Med booklet BB

Question 1

What renal function blood tests can we do

Answer 1

FBC – Anaemia, infection, allergic reactions,

 Haematinics – Iron/Folate/B12 deficiency

 U&Es – Potassium, Urea, Creatinine, Bicarbonate

 Bone profile – Calcium, Phosphate, PTH, Alkaline Phosphatase

 CRP – Infection/Inflammation

 HbA1c – Diabetic control

Question 2

What Urine tests can we do

Answer 2

 Urine Dipstick – Infection (leukocytes, nitrites); Glomerular pathology (blood, protein)

 Urine Protein:Creatinine Ratio – Quantifies the amount of all protein in the urine

 Urine Albumin:Creatinine Ratio – Quantifies just albumin (good for diagnosing and monitoring diabetic
nephropathy)

 Urine microscopy, culture and sensitivity

Question 3

What imaging can be done

Answer 3

US KUB – look for peri-nephric collection, size of kidneys, corticomedullary differentiation, hydronephrosis.

ultrasound, kidneys, urethra, bladder

Question 4

Causes of metabolic alkalosis

Answer 4

Causes
 GI losses
o Diarrohoea
Vomiting

 Renal losses
o Primary hyperaldosteronism
o Tubular transporter defects
o Diuretics

 Intracellular shift
o Hypokalaemia

Question 5

Why is anion gap useful and what is the equation

Answer 5

Can be useful to work out what could be causing the acidosis

Anion Gap = Sodium - (Chloride + Bicarbonate)

[Na+] – ([Cl-] +
[HCO3-])

Question 6

What is a normal anion gap

Answer 6

8-12

Question 7

What does high anion gap indicate and list some causes for the acidosis

Answer 7

Acidosis due to increased acid

Lactic acidosis
Anaerobic exercise; Sepsis; Organ ischaemia

Ketoacidosis
Diabetic; alcohol abuse; Starvation

Toxins
Ethylene Glycol; Methanol; Isoniazid; Aspirin; Salicylate

Renal failure

Question 8

What does normal anion gap indicate and list some causes for the acidosis

Answer 8

Acidosis due to reduced alkali

GI losses of HCO3
Vomiting; diarrhoea

Renal losses of HCOs
Renal tubular acidosis; mineralocorticoid deficiency (Addison’s)

Toxins
Ammonium Chloride; Acetazolamide

Question 9

What usually causes hypernatraemia, what does high cause (bad)

Answer 9

Usually due to water deficit.
 Causes cellular dehydration (osmotic drag).
 Creates vascular shear stress (bleeding and
thrombosis)

Question 10

Symptoms of hypernatraemia

Answer 10

Symptoms of thirst, apathy, irritability, weakness, confusion, reduced consciousness, seizures, hyperreflexia, spasticity & coma

Question 11

Hypernatraemia - hypervolaemic, euvolaemic and hypovolaemic. explain causes of hypernatraemia in each of these…

Answer 11

Hypovolaemic High Na
 Renal free water losses (Osmotic diuresis [NG feed etc], loop diuretics, intrinsic renal disease)
 Non-Renal free water losses (Excess sweating, Burns, Diarrhoea, Fistulas)

Euvolaemic High Na
 Renal Losses (Diabetes Insipidus, Hypodipsia)
 Extra-Renal Losses (Insensible, Respiratory losses)

Hypervolaemic High Na (Sodium Gains)
 Primary hyperaldosteronism, Cushing’s Syndrome,
Hypertonic dialysis, Hypertonic Sodium Bicarbonate, Sodium Chloride tablets

Question 12

Card on diabetes insidious

Answer 12

Diabetes Insipidus (differential = psychogenic polydipsia) – dilute urine (Urine osmolality <300)

Polydipsia and polyuria – not always hypernatraemic Impaired release of ADH (Cranial DI)

Causes - Trauma/post-op, tumours, cerebral sarcoid/TB, infection (meningitis/encephalitis), cerebral vasculitis (SLE/Wegener’s)
Resistance to ADH (nephrogenic DI)

Causes - Congenital, Drugs (lithium, amphoterecin, demeclocycline), hypokalaemia, hypercalcaemia, tubulointerstitial disease

Question 13

Hypernatraemia treatment?

Answer 13

Treatment
 Generally – free water

Question 14

Hyponatraemia causes

Answer 14

Causes
Pseudohyponatraemia – occurs with high lipids, myeloma, hyperglycaemia, uraemia etc.

Question 15

Hyponatraemia symptoms

Answer 15

Low Na causes decreased perception and gait disturbance, yawning, nausea, reversible ataxia, headache, apathy, confusion, seizures, coma.

Question 16

Hyponatraemia investigations

Answer 16

Investigations – plasma osmolality (if normal or raised then pseudohyponatraemia), hypokalaemia/hypomagnesaemia potentiates ADH release, Urine sodium (if <20 then non-renal salt losses, if >40 then SIADH) (diuretics may confound), TSH and 9am cortisol, Calcium, albumin, glucose, LFT, CT head or chest if suspect SIADH.

Question 17

Hyponatraemia - hypervolaemic, euvolaemic and hypovolaemic. explain causes of hypernatraemia in each of these…

Answer 17

Hypovolaemic Hyponatraemia
Renal loss [Urine Na+ >20mmol/L]
 Diuretics (thiazides), Osmotic diuresis (glucose, urea in
recovering ATN), Addison’s disease (mineralocorticoid
deficiency)
Non-renal loss [Urine Na+ <20mmol/L]
 Diarrhoea, Vomiting, Sweating, Third space losses
(burns, bowel obstruction, pancreatitis)

Euvolaemic Hyponatraemia
 Hypothyroidism, Primary polydipsia – (if urine osmolality <100), Glucocorticoid deficiency – adrenal insufficiency, SIADH

Hypervolaemia Hyponatraemia
 CCF, Nephrotic syndrome, Liver cirrhosis

Question 18

Treatment of hyponatraemia when hypervolaemic and hypovolaemic

Answer 18

Hypo
Treatment – give IV fluids (0.9% NaCl at 1-3ml/kg/hour) Give K if necessary

hyper
Treatment – fluid restrict and consider furosemide

Question 19

Risk of correcting hyponatraemia quickly?

Answer 19

Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis. Aim to correct <12 mmol/L/day

Question 20

Treatment of acute hyponatraemia?

Answer 20

Acute (tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy)
If acute hyponatraemia (within 48 hours) and symptomatic – Give 3% hypertonic saline IV boluses +/- Furosemide

Question 21

Treatment of chronic hyponatraemia

Answer 21

Chronic
If chronic (>48 hours) and symptomatic – hypertonic saline boluses if having seizures. Otherwise isotonic saline and furosemide – aim to correct 8mmol/L in 24 hours
If chronic and asymptomatic – water restriction, stop offending drug, if dehydrated – restore volume, if overloaded – Na and water restriction and diuretics

Question 22

As many causes of hyperkalaemia

Answer 22

Causes
 CKD, K rich diet with CKD (dried fruit, potatoes, oranges, tomatoes, avocados, nuts)
 Drugs (ACEi/ARBs/Spironolactone/Amiloride/NSAIDs/ Heparin/ LMWH/Cyclosporin or calcineurin inhibitors/High dose Trimethoprim/ Digoxin toxicity/B- blockers)
 Hypoaldosteronism (T4RTA), Addison’s disease, Acidosis, DKA (insulin deficiency), Rhabdomyolysis, tumour lysis, Massive haemolysis, Succinylcholine use
 Rarer – Hyperkalaemic periodic paralysis, Gordon’s syndrome
 Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis

Question 23

ECG changes in hyperkalaemia

Answer 23

ECG changes
 Tented T waves
 Prolonged QRS
 Slurring of ST segment
 Loss of P waves
 Asystole

Question 24

3 treatment stages for hyperkalaeima (detailed)

Answer 24

1. Stabilizing the myocardium to prevent arrhythmias
    10mls of 10% Calcium Gluconate over 5-10 minutes
2. Shifting potassium back into the intracellular space
   IV fast acting insulin (actrapid)
    10 units and IV glucose/dextrose 50% 50mls
   Sodium Bicarbonate
    500mls of 1.4% Sodium Bicarbonate
    Only effective at driving Potassium intracellullarly
   if the patient is acidotic
   Salbutamol
    5-10mg via nebulizer
3. Eliminating Potassium From the Body: Calcium Resonium
    15-45g orally or rectally, mixed with sorbitol or lactulose
   Frusemide
    20-80mg depending on hydration status
   Dialysis
    If resistant to medical treatment

Question 25

Hypokalaemia symptoms

Answer 25

Fatigue, constipation, proximal muscle weakness, paralysis, cardiac arrhythmias, worsened glucose control in diabetics, hypertension

Question 26

Causes of hypokalaemia

Answer 26

 Pseudohypokalaemia – acute leukaemia
 Extra-renal losses - Inadequate PO intake, Gut
losses (vomiting, NG losses, secretory Diarrhoea, laxatives, VIPoma, Zollinger-Ellison, Ileostomy, enteric fistula)
 Redistribution – Delirium tremens, beta agonists, insulin, caffeine, theophylline, alpha-blockers (Doxazosin), hypokalaemic periodic paralysis (inherited or acquired from thyrotoxicosis – Asian males)
 Refeeding syndrome, alkalosis, vigorous exercise, glue-sniffing (Toluene can cause Fanconi/RTA II with renal potassium wasting)
 Primary hyperaldosteronism (conn’s syndrome) Cushing’s syndrome, Secondary hyperaldosteronism (liver failure, heart failure, nephritic syndrome),
 Renal losses (diuretics, RTA, Tubulopathies - Bartters/Liddles/Gittelmans), liquorice, glucocorticoids, hypomagnesaemia.

Question 27

Hypokalaemia on ecg?

Answer 27

 Small T waves
 U wave (after T)
 Increased PR interval

Question 28

Treatment of hypokalaemia

Answer 28

Replace magnesium
 Oral K replacement
 IV K replacement (Usually in 0.9% NaCl - avoid in
dextrose as induces further hypokalaemia)

Question 29

All investigations for AKI

Answer 29

Investigations in AKI
- URINE DIPSTICK is vital (look for abnormal protein and blood)

• Daily FBC, U&Es, LFTs, Bone profile, CRP – incl. serum bicarbonate (CK if rhabdomyolysis suspected)
• Urine PCR, Urine MC+S, USS KUB (to rule out obstruction)
• If blood and protein on urine dipstick – perform c-ANCA (PR3) + p-ANCA (MPO) too look for vasculitis, anti-GBM, ANA,
  C3, C4 to look for lupus nephritis, serum immunoglobulins and electrophoresis to look for myeloma
• If suspected post-streptococcal GN – do Anti-Streptolysin O Titres
• In case of associated thrombocytopenia consider HUS/TTP/Disseminated Intravascular Coagulopathy, request
  haemolysis screen - blood film, LDH, bilirubin, reticulocytes, haptoglobin, and call Renal SpR urgently.
• Check cryoglobulins if unexplained rash, peripheral neuropathy, hypocomplementaemia, known hepatitis C, history of
  lymphoproliferative disorder, or +ve RhF.

Question 30

What is the general step by step management of Aki

Answer 30

Management of AKI
 Send off investigations as appropriate

 Discontinue nephrotoxic agents if possible

 Ensure volume status and perfusion pressure – If dehydrated give IV fluids, If overloaded give diuretics, aim for euvolaemia

 Be aware of third space losses (patient may look overloaded but JVP & BP may be low indicating intravascular depletion)

 Consider function haemodynamic monitoring with Central Venous Pressure (CVP) line/Arterial line

 Monitor urine output and daily bloods (catheterise if necessary)
 Avoid hyperglycaemia

 Check for changes in drug dosing (antibiotic doses etc adjusted to renal function)

 Treat underlying cause

 Refer to specialist for consideration of renal replacement therapy

 Consider ICU admission

Question 31

What are the indications for renal replacement therapy in AKI

Answer 31

 Hyperkalaemia refractory to medical therapy

 Metabolic acidosis refractory to medical therapy

 Fluid overload refractory to diuretics (anuric)

 Uraemic pericarditis

 Uraemic encephalopathy – vomiting, confusion, drowsiness, reduced consciousness

 Intoxications – ethylene glycol, methanol, salicylates, lithium

Question 32

Have a look at the booklet for glomerulonephritis stuff