Child Health- Renal Flashcards
UTI, Nephrotic and nephritic disease
define oedema
increase of interstitial fluid
clinical presentation of swelling with pitting, facial oedema, ascites, pleural effusions, pulmonary oedema
causes of increased interstitial fluid
lymph drainage
-lymphodema, obstruction or design
venous drainage
- obstruction eg DVT
lowered oncotic pressure
- low albumin/protein
-malnutrition
decreased production in liver
increased loss in the gut or kidney (nephrotic syndrome)
describe the clinical signs of nephrotic syndrome
heavy proteinuria
hypoalbuminaemia
oedema
what are the three types of nephrotic syndrome
congenital
steroid sensitive
steroid resistant
what are the differences in teh clinical signs of steroid senstive and steroid resistant NS
blood pressure
-sens= normal
-resistant= elevated
haematuria
-sens= no macroscopic
- resistant= macroscopic
renal function
-sens= normal
-resistant= impaired
resistant has features to suggest nephritis
resistant has histological changes present eg. glomerulopathy, basement membrane abnormality
clinical presentation of steroid sensitive NS
peak age of onset= 2-5 years
M>F
higher incidence in those from asian sub continent
unknown immunological aetiology
~5% continue into adult life
normal renal function if steroid responsive
what is the treatment for sSNS
standard course of prednisolone for 1st episode
-60mg/m2 for 4 weeks
-40mg/m2 on alternate days for 4 weeks
also consider
- Na and water moderation
-diuretics
-Pen V
- measles and varicella immunity and pneumococcal immunisation
describe the clinical presentation of acute glomerulonephritis
haematuria- often macroscopic (tea or coca cola coloured)
proteinuria- varying degrees
impaired GFR- rising creatinine. variable degree
salt and water retention- hypertension, oedema
what can trigger glomerulonephritis?
streptococcus
acute post streptococcal glomerulonephritis
where would a strep infection which triggers glomerulonephritis be located
nasopharyngeal or skin infection
which strains of strep cause glomerulonephritis
Gp A Beta haemolytic streptococcus
nephritogenic
what is the pathology of acute post streptococcal glomerulonephritis
antigen-antibody complexes form in the glomerulus, causing complement activation
clinical nephritis presents 10 days post infection
-haematuria, swelling, decreased urine output.
-oedema, hypertension, signs of cardiovascular overload
describe the renin angiotensin aldosterone system
reduction of blood pressure causes renin release.
renin cleaves angiotensinogen to angiotensin I.
angiotensin-converting enzyme (ACE) cleaves angiotensin I to Angiotensin II.
AII acts on the adrenal glands to release aldosterone.
causes salt retention and therefore more water moves out of the tubules and back into the blood.
what is Henoch-Schonlein Purpura (HSP)
a type of vasculitis
affects: skin, joints, gut, kidneys
what is the pathology of HSP nephritis
IgA deposition in the kidneys