary glomerular disease
Abnormally glycosylated IgA deposits in the mesangium
Mesangial cell proliferation = glomerulosclerosis and tubular scarring
Haematuria, proteinuria, hypertension, renal impairment
Outline the pathophysiology of membranous glomerulonephritis
Commonest cause of nephrotic syndrome in adults
Immune complex deposition in GBM and mesangium (antigen may be in kidney or ciculation)
Altered GBM charge affects permeability and activates mesangial cells (= tubule loss/glomerulosclerosis)
Nephrotic syndrome, hypertension and renal impairement
What is the nephrotic syndrome?
When kidney damage causes:
What is the nephritic syndrome?
When kidney disorder causes:
Haematuria (with RBC casts)
Uremia with oligouremia
What is 'minimal change disease'
Acute presentation, with a normal GFR but nephrotic syndrome and oedema
No abnormalities found in light microscopy
Ideopathic podocyte fusion occurs
Describe the RPGNs
Rapidly progressing glomerulonephritides
Group of conditions with common histology; crescent formation and acute severe damage
Examples include Goodpastures, Wegener's
Outline the pathogenesis of Wegener's and Goodpastures
: Anti-neutrophil cytoplasm Ig - necrotising granulomas in midline and necrotising vasculitis
: Anti-GBM Ig = complex deposition, glomerular destruction and epithelial proliferation = all renal clinical features
What are the common clinical features of glomerulonephritis?
What lab investiations are useful when diagnosing glomerulonephritis?
: creatinine, albumin
: Anaemia, Hb
: Monoclonal antibodies (M band)
: ANCA, RhF, ANA, anti-GBM
: Proteinuria, microscopy (RBCs)
: CXR, renal US
Define 'acute kidney injury'
Decline of renal excretory function over hours or days, recognised by the rise in serum urea and creatining
Outline the production of urea during AKI recovery
Polyuric phase for 2-3 days (>6litres daily)
'Low quality' urine; tubules cannot concentrate
Low K, Ca, Ma content
How can an underlying diagnosis be reached in known AKI?
: Urea, creatinine, CK, LDH (just raised urea = dehydration)
Clinical assessment of fluid status
GN screen (including Bence-jones)
Outline the acute management of AKI
Airway and breathing
Circulation; assess for shock, hyperkalaemia, pulmondary oedema
Remove cause, e.g. drugs/sepsis
Consider a 'renal' cause; are pre-renal causes sufficient to account for patient's condition?
What is the function of insulin/dextrose therapy in AKI?
Hyperkalaemia a result of kidney injury
Insulin/dextrose therapy activates Na/K pumps
Causes potassium uptake into cells
Outline the pathophysiology of 'salt losing' and 'salt retaining' CKD
: Tubule damage causes inability to concentrate and acidify urine, leading to excessive salt/H2O loss and dehydration/hypotension and acidosis
: Glomerular damage causes loss of filtration, meaning salt and water retention and so hypertension/oedema
How should progressive CKD be managed?
Treat underlying cause
Treat hypertension (especially RAAS inhibition)
Treat proteinuria (RAAS inhibition helps)
Stay watchful for anaemia, acidosis, calcium/phosphate levels (EPO, vit D and sodium bicarbonate)
Outline some complications of haemo and peritoneal dialysis
: Hypotension, hypoxia, air embolism, disequilibrium (sudden creatinine/urea loss), allergy
: Fluid retention/overload, fibrosis, hypertension
What are the clinical features and investigations used in assessing chronic transplant rejection?
: Increased creatinine, tenderness, haematuria
: U+Es, FBCs, US, Urinalysis, biopsy, Ig levels
Outline the structural changes which occur in diabetic nephropathy
Hyperfiltration in early diabetes
Mesangial cell hyperplasia (=glomerulosclerosis)
Loss of podocytes
Outline the management of diabetic nephropathy
Intensive plasma glucose control to reduce CV risk
Hypertension control, especially with RAAS inhibitors
RRT if ESRD occurs
Transplantation only provides temporary improvement
What factors suggests that microalbuminuria is NOT related to diabetes?
Duration of T1DM less than 10 yrs
Previously had a documented normal Alb:creat ratio, but rapid proteinuria developed
Significant haematuria present
Acute GFR loss
What are the clinical features and investigations of renal artery stenosis?
Hypertension, carotid/femoral bruits and proteinuria
CTA, MRA, CO2 angiography, biopsy
How should renal artery stenosis be managed?
Interventional radiology of severe (uncontrollable BP, pulmonary oedema)
BP control (3 or more hypertensives)
Risk factor control
Describe kidney cancer
Also called 'clear cell carcinoma'
An adenocarcinoma, arising from proximal convoluted tubule
Commonly metastasises along veins to the IVC
What is the aetiology of kidney cancer?
Polycystic kidney disease
Outline the common clinical features of kidney cancer
Paraneoplastic syndromes (hypercalcaemia, hypertension, polycythaemia)
How is kidney cancer investigated?
Differentiate from spleen mass (ballotable, resonant, doesn't move on respiration)
FBC, U&Es, LFTs
CT and US
Outline the pathology of prostate cancer
Vast majority are primary adenocarcinoma, in peripherals
Gleason grading and TNM classification
Outline the aetiology of prostate cancer
Genetics (hereditary prostate cancer 1)
Hormones (androgen production)
How does prostate cancer commonly present?
Many cases are asymptomatic
Usually presents early
Painful/slow micturation and retention
How is suspected prostate cancer investigated?
Raised PSA level; protease in semen/plasma. Tissue not tumour specific
Trans-rectal US guided biopsy
What important pieces of information should a patient be told if they request a PSA level?
Test may detect a curable cancer (in 5% of 50-65yo)
Test may fail to detect some early tumours
Teset may detect uncurable prostate cancer
PSA testing and indicated treatment may incur risk while not improving life expectancy
A biopsy may be required
What methods are used in the management of prostate cancer?
Radiotherapy (with/without LHRH analogue)
What is the aetiology of bladder cancer?
Occupation (especially working with rubbers)
Schistosomiasis (or other chronic infections)
Outline the pathology of bladder cancer
Transitional cell carcinoma; transitional epithelium found in the urinary tract
75% are superficial, 25% are invasive
Outline the presentation, diagnosis and management of bladder cancer
Frank haematuria/microscopic haematuria
Endoscopic resection (if confined), trans-urethral resection, intravesical BCG immunotherapy, cystectomy/radiotherapy
What investigations are used when investigating suspected testicular cancer?
Describe the pathgenesis of urinary calculi
Precipitation occurs due to increased solute:solvent ratio
Causes of formation include papilla formation, urinary obstruction or UTIs (increase urease production = ph change)
Calcium oxalate (54%), calcium phosphate (30%), struvite/uric acid
How do urinary calculi present?
Colicky pain, in loin or lateral abdomen
: appendicitis, gallstones, diverticulitis and especially AAA
When does a urinary calculus become an emergency, and how is this managed?
When calculus passes into ureter, obstructing fluid and leading to infection
Causes fever, tachycardia, hypotensive/septic shock
CT and US immediately given
Renal drained via nephrostomy tube
What investigations are useful when diagnosing a suspected urinary calculus?
: Previous kidney stones, fluid intake, dietary change
: Obs and abdo exam
: KUB, IV urography, US, CT KUB
: For sepsis/inflammation
: Dipstick for haematuria, cultures.
How can urinary calculi be managed, and what factors affect this?
: Conservatively. Lithotripsy. Endoscopy. Open surgery/laparoscopy
: Size, site, symptoms, depth, density