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Medicine block (Y3) > Week 8: Renal disease (1) (renal function tests and electrolyte balance) > Flashcards

Week 8: Renal disease (1) (renal function tests and electrolyte balance) Flashcards

1
Q

renal function tests

A

bloods

urine

imaging

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2
Q

blood tests

A
  • 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
  • ABG/VBG
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3
Q

urine

A
  • 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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4
Q

imaging

A

US KUB (kidneys, ureters and bladder)

  • look for peri-nephric collections
  • size of kidneys
  • corticomedullary differentiation
  • hydronephrosis
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5
Q

ABG results

A
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6
Q

the anion gap

A

useful in working out what could be causing acidosis

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7
Q

high anion gap

A

acidosis due to increased acid

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8
Q

normal anion gap

A

acidosis due tor educed alkali

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9
Q

Diabetes insipidus

A

Differential- psychogenic polydipsia (mental illness and developmental disability)

Presentation

  • Dilute urine (osmolality <300)
  • Polydipsia and polyuria
  • Impaired release of ADH (cranial DI)

Causes

  • Impaired release:Cranial DI
    • Trauma/post op tumours
    • Cerebral sarcoid/TB infections (menin/encep)
    • Cerebral vasculitis (SLE/Wegeners)
  • Resistance to ADH: Nephrogenic DI
    • Congenital, drugs (lithium, amphotericin, demeclocycline), hypokalaemia, hypercalcaemia, tubulointerstitial disease

Treatment: generally- free water

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10
Q

types of hypernatremia

A
  • Hypovolaemic high Na
    • Renal free water losses (osmotic diuresis(NG feed etc), loop diuretics, intrinsic renal disease)
  • Euvolemic High Na
    • Renal losses (diabetes insipidus, hypodipsia - dehydration)
  • Hypervolaemia High Na (sodium Gains)
    • Primary hyperaldosteronism, Cushing’s syndrome, hypertonic dialysis, hypertonic sodium bicarbonate, sodium chloride tablets
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11
Q

hypernatraemia impact on body

A
  • Causes cellular dehydration (osmotic drag)
  • Creates vascular shear stress (bleeding and thrombosis)
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12
Q

presentations of hypernatremia

A
  • Thirst
  • Apathy
  • Irritability
  • Weakness
  • Confusion
  • Reduced consciousness
  • Seizures
  • Hyperreflexia
  • Spasticity
  • Coma
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13
Q

Change in sodium is rarely a change in sodium conc, usually a change in

A

water

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14
Q

causes of hypernatraemia

A
  • Think of water- less water to sodium (not really about sodium)
  • Causes
    • Osmotic diuresis (e.g. uncontrolled diabetes)- excreting too much water
    • Fluid loss without replacement (sweating, burns, vomiting)
    • Diabetes insipidus (suspect of lots of dilute urine produced)
    • Incorrect intravenous fluid replacement
    • Primary aldosteronism
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15
Q

hyponatraemia impact on the body

A

causes cellular swelling

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16
Q

symptoms of hyponatraemia

A
  • Decreases perception
  • Gait disturbance
  • Yawning
  • Nausea
  • Reversible ataxia
  • Headache
  • Apathy
  • Confusion
  • Seizures
  • Coma
17
Q

causes of hyponatreamia

A
  • Pseudohyponatremia
    • High lipids
    • Myeloma
    • Hyperglycaemia
    • Uraemia
  • Hypovolaemic hyponatremia
  • Euvolemic hyponatremia
  • SIADH
  • Hypervolemic hyponatremia
18
Q

causes of hyponatraemia

A
  • Pseudohyponatremia
    • High lipids
    • Myeloma
    • Hyperglycaemia
    • Uraemia
  • Hypovolaemic hyponatremia
  • Euvolemic hyponatremia
  • SIADH
  • Hypervolemic hyponatremia
19
Q

investigations for hyponatraemia

A
  • Plasma osmolality (if normal or raised then pseudohyponatremia)
  • Hypokalaemia/hypomagnesemia potentiates ADH release
  • Urine sodium (if <20 then non-renal salt losses, if >40 then SiADH) (diuretics may confound)
  • TSH
  • 9am cortisol
  • Calcium
  • Albumin
  • Glucose
  • LFT
  • CT head
  • CT chest- SIADH
20
Q

Risk of correcting hyponatraemia quickly

A

Too rapid correction of chronic hyponatraemia leads to central pontine/osmotic myelinosis.

  • Aim to correct <12 mmol/L/day
21
Q

treatment of hyponatraemia

A
  • Acute (tends to be iatrogenic, polydipsia, colonoscopy prep, ecstasy)
    • If acute hyponatraemia (within 48 hours) and symptomatic – Give 3% hypertonic saline IV boluses +/- Furosemide 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
22
Q

causes of euvolemic hyponatraemia

A

normal sodium stores and a total body excess of free water

causes:

  • Hypothyroidism
  • Primary polydipsia (if urine osmolality <200)
  • Glucocorticoid deficiency- adrenal insufficiency
  • SIADH
23
Q

SIADH

A
  • Low serum osmolality
  • Inappropriately concentrated urine – Urine osmolality >100
  • Urine Na >20
  • Clinical euvolaemia
  • Not on diuretics
  • Diagnosis of elimination – normal renal, thyroid, adrenal function
24
Q

Management of SIADH

A
  • Fluid restrict <800ml/day.
  • PO sodium chloride
  • May give furosemide
  • Demeclocycline induces diabetes insipidus (reversing ADH effect), alternatively Tolvaptan
25
Q

causes of hypovolaemic hyponatraemia

A
  • Renal loss (urine Na+ >20 mmol/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)
26
Q

treatment of hypovolaemic hyponatraemia

A
  • IV fluids (0.9% NaCl at 1-3ml/kg/hour
  • Give K if necessary
27
Q

hypervolemic hyponatraemia

A

This increase in total body water is greater than the total body sodium level, resulting in edema.

Causes

  • CCF
  • Nephrotic syndrome
  • Liver cirrhosis

Treatment

  • Fluid restriction and consider furosemide
28
Q

cause sof hyperkalaemia

A
  • 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 – Hyperkaliaemic periodic paralysis, Gordon’s syndrome
  • Artifact Hyperkalaemia – haemolysis, leucocytosis, thrombocytosis
29
Q

ECG changes in hyperkalaemia

A
  • Tented T waves
  • Prolonged QRS
  • Slurring of ST segment
  • Loss of P waves
  • Asystole
30
Q

treatment of hyperkalaemia

A
  • 10mls of 10% calcium gluconate over 5-10 minutes
    • Stabilises myocardium to prevent arrhythmias
  • IV fast acting insulin (actrapid)
    • With 10 units IV glucose/dextrose 50% 50mls
    • Shifting potassium back into the intracellular space
  • Calcium resonium
    • 15-45g orally or rectally
    • Eliminating potassium from body
  • Furosemide
    • Eliminating potassium from the body
  • Dialysis
    • Eliminating potassium from the body
31
Q

Hyporeninaemic hypoaldosteronism (Type IV renal tubular acidosis)

A
  • Hypochloraemic acidosis in about 50%
  • hyperkalaemia
  • Often hypertensive with increased extra-cellular fluid volume (renin often down regulated by fluid overload

Risk factors

  • Increased age
  • Reduced eGFR
  • Diabetes nephropathy
  • Nephritis
  • TIN/sickle cells
  • NSAIDs CNI
  • Lupus nephritis
32
Q

symptoms of hypokalaemia

A
  • Fatigue
  • Constipation
  • Proximal muscle weakness
  • Paralysis
  • Cardiac arrhythmias
  • Worsened glucose control in diabetics
  • Hypertension
33
Q

ECG treatment in hypokalaemia

A
  • Small T waves
  • U wave (after T)
  • Increased PR interval
34
Q

causes of hypokalaemia

A
  • 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.
35
Q

treatment of hypokalaemia

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

Medicine block (Y3) (38 decks)

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