Urology - Renal Failure Flashcards
define AKI
Rapid decline GFR
- Nitrogenous and non-nitrogenous waste products
- Electrolyte (K+)
- Acid-base
- Fluid balance
purley based on blood tests - creatinine
what do you look at in AKI
level of creatinine
what is the classification of AKI
Serum Cr ≥ 26.5 micromol/l in 48 hrs
Serum Cr ≥ 1.5 (base) within last 7 days
Urine Output < 0.5ml/kg/hr for 6 hrs
what is a stage 1 AKI
what is stage 2 and 3 AKI
what are the 3 causes of AKI
pre-renal, intrinsic, post-renal
which of the causes is most common
pre-renal
anything that inpaires blood flow to kidney
dehydration, sepsis, heart failure
You are the FY1 on call and are asked to see a 52 year-old gentlemen in A&E by your registrar; apparently sent in by his GP generally unwell.
52 yrs old
BG: Obesity (BMI>40), Hypertension,Ischaemic Heart Disease,Leg ulcers
PC: Unwell,recent diarrhoea and vomiting,not eating and drinking.
SH: Lives with wife, increasing difficulty with ADL.
Drugs: Lisinopril and Naproxen
Generally Unwell.Temp 40 deg C
CVS: P110/min, BP 74/30, JVP not visible, dry mucus membranes, HS I+II
Resp: RR 24, Sats 94% on 21% FiO2, Chest clear
Abdomen: difficult to examine as sitting, grossly non-tender, BS+ ve
WBC 24
Neut 19
Hb 10.1
Plt 469
Cr 823
Ur 39
K 6.6
CRP 275
What is the cause, give possible diagnosis
pre-renal
Hypovolemia, SepsisShock, Nephrotoxic drugs, Renovascular disease, Left ventricular dysfunction
STAGE 3 kidney injury
what 3 factors are considered for eGFR
Cardiac output (pump)
Effective Circulatory volume (blood)
Peripheral Vascular Resistance (BP)
what are the 3 protective mechanisms for renal autoregulation
Myogenic Reflex
Tubuloglomerular feedback
Renin-Angiotensin system
what happens if arterial pressure decreases
who is at high risk of pre renal AKI
Elderly
Arteriosclerosis (HTN, DM)
Pre-existing renal disease
Underlying cardiovascular disease
ARB/ACEI/NSAID/Anti-hypertensives/Diuretics
how do NSAIDS, ACEi/ARB cause kdney injury
act on autoregulators
what is the management of AKI in dehydrated and septic patient
IV access and Bloods (CRP and cultures)
ABG/VBG
ECG
Wound swabs
Urine dip and I/O monitoring
CXR
what are some of the ECG signs seen for hyperkalaemia
how would you assess fluid balance
Peripherally:
Pulse, CR > secs
Warm/vasodilated/hyperdynamic
Weak/thready/cool
Centrally:
JVP
BP (postural)
Skin turgor/ Mucus membranes
Ausc chest
You’re the FY1 on call and are asked to see a patient in A&E.81 year old gentlemen, GP has sent in as generally “off legs”. A&E have kindly done some bloods for you
Hb 12.0g/dl
WBC 11
Plt 200
Na 130
K 5.8
Ur 40
Cr 1550
81 yr male
BG: Hypertension, Ischaemic Heart Disease, BPH – TURP 1997
PC: Generally unwell, hesitancy, abdominal pain
SX: Independent, Smoker, no ETOH
Drug: Ramipril, Bisoprolol, Furosemide, Aspirin, Simvaststain, Tamsulosin
T 36.1
CVS: P 110 bpm, BP 182/90, JVP 1cm, skin turgor normal, HS I+II
Resp: RR 16, Sats 98% RA, Chest clear
Abdomen: large abdominal mass with suprapubic dullness. DRE: craggy enlarged prostate
What is the cause of AKI
post renal obstruction
what are intrinsic and extrinsic causes of post renal obstruction
Intrinsic
Intraluminal (stone, blood clot, papillary necrosis)
Intramural (bladder tumour, urethral stricture)
Extrinsic
Prostate
Pelvic
RPF - retro peritoneal fibrosis
how would you manage an obstruction
Urinary catheter (SPC)
Polyuric phase – careful input/output monitoring, IVF
USS renal tract
Treat underlying infection
Check PSA/DRE (prostate)
what are the 4 intrinsic renal disease
acute tubular necrosis
acute glomerulonephritis
acute tubular interstitial nephritis
acute vascular issues
what causes Acute tubular necrosis
Ischaemia
Any cause of renal hypoperfusion (hypovolaemia, hypotension)
End of spectrum
Toxins
Endogenous
- Myoglobin – rhabdomyolysis
- Haemoglobin –massive haemolysis
- Myeloma – light chains
- Uric acid – tumour lysis syndrome –
Key mechanisms: direct toxicity and obstruction
Exogenous
Contrast
Antibiotics: aminoglycosides, Amphotericin B
Chemotherpeutic agents (cisplatin)
what is wrong
Acute interstitial nephritis
Normal tubule bottom centre
Amount of inflammatory cells – purple nucleus is WBC – lots in interstitial compartment
what 3 things make up glomerulonephritis
nephrotic syndrome
nephritic syndrome
asymptomatic urinary abormalities
what are key features of nephrotic syndrome
Proteinuria >3.5g/day
Hypoalbuminaemia
Oedema (periorbital)
Hyperlipidaemia
Lipiduria
what are some causes of nephrotic syndrome
Minimal Change
Membranous
Mesangiocapillary
Diabetes
FSGS
Amyloidosis
HIV
Lupus
what are key features of nephritic syndrome
Haematuria (dysmorphic)
Proteinuria (<3g/day)
Oedema
Oligouria
Hypertension
what are some causes of nephritic syndrome
IgA and HSP
Small vessel vasculitis (WG, MPA)
Anti-GBM
Post infectious
Mesangiocapillary
Lupus
what blood tests would you perform for AKI
Haematology (FBC, ESR)
Biochemistry (U&E, CK, CRP, LFT)
Immunology (
ANA – autoimmune
dsDNA – systemic lupus
ANCA – systemic vasculitis
Anti-GBM – Goodpastures
ASO titres, Anti-Dnase B titres – post-strep
Complement
Myeloma screen (SPE, SFLC, BJP)
Virology (hep B, C, HIV)
what are some urgent indications for dialysis
Hyperkalaemia – resistant
Pulmonary Oedema – resistant
Uraemic – encephalopathy, pericarditis
Acidosis
Drug overdose
what does a normal urine dip imply as a diagnosis
pre-renal, ATN and post renal
what does haematuria and proteinuria urine dip imply as a diagnosis
Acute GN
Vasculitis
Thrombotic Microangiopathy
What does WBC and casts urine dip imply as a diagnosis
Acute TIN
Obstruction
Pyelonephritis
what are 3 conditions that require immunosuppression
Glomerulonephritis
Tubulointerstital nephritis
graft rejection
Name different causes of glomerulonephritis and their treatment
Minimal change disease - Normally steroid-responsive
FSGS - Variable steroid response
Membranous nephropathy - Limited response to immunosuppression
IgA nephropathy - Poor response to immunosuppression
Diabetic nephropathy - Adverse effect of steroids
Goodpasture’s Disease - ?Plasma exchange + immunosuppression
Systemic vasculitis - Often responds to immunosuppression
what is the treatment for interstitial nephritis
steroids
common drugs which cause interstitial nephritis
NSAIDS, furosemide/bumetanide, PPIs (lanzoprazole)
when is hyperacute transplant rejection
immediate
Can cause graft loss within minutes to hoursDue to pre-formed anti-donor antibodies in recipient
Avoided by pre-operative cross-match
Untreatable
at what GFR do you need dialysis
10-12
how much more does dialysis give
5-10
what are some small molecules immunosuppressive drugs
what are some immunosuppressive drugs - antibodies (polyclonal and monoclonal)
Polyclonal“IVIg” (pooled immunoglobulin)Anti-lymphocyte globulin (ALG)Anti-thymocyte globulin (ATG)
MonoclonalAnti-CD3 – OKT3Anti-CD25 (IL-2 receptor) – basiliximab, daclizumabAnti-CD52 – alemtuzumab (Campath)Anti-CD20 – rituximab
how are T cells activated and what drugs inhibit what aspects of T cell activation
how does prostate cancer present
insidental finding - rarely have many symptoms
where does prostate cancer spread
bones mainly
how do you diagnosie prostate cancer
PSA,
rectal examination
MRI - biopsy can miss the cancer
biopsy
ISUP - prostate cancer are graded
from what grade do you want to treat protate cancer
Gleason 4 and up.
below this and the cancer is rarely an issue - aged 80+
how do you stage prostate cancer
Bone scan (PSA >20ng/ml)
CT (very high PSA or high grade disease on Bx)
PET-CT (choline, PSMA)
WB-MRI
what is the diagnosis if you see an osteoblastic lesion on an x-ray
its prostate cancer until proven otherwise
what are the top 4 primary metastisis to bone
breast, prostate, lung, kidney
how do bone mets present
pain
cauda equina compression
what is the treatment for prostate cancer
Active surveillance
- GG1, PSA <10
- Life expectancy
Radiotherapy
Prostatectomy
Hormone therapy (anti androgens)
58 yr male patient, smoker
On and off blood in urine for one month
Physical examination unremarkable
Haematology- mild anaemia
You are the junior doctor assessing him. How would you investigate?
bloods and blood films - macrocytic anaemia
ultrasound the kidney
58 yr male patient, smoker
On and off blood in urine for one month
Physical examination unremarkable
Haematology- mild anaemia
How would you investigate ?
ultrasound
what are malignant renal tumors
what are benign renal tumors
Angiomyolipoma
Oncocytoma
what is the most common location of TCC
bladder
how do you investigate haematuria
USS urinary tract
cystoscopy
where do you look for ureter cancer
IVU
CT urogram
ureteroscopy
how do you stage a bladder cancer
MRI
what imaging do you do for testicular tumors
ultrasound
where would you find the sentinal node in testicular cancer
it skips the pelvis and you see in upper abdomen by the aorta
what is chronic kidney disease
A reduction in kidney function, characterised by a reduction in GFR, which is not reversible and may be progressive
what is normal gfr (in mL/min/m2)
120mL/min/1.73m2
what are the 2 GCA stages of CKD
glomerular and albuminuria stage
what 2 things considerable increase the risk of having CKD
albuminuria and impaired glomerular filtration
what are some markers of kidney disease
GFR <60 ml/min/1.73m2
Albuminuria / Haematuria
Electrolyte abnormalities due to tubular disorders
Structural / histological abnormalities (e.g. on imaging, biopsy)
Kidney transplantation
how is CKD definitlvely diagnosed - what tests and results would you see
2 Samples 90+ days apart
eGFR calculated from Creatinine levels (more accurate than Creatinine alone)
Haematuria detected best on dipstick
Albuminuria detected best on alb:creat ratio
Structural disease detected best on US
what are the 3 equations which are used to estimate eGFR
Cockroft-Gault Calculated Creatinine Clearance
(140-age) x (1.23 if male/1.04 if female) x weight / serum creatinine
MDRD eGFR formula
32788 x serum creatinine-1.153 x age-0.203 x 0.742 if female x 1.21 if black
CKD-EPI formula
141 x min(creatinine/k,1)a x max(creatinine/k,1)-1.209 x 0.993age x 1.018 if female x 1.159 if black
If female, k=0.7, a=-0.329; if male k=0.9, a=0.411
what are the 2 main causes of chronic kidney disease
diabetes - 20-40%
hypertension - 10-25%
what are some other less common causes of chronic kidney disease
Renovascular disease
Reflux disease
Obstructive uropathy
Autosomal dominant polycystic kidney disease
Glomerulonephritis
Unknown- idiopathic
how would you manage CKD stage IIIb and IV
Ongoing risk factor management
Non-glomerular functions start to be relevant
Iron-erythropoietin balance
Calcium-phosphate balance
Tubular function can start to decline
Low potassium diet, oral bicarbonate
Most common with diabetic nephropathy due to a Type IV renal tubular acidosis.
what are some complications of CKD
Anaemia of CKD
Mineral Bone Disorder of CKD
Salt & Water, Acid-Base disorders
‘Uraemia’
Disease-specific complications
how would you manage CKD managment for stage V
Preparation for renal replacement
Low Clearance Clinic for discussion of options
Definitive dialysis access in good time
Listing for pre-emptive transplantation / planned living donation if appropriate
Close monitoring of progression
Little margin of error
Can start to get problems with salt & water
May need fluid ration
what are the 3 renal replacement therapies
Haemodyalyisis
peritoneal dialysis
transplantation
Identify most important or frequent ADR of specified drug.
Patient given iv morphine stat after hip replacement. What important ADR to monitor?
Sweating
Itching
Constipation
Respiratory rate/ depression
Lethargy
Respiratory Depression
Identify most likely cause of specified ADR.
82 year old lady, history of hypertension. 3 months of ankle swelling. Treated with diuretics – no improvement. What is most likely cause?
Aspirin
Amlodipine
Alendronate acid
Bendroflumethiazide
Bisoprolol
amlodipine
Patient with hypertension and heart failure. Routine bloods K+ 5.9 mmol. (3.5 – 5.1 mmol).
Select two drugs most likely to interact to cause this:
Aspirin
Bendroflumethiazide
Bisoprolol
Digoxin
Isosorbide Mononitrate
Ramipril
Spironolactone
ramipril and spironalactone
Patient with hypertension and heart failure. Pulse rate: 48 beats per minute.
Select two drugs most likely to interact to cause this:
Aspirin
Bendroflumethiazide
Bisoprolol
Digoxin
Isosorbide Mononitrate
Ramipril
Spironolactone
bisoprolol and digoxin
what drugs have poor kinetics (narrow range of safety)
Gentamicin, vancomycin
Theophylline
Phenytoin
what drugs affect the liver
Anticonvulsants
Anti-TB drugs
what drugs affect the kidney
Aminoglycosides
Diuretics & other drugs for heart failure
how do calcium blockers cause interactions
Calcium blockers →relax smooth muscle → vasodilatation → headache, flushing, oedema
what are the 4 adverse drug reactions that need to be memorised
Bisphosphonate – osteonecrosis of the jaw
Metformin – lactic acidosis
Carbimazole, clozapine – marrow suppression
**Statins - myositis
what mechanisms help to show possible ADRs
Block A-V node conduction – bradycardia
Arterial dilatation – hypotension
CNS drugs – sedation
Antiplatelets /Anticoagulants – haemorrhage
Drugs acting on aldosterone and kidney – potassium and other electrolyte abnormalities
how do you predict issues of Treatment of atrial fibrillation – rate control with beta-blocker
what are the main ADRs for salbutamol
patient presents with tremor or tachycardia after using inhaler what is the most likely drug
salbutamol
why do some drugs interact (3)
what are bradycardia with the same drug interactions
alchohol
GTN and alcohol are both vasodilators
increased risk of hypotension and fainting
especially when GTN used within 1 hour of alcohol
what are target sights of trimethoprim and methotrexate
what are important enzyme interaction inducers
Drugs for epilepsy – carbamazepine
Antibiotics – drugs for TB
Alcohol
what are important enzyme inhibitors
Antibiotics – clarithromycin, ciprofloxacin
Xanthine oxidase inhibitor - allopurinol
what is a type A ADR
dose dependent, predictable
beta-blocker causes bradycardia because of action on beta-receptors in cardiac conduction
what is a type B ADR
not dose dependent, cannot be predicted pharmacologically
Anaphylaxis to penicllin
what 2 ways are you able to limit the classification
No account of duration e.g. steroid osteoporosis – cumulative dose and length of therapy are relevant
What about susceptibility – poorly mobile elderly women more likely to have steroid osteoporosis
76 year old recent acute coronary syndrome. TSH 12.6. Please prescribe thyroxine. (you can use BNF)
25mcg OD
83 year old with severe acute gout. Started on Naproxen 250 mg bd. What management options to prevent complications from Naproxen?
use lower dose
restrict time of treatment 5-10 days
assess susceptibility
30 year newly diagnosed thyrotoxicosis. Start carbimazole. What is the most important communication item?
“Patient should be asked to report symptoms and signs suggestive of infection, especially sore throat.
A white blood cell count should be performed if there is any clinical evidence of infection.”
