Renal Flashcards
(111 cards)
grade 1 chronic kidney disease description
- eGFR over 90
- urine findings, genetic traits or structural abnormalities which point to kidney disease
grade 2 chronic kidney disease description
- eGFR 60-89
- mildly reduced kidney function
- urine findings, genetic traits or structural abnormalities which point to kidney disease
grade 3a and 3b chronic kidney disease description
- G3a = eGFR 45-59
- G3b = eGFR 30-44
- moderately reduced kidney function
grade 4 chronic kidney disease description
- eGFR 15-29
- severely reduced kidney function
grade 5 chronic kidney disease description
- eGFR less than 15
- established renal failure
what is a high risk albumin creatinine ratio
over 30 mg/mmol
what are the symptoms of uraemia?
- yellow colour of skin
- uraemic frost
- twitching (restless legs)
- confusion
- encephalopathic flap
- pericardial rub/effusion
- kussmaul breathing
- itch
common diet restrictions in those with CKD
- low salt
- restricted fluid
- low K+
- low phosphorus i.e. no dairy (lots of phosphate in blood leached calcium from bones)
-protein (sometimes, depends on dialysis status)
useful drugs in CKD
- calcium resonium (stops absorption of K+ in GI tract)
- adcal, aluminium, lanthanum (phosphate binders)
- alfacalcidol (active vit D to increase calcium absorption)
- iron supplements
- sodium bicarbonate (for acidosis)
electrolyte abnormalities in CKD
- hyperkalaemia
- hypocalcaemia
- hyperphosphataemia
- metabolic acidosis (bicarb deficiency)
AKI definition
abrupt decline in kidney function:
- increase in creatinine by 26.4umol/l or more than 50%
- reduction in urine output
ABOVE CAN ONLY BE APPLIED AFTER ADEQUATE FLUID RESUSCITATION
what are the ECG changes seen in hyperkalaemia
- tall ‘tented’ T waves
- P wave flattens, prolonged PR, depressed ST
- broad QRS complexes
- sine wave pattern
- ventricular fibrillation
what are the indications for dialysis in AKI
- K+ over 7 (or 6.5 post medical intervention)
- PH under 7.15 (severe acidosis)
- fluid overload
- urea over 40 (may cause pericardial effusion)
Man post MI with an AKI. why?
- AKI caused by intra-arterial contrast used in coronary angiogram post MI
- can reduce risk by giving fluid before and after
main features of nephrotic syndrome
- proteinuria over 3g/day
- hypoalbuminaemia
- oedema
- hypercholesterolaemia
- increased susceptibility to infection (due to loss of antibodies in urine)
Type of damage in nephrotic syndrome
- podocyte damage
- non-proliferative process
main features on nephritic syndrome
- oliguria (little/no urine output)
- oedema/fluid retention
- hypertension
- haematuria and proteinuria with granular casts
- AKI
type of damage in nephritic syndrome
- damage to endothelial and mesangial cells
- proliferative
patient intermittent claudication is perscribed ACEI/ARB. Develops an AKI Why?
- he had renal artery stenosis
- kidney now super hypoperfused
side effects of renal artery stenosis
- malignant hypertension due to kidney being hypoperfused and over-activating RAAS
- flash pulmonary oedema in those with congestive heart failure
features of minimal change disease
- antibodies against podocytes
- nephrotic syndrome
- kids
- biopsy of glomerulus will look pretty normal
- responds well to steroids
features of focal segmental glomerulosclerosis (FSGS)
- areas of damage
- risk factors: heroin, HIV, obesity, reflux nephropathy
- kids and adults can get it
- responds well to steroids
features of membranous nephropathy
- immune complex deposition in basement membrane
- often caused by infection e.g. HepB malaria, syphilis
- also CTD (esp. SLE) , malignancy, drugs
- respond to steroids, alkylating agents and B cell monoclonal antibodies
features of IgA nephropathy
- misfolded IgA forms complexes that can’t be cleared
- causes mesangial cell porliferation with IgA deposits
- worse after resp/GI infections (secretory areas)
- associate with HSP and coeliac disease
- nephritic
- no cure only management or symptoms