Renal and Urology Flashcards
Name some hormones that act on the kidney
- Vasopressin from posterior pituitary - water resorption
- Aldosterone from adrenal cortex - Na+ resorption
- Natriuretic peptide - Na+ excretion
- Parathyroid hormone - phosphate excretion, calcium resorption
Name some hormones produced by the kidneys
- Renin (juxtaglomerular apparatus) - forms angiotensin II
- Na+ retention and vasoconstriction
- Vitamin D (metabolised by kidney into 1,25-DH cholecalciferol
- Ca2+ and phosphate absorption from gut
- Erythropoeitin
- Red blood cell formation in bone marrow
- Prostaglandin
- Renal tone control
How is GFR regulated?
- Myogenic - inc in BP stretches receptors in smooth muscle of vessels = vasoconstriction = inc resistance to flow = dec renal blood flow
- Tubuloglomerular feedback mechanism - macula densa detects inc in NaCl (osmolarity) or inc flow rate
- JGA signals via ATII or prostaglandins to vascoconstrict
- Dec renal plasma flow = dec GFR = inc NaCl resorption = dec NaCl concentration at macula densa
Describe the RAAS system
- Dec ECF volume/dec BP detected by baroreceptors in arch of Aorta or carotid sinus
- Inc sympathetic activity to JGA = renin release
- Conversion of angiotensinogen to angiotensin I to angiotensin II via ACE
- ATII simulates glomerulosa to release aldosterone
- Vasoconstricts
- Increases Na+ resorption from PCT
- Releases ADH - inc water retention - inc BP
How are UTIs classified?
- Uncomplication
- Complicated
- Men
- Abnormal renal tract/catheter/stent/
- Impaired renal function
- Immunosuppression/diabetes
- Pregnancy
- Elderly
- Recurrent (further infections with new organism)
- Relapse (further infections with same organism)
Name some risk factors for developing a UTI
- Female
- Sexual intercourse
- Diabetes
- Immunnosuppression
- Pregnancy
- Menopause
- Urinary tract obstruction
- Renal stones
- Instrumentation
- Diaphragm contraceptive
Name some common UTI organisms
- E coli
- Staph saprophyticus
- Enterococcus faecalis
- Klebsiella
- Enterobacter
- Pseudomonas aeruginosa
Describe the clinical features of UTI
- Fever
- Abdominal/loin/suprapubic tenderness
- Frequency
- Dysuria
- Urgency
- Haematuria
- Polyuria
- Cloudy urine
How is a UTI diagnosed?
- Urine dip - proteinuria, leucocytes, nitrites, RBCs
- MSU - M, C & S - if complicated, child or ill patient
- Growth of >108 colony-forming units
- Bloods if systemically unwell - FBC, U&E, CRP, blood cultures
- Consider US/cystoscopy if child, men, recurrent, pyelonephritis
How is a UTI treated?
- Advice - drink plenty, urinate often, post-intercourse voiding, wipe front to back
- Antibiotics
- Nitrofurantoin if GFR>45 100mg/BD
- Uncomplicated 3 days
- Complicated 7 days
- Trimethoprim if allergic to nitro
- Change to sensitive when MSU results come back
- Nitrofurantoin if GFR>45 100mg/BD
Name some causes of acute kidney injury
- Pre-renal - reduced circulating volume
- Hypovolaemia (haemorrhage, dehydration etc)
- Cardiac failure
- Liver failure
- Shock
- Renal artery stenosis/emboli
- Intrinsic/renal
- Acute tubular necrosis (ischaemia, drugs/toxins)
- Drugs = gentamicin, NSAIDS, methotrexate, ACE-i, aminoglycosides
- Toxins = myoglobin, sepsis, rhabdomyloysis
- Glomerular disease (glomerular nephritis)
- Post-renal = obstruction
- Bladder outflow obstruction (BPH, strictures)
- Tumour (prostate, bladder, gynae)
- Stone (bilateral)
- Retroperitoneal fibrosis
How is AKI investigated?
- Low urine output ≈ <400ml/d
- Urine dip - leucocytes, nitrites, blood, protein, glucose, ketones
- Urine culture - M, C & S
- Bloods - U&E (high urea, K+), high creatinine, osmolarity, FBC, LFT, clotting, CK, CRP
- ABG (met acidosis)
- Blood culture
- If cause unclear consider - serum immunoglobulins, C3/C4, autoantibodies (ANA, ANCA, anti-ds DNA)
- CXR - pulmonary oedema
- ECG - hyperkalaemia?
- Renal US
How can urine test results be used to distinguish pre-renal and renal causes of AKI?
How is AKI managed?
- If bladder palpable - insert catheter
- Stop nephrotoxic drugs
- Treat underlying cause
- Shock - fluids
- Post-renal = catheter/nephrostomy
- Dialysis if severe hyperkalaemia/metabolic acidosis, uraemic encephalopathy, pericarditis
Name some complications of AKI
- Hyperkalaemia
- Pulmonary oedema
- Bleeding
- Impaired haemostasis
- Uraemic encephalopathy
- Uraemic pericarditis
How is chronic kidney disease defined?
Progressive and irrervisble loss of renal function over years
- 1 = GFR >90
- 2 = GFR 60-89
- 3 = GFR 30-59
- 4 = GFR 15-29
- End-stage = GFR < 15
Name some causes of CKD
- Intrinsic
- Glomerulonephritis/pyelonephritis
- Polycystc kidneys
- Bladder/urethral obstruction (BPH
- Amyloidosis
- Systemic
- Diabetes
- Hypertension
- Gout
- Heart failure
- SLE
- Renovascular
- Drugs (gold, ciclosporin, analgesics)
Describe the clinical features of CKD
- Yellow skin pigmentation
- Brown nails
- Purpura
- Bruising
- Hypertension
- General - fatigue, weakness
- Pulmonary oedema/dyspnoea
- Cardiomegaly
- Ankle swelling/peripheral oedema
How is CKD diagnosed?
- Bloods - eGFR, normochromic, normocytic anaemia, U&E (high urea, creatinine) low calcium, high phosphate, high ALP, high PTH, high urate, CRP, glucose
- Urine
- Urinanalysis - blood, protein
- Microscopy - WCC< granular casts, red cell casts
- Imaging
- Renal ultrasound - obstruction, PCKD
- CXR - pulmonary oedema, cardiomegaly
- Biopsy
How is CKD treated?
- BP control (<130/80)
- ACE-i with careful monitoring
- Treat hyperlipidaemia with statins
- Decrease risk of renovascular disease
- Treat oedema with furosemide and metolazone
- Treat anaemia
- Consider erythropoeitin
- Treat renal osteodystrophy (bone disease) with vit D analogues (alfacalcidol) and calcium supplements
- Diet - protein restriction, Na+ and K+ restriction may be necessary
- Dialysis
- Peritoneal - insert Tenchkoff catheter
- Haemo - AV fistula
- Transplant
Name some complications of CKD
- Fluid retention - oedema
- Hypertension
- CVS risk
- Osteodystrophy (dec activated vit D = dec Ca2+ = PTH activation = bone resorption
- Anaemia (dec erythropoeitin)
- Electrolyte disturbance
- Acidosis
- Uraemia - anorexia, nausea, vomiting, pruritis
Name some common nephrotoxic drugs
- NSAIDS
- Incl. COX-2 inhibitors
- Diuretics, ACE-i, ARB
- Antibiotics - aminoglycosides, vancomycin
- Immunosuppressants - ciclosporin, tacrolimus
- Chemo - cisplatin
- IV contrast
What is Acute Tubular Necrosis (ATN)?
A cause of AKI due to the death of tubular epithelial cells that form the renal tubules.
It is classified into toxic or ischaemic
What causes ATN?
Which patient groups are screened for CKD?
- Hypertension
- Diabetes
- CCF
- Atherosclerotic disease (coronary/cerebral/peripheral)
- Multisystem diseases (SLE, myeloma)
- Urological problems (outflow obstruction, renal stones)
- Chronic nephrotoxin use
- Unexplained haematuria or oedema
Describe the process of haemodialysis
Removal of toxins across a semi-permeable membrane
- Concentration differences between dialysate (dialysis fluid containing physiological concentration of electrolytes) allow excess solutes to move down a contration gradient from blood to dialysate
- Allows removal of waste products and excess water
- Allows replacement of desirable molecules
- 4 hours of treatment, 3 times a week in hospital or at home
- Access via AV fistula or PTFE graft
How should AV fistulas be cared for?
- No IV cannulae between elbow and wrist
- Never use a tourniquet or BP cuff on fistula arm
- Do not use fistula to take blood
- Avoid using same site repetitively
- Complications need immediate attention
- Thrombosis
- Infection
- Aneurysm
- Distal ischaemia
- Extravasation
Name some complications of haemodialysis
- Hypotension
- Cramps
- Infection
- Nausea and vomiting
- Headache
- Haemolysis
- Air emboli
- Clotting of extracorporeal circuit
- Malnutrition
Describe the process of peritoneal dialysis
Dialysate introduced into the peritoneal cavity via a Tenchkoff catheter. The peritoneal membrane acts as a semi-permeable membrane
- 4-5 times a day
- Loss of function after 5 years
- At home by patient
What are the advantages of peritoneal dialysis?
- Preservation of residual renal function
- No need for vascular access
- Mobility (holidays etc)
- Patient engagement
- Home-based therapy
- Less expensive than haemo
- Less risk of transmission of BBV
Name some contraindications of peritoneal dialysis
- Patient/carer unable to train adequately in technique
- Inguinal/umbilical/diaphragmatic hernias
- Ileostomy or colostomy
- Abdominal wall infections
- Active diverticular disease
- Peritoneal adhesions
Name some complications of peritoneal dialysis
- Peritonitis
- Catheter exit site infection
- Drainage problems/occlusion
- Peritoneal leaks
- Pleural effusion
Name some contraindications for renal transplant
- Active infection - CMV, zoster, HBV, hep B, TB, HIV
- Cancer
- Severe heart disease
- Life expectancy < 5 years
- Cirrhosis
- Substance abuse
- Morbid obesity
What types of graft are there in renal transplants?
- Living Related Donor
- HLA haplotype matching
- Improved graft survival
- Living unrelated Donation
- Cadaveric
- Donation after brain death (DBD)
- Donation after cardiac death (DCD
Name some complications of renal transplants
- Bleeding
- Thrombosis
- Infection
- Oliguria
- Rejection
- Rising serum creatinine +/- fever, graft pain
- Proteinuria
- Ciclosporin nephrotoxicity
- Infection
- Malignancy
- Hypertension
What investigated are needed before a transplant?
- Immunological - blood group, HLA type, HLA antibody screen
- Virology - HIV, Hep B/C, EBV, CMV, Varicella, toxoplasma, syphilis
- Haematology - FBC, INR, Thrombophilia screen
- CXR
- ECG +/- additional cardiac assessments
- Iliac doppler studies
- US of native kidneys
What immunosuppressive drugs are used in renal transplants?
- Ciclosporin
- +/- azathioprine/prednisolone
OR
- Tacrolimus
- Mycophenylate
What is nephrotic syndrome?
The combination of proteinuria (>3.5/24hrs), hypoalbuminaemia (<30g/L) and oedema thought to be due to protein loss resulting in low albumin and low plasma oncotic plasma
Name some causes of nephrotic syndrome
Primary:
- Minimal change glomerulonephritis (common in young)
- Focal segmental glomerulosclerosis
- Membranous glomerulonephropathy (common in older)
Secondary:
- SLE
- Diabetes
- Amyloidosis
Name some clinical features of nephrotic syndrome
- Facial swelling/peripheral oedema
- Xanthelasma/xanthomata
- Hypertension
- Pleural effusion
- Hepatomegaly
- Ascites
- Recurrent infections
Name some complications of nephrotic syndrome
- Susceptibility to infections
- Thromboembolism
- Hyperlipidaemia
- Acute renal failure/AKI
How is nephrotic syndrome investigated?
- Urine dip - blood, proteins
- Urine microscopy - RBCs, casts, M, C & S
- Bloods - FBC, U&E, LFT, CRP, cholesterol, IGs, C3/C4, autoantibodies (ANA, ANCA)
- Imaging
- CXR
- Renal US
- Renal biopsy
How is nephrotic syndrome treated?
- Fluid and salt restriction
- Avoid excess dietary protein
- Control blood pressure
- Control hyperlipidaemia
- Diuretics (furosemide PO +/- metolazone (thiazide) or spironolactone
- Reduce proteinuria
- Treat underlying cause
- Eg steroids in minimal change
- Immunosuppressants in membranous
- Heparin thromboprophylaxis if immobile
What is nephritic syndrome?
Clinical syndrome associated with underlying glomerulonephritis:
- Haematuria
- Proteinuria
- Hypertension
Describe the clinical presentation of nephritic syndrome
- Haematuria
- Macro or microscopic +/- red cell casts
- Proteinuria
- Hypertension
- Nephrotic syndrome signs
- Renal failure
- Oliguria
- Signs of water and salt retention
Name some causes of nephritic syndrome
Primary:
- Glomerulonephritis
- Minimal change
- Rapidly progressive
- IgA nephropathy/HSP
Secondary:
- SLE (deposition of immune complexes)
- Vasculitis
- Diabetes
- Post-streptococcal
- Goodpasture’s
What is Goodpastures syndrome?
Autoimmune attack of the type IV collagen in the basement membranes of the lungs and kidneys
Describe IgA nephropathy
- Primary glomerulonephritis cause of nephritic syndrome
- Macroscopic haematuria
- Precipitated by infection
- Diagnosed via renal biopsy
- No treatment
How is nephritic syndrome diagnosed?
- Bloods - FBC, U&E, LFT, CRP, Igs, complements, autoantibodies, anti-GBM, cultures, antistreptococcal antibody titres (ASOT) virology, creatinine
- eGFR
- Urine microscopy - RBC casts, M, C & S
- Urine dip = blood, proteins
- 24hr - protein/creatinine clearance
- Imaging
- CXR
- Renal ultrasound
- Renal biopsy
How is nephritic syndrome treated?
- Keep BP < 130/80
- Salt and water restriction
- Refer to nephrologist
- Steroids / immunosuppressants
- Need biopsy results to tailor to diagnosis
- Dialysis
What elements make up the glomerular filter?
- Endothelial fenestrations
- Glomerular basement membrane
- Podocytes
What is Alport’s syndrome?
Inherited genetic disease - defective type IV collagen genes result in thickened glomerular basement membrane with splitting of the lamina densa.
SIgns:
- Progressive haematuria
- Sensorineural deafness
- Bulging of lens capsule
What is respiratory acidosis? Name some causes
Lungs cannot remove enough CO2
- Respiratory failure
- COPD
- Airway obstruction
- Asthma
- Mechanical chest injuries
- Drugs - aneathesia, barbiturates
- Injuries to respiratory centre in brain
What is respiratory alkalosis? Name some causes
Too much CO2 is breathed off
- Hyperventilation
- Hypoxia detected by chemoreceptors
- High altitude
- Fever
- Hysterical overbreathing
- CNS causes
- Stroke
- Subarachnoid haemorrhage
- Meningitis
What is metabolic acidosis? Name some causes
The increased production of acids or excess loss of bicarbonate
- High lactate (shock, infection, hypoxia)
- Anaerobic respiration due to tissue hypoxia
- DKA
- Alcohol
- Diarrhoea (loss of carbonate)
- Renal disease (urate)
What is metabolic alkalosis? Name some causes
Excess loss of acid
- Vomiting/diarrhoea
- Alkali ingestion
- Diuretics (K+ depletion)
- Decrease in ECF
- Haemorrhage
- Burns
What are the parameters of pH, pCO2, HCO3-?
pH 7.35-7.45
pCO2 4.7-6.0kPa
HCO3- 22-28mmol/L
Describe an approach to ABGs
- pH: acidosis or alkalosis?
- Is CO2 normal?
- If raised - respiratory
- If no change or opposite - compensated
- Is HCO3- normal?
- High - metabolic
- No change or opposite - compensated
What is the anion gap?
- Estimates unmeasured anions
(Na+ and K+) - (Cl- and HCO3-)
- Normal range 10-18mmol/L
- Increased in metabolic acidosis due to increased production of fixed/organic acids (lactate, ketones, phosphate)
Describe the appearance of respiratory acidosis, respiratory alkalosis, respiratory acidosis/alkalosis with metabolic compensation
Describe the appearance of metabolic acidosis, metabolic alkalosis, metabolic acidosis/alkalosis with respiratory compensation
What is base excess?
Marker of metabolic acidosis or alkalosis
- High base excess (>2) indicated higher than normal HCO3-
- Primary metabolic alkalosis
- Compensated respiratory acidosis
- Low base excess (<-2) indicates lower than normal HCO3-
- Primary metabolic acidosis
- Compensated respiratory alkalosis
Name some signs and symptoms of hyponatraemia
- Confusion
- Seizures
- Hypertension
- Cardiac failure
- Oedema
- Nausea
- Muscle weakness
What causes hyponatraemia?
- Loss through kidneys
- Addisons
- Renal failure
- Excess diuretics (thiazides)
- Loss elsewhere
- Diarrhoea and vomiting
- Burns
- Small bowel obstruction
- Water excess (oral/dextrose 5%)
- SIADH
- Organ failure - cardiac, liver, renal
- Pseudohyponatraemia - serum volume increases from high lipids or proteins, Na+ falls but osmolarity is normal
- Or taking blood from an arm with IV drip
How is hyponatraemia diagnosed?
- Is patient dehydrated?
- Plasma Na+ < 135?
- Is urinary Na+ > 20mmol/L?
- Is patient oedematous?
- Is urine osmolality > 500mmol/kg?
How is hyponatraemia managed?
- Correct underlying cause
- Saline infusion
- Furosemide
Name some signs and symptoms of hypernatraemia?
- Thirst
- Confusion
- Coma
- Fits
- Dehydration
- Dry skin
- Decreased skin turgor
- Postural hypotension
- Oliguria
Name some causes of hypernatraemia
Plasma Na+ > 145
- Fluid loss without replacement (diarrhoea, vomit, burns)
- Incorrect IV fluid replacement (excess saline)
- DIabetes insipidus
- WIth large urine volume
- Primary aldosteronism
- If high BP, low K+ and alkalosis
How is hypernatraemia managed?
- Water orally if possible
- Or dextrose 5% IV (4L/24hrs)
- Guided by urine output
Name some signs and symptoms of hyperkalaemia
Plasma K+ > 6.5
- Cardiac arrhythmias
- Palpitations
- Sudden death
- Muscle weakness
What causes hyperkalaemia?
- AKI/CKD
- Excess K+ therapy
- K+-sparing diuretics
- Addisons (low aldosterone)
- Low insulin
- Rhabdomylosis
- Massive blood transfusion
- Metabolic acidosis (DKA)
- Drugs - ACE-i, suxamethonium
Describe the appearance of hyperkalaemia on an ECG
- Tall tented T waves
- Small P wave
- Wide qrs complex
- VF
How is hyperkalaemia managed?
- 10ml calcium gluconate IV over 2 mins
- Provides cardioprotection
- Insulin and glucose (20U soluble insulin and 50ml of glucose 50% IV)
- Insulin moves K+ into cells
- Nebulised salbutamol (2.5mg)
- Polystyrene sulfonate resin + colonic irrigation
- Dialysis
Name some signs and symptoms of hypokalaemia
- Muscle weakness
- Paralysis of resp muscles
- Hypotonia
- Cardiac arrhythmia
- Hyperpolarisation = decreased excitability = decreased APs
Name some causes of hypokalaemia
K+ < 2.5
- Diuretics
- Cushings/steroids/ACTH
- High insulin
- Vomiting and diarrhoea
- Conns syndrome
- If high BP and alkalosis without diuretics
- Pyloric stenosis
- Alkalosis
How is hypokalaemia managed?
If mild: >2.5
- Oral K+ supplement (Sando K 2 tabs)
If severe: <2.5
- IV potassium cautiously (no more than 20mmol)
- Never as bolus
How is calcium metabolism controlled?
- Parathyroid hormone - inc PTH = inc plasma Ca2+ and dec PO43- due to reabsorption from bone and kidney
- Vit D - inc Ca and Phos absorption from gut and kidney
- Inhibits PTH
- Calcitonin - dec Ca and Phos
- Magnesium - Low Mag prevents PTH release
What are the signs and symptoms of hypocalcaemia?
- Tetany
- Convulsions
- Depression
- Perioral parasthesia
- Carpo-pedal spasm
- Troussaeus sign (with BP cuff)
- NM excitability
- Cardiac arrhythmia
What causes hypocalcaemia?
- Thyroid/parathyroid surgery
- If phosphate raised
- Chronic renal failure
- Hypoparathyroidism
- Acute rhabdomyolysis
- If phosphate normal or low
- Osteomalacia (with high ALP)
- Pancreatitis
- Respiratory alkalosis
How is hypocalcaemia treated?
- Mild = calcium 5mmol/6hrs PO
- Severe = 10ml of 10% calcium gluconate IV over 30min
- Alfacalcidol
- Correct underlying cause
Name some signs and symptoms of hypercalcaemia
- Bones = fractures, bone pain
- Stones = renal stones/renal failure
- Groans = abdo pain, constipation
- Psychic moans = depression
- Polyuria/polydipsia
- Hypertension
What are the causes of hypercalcaemia?
- Malignancy - myeloma, bone mets, PTHrP
- Primary hyperparathyroidism
- Sarcoidosis
- Acidosis
- Increases free ca2+
- Bone destruction
- Drugs = thiazide
How is hypercalcaemia diagnosed?
- Albumin
- Urea
- Phosphate
- ALP
- PTH
How is hypercalcaemia managed?
- Fluids - rehydrate with saline
- Treat hypokalaemia and hypomagnesaemia
- Diuretics - furosemide 40mg/12hrs
- AVOID thiazides
- Bisphosphonates (pamidronate) - inhibit osteoclast activity
- Treat underlying cause
- Eg steroids for amyloidosis
What is SIADH?
Hyponatraemia secondary to the dilutional effects of excessive water retention caused by increased ADH secretion
- Decreased plasma osmolality
- Increased urine osmolality (Na+ > 20)
- Dehydrated
Name some causes of SIADH
- Small cell lung cancer
- Pancreas/prostate malignancy
- Stroke
- Infections - pneumonia/TB
- Drugs - sulfonylureas (glipizide) SSRIs
How is SIADH managed?
- Remove underlying cause
- Fluid restriction
- Slow correction of electrolyte imbalances with 0.9% saline and/or furosemide
- Avoids central pontine myelinolysis
- Demeclocycline = reduce responsiveness of collecting tubules to ADH
- ADH (vasopressin) receptor antagonists
Give examples of diuretics, where they work in the kidney and on what transporter
What is the most common organism of an infected transplanted organ?
Cytomegalovirus
