Renal Flashcards
Nephrotic syndrome what is it and path
proteinuria
= low serum albumin
= which provokes Oedema
& hyperlipidemia
cause = podocyte effacement = more permeable to protein
thefor no renal impairment bc diseases of only filtration barrier (podocytes) (bc nephrin bridges between the podocyte feet are lost which usually filter proteins
normal renal fxn normal Cr
Minimal change disease (MCD), what is it
pt
ix
tx
non immune depositing nephrotic syndrome
pt: children post viral infection w nephrotic syndrome (oedema)
Ix: only finding is podocyte effacement on electron microscopy (but normal glomeruli)
tx: corticosteriods resolution and complete recovery & no recurrence is norm. if dont respond = progress to FSGS
ATN types and area
TOXIC ATN (PCT)
rhabdo (myoglobin), amphoterecin, contrast dye
ISCHAEMIC/hypoperf ATN (PCT, TA, DCT)
ATN phases
PRODROMAL
Apoptosis of epithelial cells and sloughing
= Inc Cr
OLIGURIC
Filtration impaired (cast obstructing)
hyperkalaemia (ions not filtered)
volume overload (water not filtered)
Increased urea and Cr (ratio<10)
- haemodialysis
POLYURIC
Resorption impaired (cast washed away but epithelium still dont work)
volume depleted
reduced urea and CR
tx - iv fluids n ion replace
types of AIN
pyelonepthritis
allergic nephritis
NSAID caused
Pyelonephritis fx
urgency freq and dysuria + fever and loin tenderness
WBC casts (macrophages n neutrophils)
Urine micro: gram -ve ie klebsiella Uti ones
allergic nephritis fx
Eosinophilia + fever + rash post starting new sulf med:
either duiretics or abx eg PCN, cephalo, trimeth
NSAID nephropathy
reduced prostaglandins = arteriole constriction = hypoperf –> pupillary necrosis
= haematuria
and fibrosis (may lead to urothelial ca of renal pelvis)
hypocalcaemia tx
prolonged QT = urgent iv calcium gluconate
SGLT2 inhibitor example and adverse effects
dapagliflozin
Urinary genital infection (bc glycosuria)
Fourniers gangrene
normoglycaemic ketoacidosis
inc risk of lower limb amputation: closely moniter feet
fourneiers gangrene
necrotizing faciatis of the genetalia or perineum
prenal AKI
hypovolaemia ie diarohea vomiting
renal artery stenosis
renal AKI cause
glomerulonephritis
ATN
AIN
rhabdomyolysis
tumor lysis
post renal aki
stone
bph
external compression
unknown cause of aki ix
renal tract USS in 24 hrs
hypercalaemia features
bones stones groans and psychic moans
corneal calcification
shortened QT on ecg
hypertension
young pt started on acei for htn and then has deterioation in renal function
undiagnosed bilateral renal artery stenosis
causes of CKD
htn
diabetic nephropathy
chronic pyelonephritis
chronic glomeruloneph
adult polycyctic kidney disease
renal USS in CKD why
exclude obstruction
renal size (small in ckd)
exclude polycystic kidneys
drugs in CKD to slow disease
ACEi
SGLT2 - dapafloglzin
signs of CKD on examination
oedema, pallor, uremic tinge, purpura, bruising, evidence of scratching
pericardial rub
pleaural effusion
how does haemodialysis work
Blood and dialysis fluid flow either side o f a semi permeable
membrane, molecules diffuse down their concentration gradients,
plasma biochemistry changes to become more like the dialysis fluid
peritoneal dialysis complications
Bacterial peritonitis, local infection at catheter site, constipation, failure, sclerosing peritonitis.
organ transplant rejection types
hyperacute - abo incompatible
acute - in 6 mths - T cell mediated
chronic = after 6 mths vascular changes
membranous glomerulonephritis histology
basement membrane thickening on light microscopy
subepithelial spikes on sliver stain
positive immunohistochemistry for PLA2
causes of membranous glomeruloneph
idiopathic: due to anti-phospholipase A2 antibodies
infections: hepatitis B, malaria, syphilis
malignancy (in 5-20%): prostate, lung, lymphoma, leukaemia
drugs: gold, penicillamine, NSAIDs
autoimmune diseases: systemic lupus erythematosus (class V disease), thyroiditis, rheumatoid
why does nephrotic predispose to vte
loss of antithrombin 3
iga nephro vs post strep glomer
iga = 2 days post illness
post strep = 1-2weeks
FSGS causes
LM
IF
EM
idiopathic
congenital
HIV
Sickle cell
heroin
Lm = some glomeruli some sclerosis
IF = -ve (maybe igm)
EM = effacement
membrano prolif path
lm
em
if
preformed ag-ab complexes
mesnagial prolif into BM
lm = basement mem splitting/thickening
em = subendothe
if = granular igg +c3
membranous nepthro
LM
EM
IF
lm = diffuse capillary thickening
em = subepithelial deposits
IF = granular igg +c3
acute urinary retention causes
BPH
UTI
dx - Anti cholinergic, opiods, TCAs
urethral structures
constipation
calculi
acute vs chronic urinary retention
chronic typically painless
may present with overflow incontinence
larger volume of urine in bladder ie 1.5l+
acute urine retention ix
urinalysis and culure (catheterise)
FBC U&E Cr CRP
Bladder USS