Nephrology Flashcards
DI
Hyperkalemia management
K>7mmol or 5.3 mmol with ECG changes:
10 ml of 10% calcium gluconate IV over 2 mins, repeat every 15 mins up to 50 ml (five doses) until K+ is corrected.
10 units of actrapid in 50 ml of 50% of glucose over 10 min
salbutamol 5mg nebulizer
consider calcium resonate 15 g PO or 30g PR
consider dialysis if the patient is not responding.
function of calcium gluconate, insulin, salbutamol and caclium resonium in hyperkalemia managmeent
calcium gluconate - stabilizes the cardiac membrane
insulin - shifts the k+ intracellularly
Salbutamol - also causes intracellular movement of K+ ion
calcium resonium - binds and removes k+ from the body
risk factors that precipitate hyperkalemia
Impaired excretion of K+: AKI, CKD, diuretic use(spironolactone, amiloride, epeleronone),hypoaldesterism, addison’s disease
Increase release of K+ cells: tumour lysis syndrome, trauma, DKA, rhabdomyolysis, insulin deficiency
Drugs: NSAIDs, potassium-sparing diuretics, digoxin toxicity, beta-blockers.
Hyperkalemia ECG changes
tall tented t waves, flattened p waves, widened QRs complex, sine wave pattern, VF/aystole
Hyponatremia management
Hypervolemic state: restrict fluids, daily weights check. Treat underlying cause. A loop diuretic may be used. Vasopressin receptor antagonist.
Hypovolemic hyponatremia Isotonic fluid replacement. In symptomatic patients aim for Na+ correction of 3-6mmol/l
per day. Serum sodium should be initially checked every 8-12 hours
and then every 24 hours after that.
Normal volume hyponatremia: Treat the underlying cause, SIADH management. Fluid restriction - Patients should be placed on 1L/Day or 500mls less than their
urinary output. The correction target should be for Na+ increase no greater than 8mmol/day.
If fluid restriction alone fails then vasopressin receptor antagonists (tolvaptan) may be given which will allow diuresis
Initial management of AKI
IV fluid, monitor ECG (hyperkalemia), monitor observations including fluid balance and repeat U&E to check for deterioration or improvement
Interpretation of creatinine results when in normal range
Creatinine within normal range can qualify as AKI if following criteria are met:
1. a rise of creatinine of greater than 26mmol/l over 48 hours
2. rise of creatinine of >50% over 7 days
3. a fall of urine output to less than 0.5ml/kg over 6 hours
why is the urea high after upper gi bleed without AKI
signaficant amount of blood is digested resulting in alot of urea absorbed into the blood as consequence of protein metabolism
types of nephrotic syndrome
Nephrotic syndrome can be primary (idiopathic) or secondary to systemic diseases. Common causes include:
Primary causes: Minimal change disease, focal segmental glomerulosclerosis (FSGS), membranous nephropathy.
Secondary causes: Diabetes mellitus, systemic lupus erythematosus (SLE), amyloidosis, infections (HIV, hepatitis B and C), drugs (NSAIDs, gold therapy).
Triad of nephrotic syndrome
Nephrotic syndrome is a clinical complex characterised by a triad of:
1. Proteinuria (> 3g/24hr) causing
2. Hypoalbuminaemia (< 30g/L) and
3. Oedema
Initial investigation for nephrotic syndrome
Initial investigations
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
How is chronic kidney disease classified
Albumin:creatinine ratio
1 Normal <3.0 mg/mmol
2 Moderately increased 3 - 30 mg/mmol
3 Severely increased >30 mg/mmol
EGFR:
1 Normal ≧90
2 Mild Decrease 89 - 60
3A Moderate Decrease 59 - 45
3B Moderate Decrease 44 - 30
4 Severe Decrease 29 - 15
5 ESKD (Kidney failure) <15
Complications of CKD
Metabolic acidosis - due to inability of the kidneys to excrete acid. Managed: oral bicarbonate supplements or dialysis
pulmonary oedema: due to fluid overload, which build up in the lungs. Management: avoid excessive water and sodium intake, treated with loop diuretics(furesemide_ or dialysis
anaemia of CKD: insufficiency of erythropoietin which is secreted by the kidneys. Management: erythropoietin stimulating agents. Often require iron supplementation too.
Uremic encephalopathy: build up of toxin in the blood therefore affects the brain. Treatment: dialysis
CVD:combination of salt and water overload, hypertension and accelerated atherosclerosis. Mangage CVD risk factors
hyperkalemia: kidneys inability to excrete K+. Treatment: K restricted diet, avoidance of drugs promoting hyperkalemia ) ACE inhibtors, use of potassium binder (calcium resonium), or dialysis
Bone mineral disorder of CKD : increased secretion of PTH (2nd hyperparathyroidism) because of impaired renal hydroxylation of vitamin D, and renal phosopate retention. Management: administration of hydroxylated vit d and control of hyperphosphatemia by restriction of dietary phosphate and administration phosphate binders (Sevelamer).
Indications to start renal replacement therapy (AEIOU)
aeiou in acute renal failure
A – Acidosis with a pH <7.1
E – Electrolyte imbalance: K+ >7.0mmol/L or
refractory hyperkalaemia with ECG changes
I – Intoxication: poisons such as ethylene glycol and
lithium
O – Overload: severe pulmonary oedema with oliguria
or diuretic resistant
U – Uraemia symptoms: encephalopathy or
pericarditis
CKD with eGFR <10mls/min
Symptomatic uraemia: pruritus, encephalopathy, pericarditis,
anorexia, nausea
assessment of fluid status
- blood pressure - high/low/postural drop
- Jugular venous pressure - can be misleading cor pulmonale
- edema examination: peripheral, sacral, or pulmonary
- daily weights and fluid balance charts
- skin turgor and mucous membranes
