Med booklet BB Flashcards by Aditya Viswanath

What renal function blood tests can we do

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

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What Urine tests can we do

 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

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What imaging can be done

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

ultrasound, kidneys, urethra, bladder

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Causes of metabolic alkalosis

Causes
 GI losses
o Diarrohoea
Vomiting

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

 Intracellular shift
o Hypokalaemia

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Why is anion gap useful and what is the equation

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

Anion Gap = Sodium - (Chloride + Bicarbonate)

[Na+] – ([Cl-] +
[HCO3-])

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What is a normal anion gap

8-12

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

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

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

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

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

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

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Symptoms of hypernatraemia

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

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

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

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Card on diabetes insidious

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

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Hypernatraemia treatment?

Treatment
 Generally – free water

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Hyponatraemia causes

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

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Hyponatraemia symptoms

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

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Hyponatraemia investigations

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.

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

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

Treatment of hyponatraemia when hypervolaemic and hypovolaemic

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

hyper
Treatment – fluid restrict and consider furosemide

Risk of correcting hyponatraemia quickly?

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

Treatment of acute hyponatraemia?

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

Treatment of chronic hyponatraemia

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

As many causes of hyperkalaemia

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

ECG changes in hyperkalaemia

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

3 treatment stages for hyperkalaeima (detailed)

Stabilizing the myocardium to prevent arrhythmias
 10mls of 10% Calcium Gluconate over 5-10 minutes
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
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

Hypokalaemia symptoms

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

Causes of hypokalaemia

 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.

Hypokalaemia on ecg?

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

Treatment of hypokalaemia

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

All investigations for AKI

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.

What is the general step by step management of Aki

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

What are the indications for renal replacement therapy in AKI

 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

Have a look at the booklet for glomerulonephritis stuff