PassMedicine Flashcards
What is the dose given for maintenance fluids
25-30ml/kg/day of water
1mmol/kg/day of potassium and chloride
50-100g/day of glucose
What is the fluid prescribed in a fluid challenge
500mls of 0.9% normal saline STAT
What are the paediatric fluid requirements for 24 hours
0-10kg = 100ml/kg
11-20kg = 50ml/kg
Anything above = 20ml/kg
What are the features of IgA nephropathy
- 2 days after an infection (URTI)
- Macroscopic haematuria
- Caused by mesangial deposition of IgA immune complexes
What are the features of rhabdomyolysis
AKI + Disproportionately raised creatinine kinase
CK >5x normal
Tea coloured urine
What are the causes of rhabdomyolysis
Statins (especially + clarithromycin)
Seizure
Collapse + Long lie
Crush injury
Ecstasy
What is the management for ADPKD
Tolvaptan - To slow down progression to CKD
What is anti-glomerular basement membrane disease
AKA Goodpastures syndrome
A rare type of small vessel vasculitis associated with pulmonary haemorrhage and rapidly progressive glomerulonephritis.
Caused by anti GBM antibodies against type IV collagen.
What is the treatment for Anti GBM disease
Plasma exchange
Steroids
Cyclophosphamide
What are the signs of good pastures syndrome?
Haemoptysis (pulmonary haemorrhage)
Rapidly progressive glomerulonephritis (proteinuria + haematuria + AKI)
How do you calculate the anion gap
(Sodium + Potassium) - (Bicarbonate + Chloride)
Normal = 8-14
What are the causes of acidosis with a normal anion gap
GI Bicarbonate loss: Diarrhoea, fistula
Renal tubular acidosis
Drugs (acetazolamide)
Ammonium chloride injection
Addisons disease
What are the causes of acidosis with a raised anion gap
Lactate (shock, hypoxia)
Ketones (DKA, alcohol)
Urate (renal failure)
Acid poisoning (methanol, salicylates)
Chronic paracetamol use
What causes death in dialysis patients
Cardiovascular events (50%)
What are the two main intrinsic causes of AKI
Acute interstitial nephritis - inflammatory process (higher white cell count - leukocytes)
Acute tubular necrosis -
What are the features of minimal change disease
- Almost always a nephrotic syndrome
- 1/3 have only one episode
- 1/3 have infrequent episodes
- 1/3 have frequent relapses which stops before adulthood
What is the treatment for minimal change disease
Oral corticosteroids - Prednisolone + Urgenzassero outpatient referral to paediatrics
Next line - Cyclophosphamide
Biopsy is only needed if there is no response to treatment
What are the features of post streptococcal glomerulonephritis
- Typically occurs 7-14 days after strep infection
- Caused by immune complex (IgG, IgM, C3) deposition in the glomeruli
- Starry sky on immunofluorescence
How is post streptococcal glomerulonephritis
Bloods:
- Raised anti-streptolysin O titre
- Low C3
What is the most common presentation of transitional cell carcinoma of the bladder
80% present with painless, visible haematuria.
When should someone have an urgent referral for haematuria
> 45 years and visible haematuria without UTI
45 and visible haematuria that recurs or persists after treatment for UTI
> 60 years and nonvisible haematuria and either dysuria or raised white cell count on a blood test
When should someone have a non-urgent referral for haematuria
> 60 with recurrent or persistent unexplained UTI
What are the symptoms of a Wilms nephroblastoma
- <5 years old
- Abdominal mass (most common presentation)
- Flank pain
- Painless haematuria
- Anorexia
- Fever
- Unilateral 95% of time
- Metastasis in 20% (most commonly the lungs)
what is CKD stage 1
> 90ml + Some sign of kidney damage
what is CKD stage 2
60-90ml + Some sign of kidney damage
If kidney tests normal - no CKD (if normal U and E and no proteinuria)
What is CKD stage 3a
45-59ml
What is stage 3b CKD
30-44ml
What is stage 4 CKD
15-29ml
What is stage 5 CKD
<15 ml = Established kidney failure.
Dialysis or transplant most likely needed
When is haemodialysis indicated
Stage 5 CKD
AEIOU
Acidosis
Electrolyte imbalance (hyperkalaemia >6.5)
Intoxication
Overload (of fluid - can be pulmonary)
Uraemia (pericarditis or encephalopathy)
What is used to treat hyperphosphataemia in CKD
Sevelamer
Phosphate is really excreted so will build up if there is impaired renal function. This drags the calcium out of the bone and causes osteomalacia.
What is used in CKD to supplement a lack of vitamin D
Alfacalcidol
What are the mineral bone diseases that occur with CKD
Low vitamin D - Causes low calcium
High Phosphate
Secondary Hyperparathyroidism: Due to low calcium, high phosphate, high vitamin D
how is ADPKD diagnosed
Ultrasound
diagnostic criteria (in patients with positive family history):
- two cysts, unilateral or bilateral, if aged < 30 years
- two cysts in both kidneys if aged 30-59 years
- four cysts in both kidneys if aged > 60 years
what investigation should be done for patients with AKI of unknown origin
ultrasound
What is the criteria for a stage 1 AKI
Increase in creatinine 1.5-1.9x baseline
Increase in creatinine by >26umol/L
Reduction in urine output to <0.5ml/kg/hour for > 6 hours
What is the criteria for stage 2 AKI
Increase in creatinine to 2-2.9x baseline
Reduction in urine output to <0.5ml/kg for > 12 hours
What is the criteria for stage 3 AKI
Increase in creatinine >3x baseline
Increase in creatinine to >353.6umol/l
Reduction in urine output to <0.3ml/kg/hour for > 24 hours
Initiation of kidney replacement therapy
eGFR <35ml in patients < 18 years
what are the causes of peritonitis in peritoneal dialysis
Staphylococcus epidermidis - most common cause
Staphylococcus aureus
what is the pH of prolonged diarrhoea
Metabolic acidosis with hypokalaemia
What is diabetes insipidus
A condition where either:
- Theres a decreased secretion of ADH from the pituitary gland
OR
- Theres an insensitivity to ADH from the kidney
What are the pre-renal causes of an AKI
Ischaemia:
- Hypovolaemia secondary to diarrhoea or vomiting
- Renal artery stenosis
- DEHYDRATION
NORMAL URINE OSMOLARITY
URINE SODIUM <20
What are the intrinsic causes of an Aki
- Glomerulonephritis
- Acute tubular necrosis
- Acute interstitial nephritis
- Rhabdomyolysis
- Tumour lysis syndrome
What are the post renal causes of an AKI
- Kidney stone in the ureter or bladder
- BPH
- External compression of the ureter
Which drugs have a nephrotoxic potential
NSAIDs
Aminoglycosides
ACE inhibitors
ARBs
Diuretics
When should Hartmanns solution not be used
In patients with hyperkalaemia (Contains potassium)
What are the features of an acute Graft failure
- < 6 months
- Usually due to mismatched HLA
- Asymptomatic + picked up by rising creatinine, pyuria and proteinuria
- may be reversible with steroids and immunosuppressants
What are the features of chronic graft failure
- > 6 months
What is dialysis
A method for performing the filtration of the blood artificially in patients with renal failure
It removes excess fluid, solutes and waste products
What is peritoneal dialysis
A dialysis solution (containing dextrose) is added into the peritoneal cavity.
Ultrafiltration occurs across the peritoneal membrane into the dialysis solution.
The solution is then replaced and the waste products are taken away.
How is peritoneal dialysis done
Via a tenckhoff catheter.
- Continuous ambulatory peritoneal dialysis - Where dialysis solution is in the peritoneum at ALL TIMES. The fluid is then changed at regular intervals.
- Automated dialysis - Occurs overnight. A machine continuously replaces fluid to optimise filtration. This takes 8-10 hours.
What are the complications of peritoneal dialysis
Bacterial Peritonitis
Peritoneal sclerosis
Ultrafiltration failure - If the patient absorbs the dextrose in the solution, this reduces the filtration gradient
Weight gain
Psychosocial effects
What is haemodialysis
When the blood is filtered using a machine.
This requires good access to an abundant blood supply.
What are the main access points for haemodialysis
Tunnelled cuffed catheter:
- Tube inserted into the subclavian or jugular vein with a tip that sits in the SVC or right atrium.
- Two lumens - one where blood exits (red) and one where blood enters (blue).
Can cause infection and blood clots.
A-V Fistula
What are the features of an A-V Fistula
- Connection between artery and vein
- Bypasses the capillary system - allows blood to flow under higher pressure
- Requires surgery
- 4 -1 week maturation period without use
- Radiocephalic
- Brachio-cephalic
- Brachio-basilic
What should be done when examining an AV fistula
- Skin integrity
- Aneurysm
- Palpable thrill (fine vibration)
- Machinery murmur on auscultation
- Pin prick marks - to suggest active use
- Blood supply to distal limb
Murmur and thrill will be absent if the fistula is thromboses or has been surgically ligated like after a renal transplant
What are the complications of A-V fistulas
- Aneurysm
- Infection
- Thrombosis
- Stenosis
- STEAL syndrome - Inadequate blood flow to the limb distal to the AV fistula
- High-output cardiac failure - increased preload and hypertrophy of the heart muscle
Which organism most commonly causes bacterial peritonitis
Staphylococcus epidermidis
What are the physiological functions of the kidney
- Remove waste products/medications - urea
- Reabsorbs vital nutrients - Sodium, Potassium, water
- Hormone secretion - Erythropoietin, Renin, Calcitriol
What is acute interstitial nephritis
An acute inflammation of the tubules and interstitium
Usually a hypersensitivity reaction
What are the signs of acute interstitial nephritis
- Urticarial-like rashes
- Fever
- Arthralgia
- Elevated white cell count in urine
- Eosinophils
- IgE elevated
- Hypertension
- Sterile pyuria
- White cell casts (eosinophilic casts)
What are the causes of acute interstitial nephritis
Drugs - Especially antibiotics
Penicillin
Rifampicin
NSAIDs
Allopurinol
Furosemide
What is the main cause of anaemia in CKD
Due to reduced erythropoietin levels
Normochromic, normocytic anaemia.
Occurs when the eGFR is <35ml/min.
Predisposes the patient to left ventricular hypertrophy
What is the management of anaemia in CKD
Optimising iron status first
Erythropoietin
What is Henoch-Schonlein Purpura
An IgA mediated small vessel vascilutus.
Causes a purpuric rash in the buttocks and lower limbs.
Often triggered by URTI or a gastroenteritis.
IgA deposits in blood vessels causing inflammation:
- Skin
- Kidneys
- GI Tract
What are the features of Henoch-Schonlein Purpura
- Usually seen in children after infection
- Palpable purpuric rash over buttocks and extensor surfaces of arms and legs
- Abdominal pain
- Poly arthritis
- Some features of IgA nephropathy (haematuria, renal failure)
- Purpura (100%)
- Joint pain (75%)
- Abdominal pain (50%)
- Kidney involvement (50%) - IgA nephritis (microscopic or macroscopic haematuria, and proteinuria)
What is the treatment for henoch-Schonlein Purpura
Analgesia
Supportive
Blood pressure and urinalysis should be monitored to detect progressive renal involvement.
What are the differentials for a nonblancing rash
Meningococcal septicaemia
Henoch-schonlein purpura
idiopathic thrombocytopenia purpura
leukaemia
Haemolytic uraemia syndrome
How is the diagnosis of henoch-schnlein purpura made
Rule out other more serious causes of a non blanching rash:
- FBC
- Blood film
- Albumin
- CRP
- Blood cultures
- Urine dipstick
- Blood pressure
- Urine protein : creatinine ratio
What is the criteria for henoch-schonlein purpura
Palpable purpura
+ 1 other from:
- Diffuse abdominal pain
- arthritis or arthralgia
- IgA deposit on histology
- Proteinuria/Haematuria
What are the complications of hence-schonlein purpura
- 1/3rd have a reoccurrence within 6 months
- a small minority of patients develop end stage renal failure
- most get better within 4-6 weeks
What is haemolytic uraemia syndrome
Occurs when there is thrombosis within small blood vessels throughout the body. Usually trigger by the shiga toxin (E. coli 0157).
Increased risk if used antibiotic or loperamide to treat gastroenteritis.
Triad:
- Haemolytic anaemia (caused by the breakdown of RBCs)
- Acute kidney injury
- Thrombocytopenia
What is the presentation of HUS?
E. coli 0157 - presents as a bloody diarrhoea (gastroenteritis)
Haemolytic uraemia syndrome usually develops 5 days later:
- Reduced urine output
- Haematuria
- Abdominal pain
- Lethargy
- Hypertension
- Confusion
- Bruising
What is the treatment
Medical emergency - mortality 10%
Supportive:
- Haemodialysis if AKI
- Blood transfusion if severe anaemia
- Antihypertensive medication
70-80% make a complete recovery
What are signs of dehydration in a blood test
The increase in urea is proportionately higher than the rise in creatinine
(dehydration causes a release in ADH which also increases urea absorption at the collecting ducts)
What are some of the main features between AKI and CKD
Ultrasound:
- Most patients with CKD will have bilateral small kidneys
- Exceptions to this are - ADPKD, early stages of diabetic nephropathy, amyloidosis, HIV associated nephropathy
Calcium will be LOW in CKD (due to lack of vitamin D) but normal in AKI
What are signs of ADPKD
Hypertension
Recurrent UTIs
Flank pain
Haematuria
Palpable kidneys
Renal impairment
Renal stones
Extra renal manifestations:
Liver cysts (most common extra Rena manifestation)
Berry aneurysm (can cause SAH)
Mitral valve prolapse
Aortic dissection
Aortic root dilatation
Mitral-tricuspid incompetence
Cysts: Pancreas, spleen, thyroid, oesophagus, ovary
What is idiopathic thrombocytopenia purpura
It is a spontaneous low platelet count which causes a purpuric (non-blanching) rash.
It is a type II hypersensitivity reaction. Caused by antibodies that destroy platelets.
Can be spontaneously or triggered by a viral infection.
What is the presentation of idiopathic thrombocytopenia purpura
- Usually presents in <10 years old
- Often a history of recent viral infection
- Onset over 24-48 hours:
Bleeding (gums, epistaxis, menorrhagia), bruising, petichael or purpuric rash.
What is the difference between petichae, purpirae and ecchymoses
ALL are non-blanching lesions
Petechiae - pin prick (1mm)
Purpura - larger (3-10mm)
Eccymoses - Large (>10mm)
What does diarrhoea cause
Metabolic acidosis with hypokalaemia
What is the prognosis of minimal change disease
1/3rd - have only one episode
1/3rd - have frequent relapses that stop before adulthood
1/3rd - have infrequent replaces
Which medications are usually safe to continue in an AKI
Paracetamol
Aspirin
Warfarin
Statin
Aspirin (at cardio protective dose 75mg)
Clopidogrel
beta blockers
Which drugs may have to be stopped in AKI for risk of toxicity (rather than kidney injury)
Metformin
Lithium
Digoxin
Which drugs should be stopped in an AKI because they worsen renal function
NSAIDs (except aspirin at 75mg)
Aminoglycosides
ACE inhibitors
Angiotensin II receptor antagonists
Diuretics
What is aport syndrome
An X-linked disease caused by a defect in type IV collagen
This causes an abnormal glomerular basement membrane
What are the features of aport syndrome
- Microscopic haematuria
- Progressive renal failure
- Bilateral sensorineural deafness
- protrusion of the lens surface into the anterior chamber
What is one of the common ways to tell the difference between acute tubular necrosis (renal cause) and a pre-renal cause
Pre- renal: A fluid challenge would cause an increase in urine
Renal: There is a poor response to fluid challenge
What is the management of IgA nephropathy
Isolated haematuria, no proteinuria:
- No treatment needed
- Follow up to check renal function
Persistent proteinuria, normal or slightly reduced eGFR:
- Treatment with ACE inhibitors
Active disease (falling eGFR) or failure to respond to ACE inhibitors:
- Immunosuppression with corticosteroids
What is the prognosis of IgA nephropathy
25% develop end stage renal failure
How is proteinuria tested for in CKD
Urinary albumin:Creatinine ratio testing.
Positive if ACR is >3mg/mmol.
What is an autologous transplant
From one donor to themselves
What is an allogenic transplant
From one donor to another recipient
What is an isograft transplantation
From one donor to their genetically identical recipient
What is a xenotransplantation
From a donor to another species
What are the signs of acute graft failre
Asymptomatic:
Picked up by a rising creatinine
Pyuria
Rising urea
What is acute tubular necrosis
the most common cause of acute kidney injury.
caused by the necrosis of tubular cells due to ischaemia or nephrotoxins.
On blood tests, normal serum urea:creatinine ratio would be expected. On urine tests, sodium levels higher than 40 mmol/, low osmolality, and muddy brown casts would be expected.
what can be used to determine whether a kidney injury is acute or chronic
Calcium will be LOW in chronic kidney disease
What measures should be taken for patients at. risk of contrast induced nephrotoxicity
- 0.9% sodium chloride at 1ml/kg/hr for 12 hours pre and post procedure
- Withhold metformin for a minimum of 48 hours and until renal function has been checked (due to lactic acidosis)
Who is at risk of contrast induced nephrotoxicity
known renal impairment (especially diabetic nephropathy)
age > 70 years
dehydration
cardiac failure
the use of nephrotoxic drugs such as NSAIDs
what is the most common cause of death in patients receiving haemodialysis
Ischaemic hear disease
How is cranial diabetes insipidus treated
Desmopressin
How is nephrogenic diabetes insipidus treated
Thiazides (chlorothiazide)
why are patients with nephrotic syndrome at an increased risk of thromboembolism
Loss of antithrombin III
What bone mineral problems are seen in CKD
Low vitamin D (Kidney usually converts vitamin D)
High phosphate (kidney usually excretes phosphate)
What steps should be taken in CKD to increase vitamin D
Increase dietary consumption
Supplements:
- Alfacalcidol
- Calcitriol
What steps should be taken in CKD to reduce phosphate
First line - recommend a low phosphate diet
Supplementation:
- phosphate binders - sevelamir is now used
Severe cases - parathyroidectomy
what medication should be given if someone has nephrotic syndrome
prophylactic low molecular weight heparin
Puts you at an increased VTE - due to a decrease in antithrombin III
what is one of the signs of acute tubular necrosis
A poor response to fluid challenge
