renal and urology Flashcards
risk factors of kidney stones
dehydration
hypercalciuria, hyperparathyroidism, hypercalcaemia
- for the calcium related stones eg calcium oxalate which is also most common
gout for uric acid stones
presentation of kidney stones
loin (to groin) pain -
SUDDEN onset
very severe cholicky (waves of worsening due to the ureter spasms)
haematuria, patients moving around unable to find comfort
vomiting and nausea
investigation for kidney stones
urinalysis for haematuria and renal function and other bloods ect
CTKUB diagnostic
PAIN management of kidney stones
NSAIDS although be weary of cardiovascular adverdse effects
diclofenac suggested from NICE
IF NSAIDS contraindicated give IV paracetamol
if requiring admission give parenteral analgesic eg IM diclofenac
can also give alpha blocker for distal ureteric stone
treatment of kidney stones
if <5mm watchful wait
if 5-10 mm? shockwave lithotripsy
10-20 mm shockwave lithotripsy OR ureteroscopy
>20 percutaneous nephrolithotomy
differentials of severe loin (to groin) pain
renal colic
ruptured AAA!- look for hypotension and tachy - systemic upset
pyelonephritis
MSK pain
radiculopathy ( compression or inflammation of spinal nerve roots)
most common type of kidney stone and some others
calcium oxalate
some others:
calcium phosphate
uric acid – where gout is risk factor
CKD clinical presentation
usually asymptomatic unless late stage and undiagnosed: polyuria, lethargy, peripheral oedema, pruritus due to uraemia, anorexia, nausea and vomiting, HT
CAUSES of CKD
chronic pyelonephritis,
chronic glomerulonephritis,
DIABETIC nephropathy,
HT,
adult polycystic kidney disease
what does eGFR calculation take into account?
age
sex
ethnicity
creatinine – all put in MDRD equation
factors that can affect creatinine levles that are not accounted for in eGFR calc
red meat consumption
pregnancy
muscle mass
KEY pathologies and findings in CKD
Anaemia (erythropoetin related prob)
calcium/ phosphate related problems
proteinuria
general picture:
deranged U+E
low eGFR
CLASSIfication of stages of CKD
STAGE 1 eGFR> 90 (WITH DERANGED u+e)
stage 2 gfr<90
st 3<60
st4<30
renal failure <15
with what levels of GFR can you get anaemia of CKD
GFR is less than 35 ml/min (other causes of anaemia should be considered if the GFR is > 60 ml/min)
management of anaemia of CKD?
DETERMINATION And optimisation of IRON STATUS BEFOREEEE giving erythropoiesis-stimulating agents (ESA).
when to give oral or iV iron in anaemia of CKD?
oral iron should be offered for patients who are NOTTT on ESAs or haemodialysis.
(If target Hb levels are not reached within 3 months then IV)
patients on ESAs or haemodialysis generally require IV iron!!!!!
WHAT IS THe best ratio to measure proteinuria
its ACR
WHAT IS considerd a clinically significant proteiniuria in acr
3 mg/ mmol and above
what acr indigates nephrologist referral
ACR >70 mg/mmol
management options of proteinuriaaa
ACE inhibitors if ACR is >30 and coexistent HT
AND >70 indicated regardless of HT
sglt2 other option
what are the clacium phospahte related abnormalities arisIng in CKD
the high phosphate level ‘drags’ calcium from the bones, resulting in osteomalacia
low calcium: due to lack of vitamin D, high phosphate
secondary hyperparathyroidism: due to low calcium, high phosphate and low vitamin D
management of calcium/ phosphate related abnormalities in ckd?
reduced dietary intake of phosphate is the first-line management
phosphate binders
vitamin D: alfacalcidol, calcitriol
parathyroidectomy may be needed in some cases
MASTItis what is it
breast pathology
typically in breastfeeding stage
mastitis features
red hot swollen painful one breast in breastfeeding stage
management of mastitis
keep breastfeeding and analgesia nd warm compresses is conservative management
how to manage mastitis if not resolved conservatively
flucloxacillin 10-14 days
other indications for mastitis flucloxaxillin
systemically unwell fever ect
nipple fissure
what is nephrotic syndrome
a syndrome, so a collection of symptoms
a triad:
proteinuria (massive usually)
oedema
hypoalbuminaemia
nephrotic vs nephritic syndrome
different causes and the NEPHRITIC features include: hypertension, haematuria in addition to proteinuria
pathophysiology of nephrotic syndrome conditions
damage to glomerular basement membrane leading to increased permeability to proteins in the urine
this means that theres less of all sorts of proteins in blood
1) less in general- low oncotic pressure so fluid moves to exracellular space: oedema
2) less antithrombin-III leads to predisposition to thrombosis
3) loss of thyroxine binfing globulin leads to low TOTAL but not FREE THYROXINE levels
nephrotic syndrome most common primary cause and other primary causes
minima change disease (most common in children 2-5)
focal segmental glomerulosclerosis
membranous nephropathy
nephrotic syndrome secondary causes
diabetes mellitus, SLE, amyloidosis, infections (HIV, HEP B AND C) nsaids and gold therapy?
initial investigations for nephrotic syndrome
Urine dipstick: proteinuria and check for microscopic haematuria
MSU to exclude urinary tract infection.
Quantify proteinuria using an early morning urinary protein:creatinine ratio or albumin:creatinine ratio.
FBC and coagulation screen
Urea and electrolytes
complications of nephrotic syndrome
immunosupressed due to loss of immunoglobulins,
thrombosis
management of nephrotic syndromes
from specialist paediatrician with nephrologist
high dose steorids- 4 weeks and gradually wheene over 8 weeks.
low salt
siuretics for oedema
albumin infusion in svere hypoaplbuminemia
what are some conditions under interstitial lung disease
idiopathic pulmonary fibrosis
secondary pulmonary fibrosis
asbestosis
hypersensitivity pneumonitis
presentation of interstitial lung diseases
SOB particularly on exertion
dry cough
fatigue
typical findings on examnation of idiopathic pulmonary fibrosis
bibasal FINE end-inspiratory crackles
clubbing
DIAGNOSIS of ILD
CLINICAL features, high resolution CT thorax (ground glass features)
spirometry
if in doubt: lung biopsy, bronchoalveolar lavage
FINDINGS oF ILD in spirometry
restrictive pattern so FVC and FEV1 significantly reduced
and FEV1:FVC ratio> 70%
general management of ILD AND prognosis
POOR prognosis
management is limited and supportive:
remove or treat underlying cause if secondary or allergic
home oxygen if hypoxic
physiotherapy and pulmonary rehab
pneumococcal flu vaccine
advanced care planning and palliative when appropriate
lung transplant is an option but careful weighing
two medications licensed specifically for idiopathic pulmonary fibrosis
pirfenidone
nintedanib (inhibits tyrosine kinase)
causes of secondary pulmonary fibrosis
Several drugs can cause pulmonary fibrosis:
Amiodarone (also causes grey/blue skin)
Cyclophosphamide
Methotrexate
Nitrofurantoin
Pulmonary fibrosis can occur secondary to other conditions:
Alpha-1 antitrypsin deficiency
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Systemic sclerosis
Sarcoidosis
what pathogenic processes does asbestos trigger and how long does it take for pathologies to develop
sbestos is fibrogenic, meaning it causes lung fibrosis. It is also oncogenic, meaning it causes cancer. The effects of asbestos usually take several decades to develop.
specific diseases caused by asbestos inhalation
Lung fibrosis
Pleural thickening and pleural plaques
Adenocarcinoma
Mesothelioma
