Medicine - Renal Flashcards
When does the Anion gap apply and what does an increased ion gap mean? What value is increased?
Applies in Metabolic Acidosis eg. DKA, Sepsis (lactic acidosis), Aspirin overdose (salicylate)
Normal anion gap is 8-12
If raised ion gap, it is due to increased acid production eg. DKA/Sepsis/Toxins
If not raised, likely due to Addison’s, renal tubular acidosis
How is the anion gap calculated?
Sodium - (Chloride + Bicarbonate)
Name some causes of Metabolic Alkalosis
Diarrhoea/Vomiting (loss of H+ and Cl-), Conn’s, Diuretics (Loop/Thiazide), Hypokalaemia
AKI Stages: Causes: Risk factors: Investigations: Management: Indications for dialysis:
Stages:
Stage 1 - 50-100% rise in creatinine and urine output <0.5ml/kg/hour for 6 hours
Stage 2 - 100-200% rise in creatinine and urine output <0.5ml/kg/hour for 24 hours
Stage 3 - 200+% rise and <0.3ml/kg/hour for 12 hours or RRT needed
Causes:
Pre-renal eg. sepsis, anaphylaxis, renal artery stenosis, ACE
Renal: ATN from hypovolaemia, myoglobin, CT contrast, Gentamicin, lupus nephritis, IgA nephropathy, drugs
Post-renal = stuff that causes hydronephrosis
Risk factors: Age, Immobilisation, Diabetes, Sepsis, Dehydration, Medications eg. ACE/NSAIDs, Gentamicin (aminoglycosides), Glomerulonephritis
Investigations: Urine dipstick to see if blood and protein on stick (think glomerulonephritis, U&Es, LFTs for hepatorenal, CK for rhabdo, USS for hydronephrosis, ASO(strep)/ANCA/ANA/C3/4 (lupus)/Anti-GBM, Bone profile
Management: Sepsis 6 if appropriate, manage oedema with diuretics/fluid restriction, give Oxygen, give low dose morphine to cause pulmonary vasodilation, GTN, stop NSAIDs/ACE, monitor via Central Venous Pressure line, consider RRT
Indications for dialysis:
- Oedema not responsive to treatment
- Metabolic acidosis not reactive to treatment
- Uraemic pericarditis/encephalopathy
- Hyperkalaemia resistant to treatment
CKD Pathophysiology: Stages: Causes: Symptoms: Management: Complications:
Pathophysiology: > 3 months of reduced eGFR
Stages: 1 ->90, 2 - 60-90, 3a - >45-59, 3b - 30-44, 4 - 15-29, 5- <15
Causes: Diabetic nephropathy, Hypertensive nephropathy (eg. Conn’s, Phaeochromocytoma, Cushing’s, Renal artery stenosis, hyperthyroidism), Glomerulonephritis, Polycystic kidney disease (dominant, flank pain, fever, haematuria), Heart failure, Pyelonephritis, Age
Symptoms: Nausea, vomiting, sleep problems, mental state changes
Management: Treat underlying disease, statins/BP control/smoking control for CVS risk, give ACE to reduce proteinuria, give EPO/B12/Folate, have a low phosphate/low potassium diet, take Vitamin D
Complications: Anaemia of chronic disease due to EPO prod, functional iron deficiency, bone marrow suppression due to uraemia, Mineral bone disease due to reduced Vitamin D fixation (1’OH), Hyperparathyroidism (tertiary), Cardiovascular disease (main killer), Dyslipidaemia
Nephrotic Syndrome
Triad:
Complications:
Causes:
Triad: Oedema, Hypoalbuminaemia, Proteinuria (measured by ACR >3.5g/24 hours) (Hypercholesterolaemia)
Complications: Infection, VTE (clotting factors are protein bound, so lost to urine), CKD, Hypertension, Hyperlipidaemia
Causes: Membranous, Minimal change, Focal segmental
Nephritic Syndromes
Triad:
General Management:
Triad: (Sudden AKI), Haematuria, Proteinuria <3.5g (less), Hypertension
Management: ACE for proteinuria, BP control, Diuretics if fluid overloaded, VTE prophylaxis if hypalbuminaemia, statins for hypercholesterolaemia, IV methylprednisolone pulse therapy, oral corticosteroids
Post-strep glomerulonephritis Cause: Onset duration: Target age: Markers: Management:
Causes: Group A B-haemolytic strep
Onset: 1-2 weeks after strep throat, 2-4 weeks after impetigo/cellulitis
Target age: Children
Markers: ASO, C3 - would see IgG/M and C3 deposition on biopsy
Management: Self-limiting, give ACE for hypertension/proteinuria
IgA Nephropathy Cause: Onset duration: Target age: Complication: Markers/Biopsy: Management:
Cause: URTI/GI infections leading to IgA reaction and mesangial deposits in the glomerulus
Onset: 1-2 days after infection
Age: 20-30 years old
Complication: Progresses to ESRF within 20 years
Markers: IgA increase
Management: ACE for proteinuria/hypertension
ANCA Vasculitis
Types:
Antibodies:
Management:
Types: Granulomatosis with polyangiitis (pulmonary involvement), Churg-Strauss (Asthma + Allergic Rhinitis + Purpura + Peripheral Neuropathy)
Antibodies: ANCA
Management: Immunosuppression
Anti-GBM Pathophysiology: Symptoms: Antibodies: Biopsy: Management:
Pathophysiology: Antibodies against Type 4 collagen, also found in the lungs
Symptoms: Nephritic syndrome + Haemoptysis
Antibodies: Anti-GBM
Biopsy: IgG deposition and pulmonary infiltrates in the lungs
Management: Immunosuppression
Alport Syndrome
Pathophysiology:
Management:
Pathophysiology: X-linked (male), Type 5 collagen mutation - linked to ocular and hearing changes
Management: Supportive, RRT and transplant - can lead to anti-GBM
Lupus Nephritis
Cause:
Markers:
Cause: Complication of SLE
Markers: ANA and ds-DNA antibodies
Peritoneal Dialysis
What is it?
Advantages:
Disadvantages:
What is it: Patient’s own peritoneal membrane used as a dialysis membrane - solutes pass down concentration gradient into dialysate fluid. Can be done overnight or continuous ambulatory.
Advantages: QOL - can be done at home, Individualised planning
Disadvantages: Technical, Unsuitable in those with previous surgery, Infection (peritonitis), Can lead to Hernias, Hydrothorax, Peritoneal Sclerosis
Haemodialysis
What is it?
Advantages:
Disadvantages:
What is it: Blood from patient pumped through dialysis membrane.
Advantages: Efficient (works well), Unit-based with plenty of support staff
Disadvantages: Need access to slots and need to plan life around it, Infection, Haemodynamic instability, AVF steal syndrome, Haematomas, Muscle cramps, Haemolytic anaemia
