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Y3 - Medicine > Renal > Flashcards

Renal Flashcards

1
Q

Renal function tests

Blood

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

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2
Q

Renal function tests

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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3
Q

Renal function tests

Imaging

A

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

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4
Q

Metabolic alkalosis causes

A

 GI losses
o Diarrhoea
o Vomiting

  Anion Gap = 145 – (107+13) = 25   Renal losses
o  Primary hyperaldosteronism
o  Tubular transporter defects
o  Diuretics
  Intracellular shift
o  Hypokalaemia
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5
Q

Anion gap

A

Anion gap = sodium - (chloride + bicarbonate)

Normal = 8-12

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6
Q

High anion gap

Acidosis due to increased acid

A

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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7
Q

Normal anion gap

Acidosis due to reduced alkali

A

GI losses of HCO3 - vomiting, diarrhoea
Renal losses of HCO3 - renal tubular acidosis, mineralocorticoid deficiency (Addison’s)
Toxins - ammonium chloride, acetazolamide

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8
Q

Hypernatraemia

A

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

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9
Q

Hypernatraemia

Symptoms

A

thirst, apathy, irritability, weakness,

confusion, reduced consciousness, seizures, hyperreflexia, spasticity & coma.

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10
Q

Hypovolaemic High Na

A

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

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11
Q

Euvolaemic high Na

A

 Renal Losses (Diabetes Insipidus, Hypodipsia)

 Extra-Renal Losses (Insensible, Respiratory losses)

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12
Q

Hypervolaemic high Na (sodium gains)

A

Primary hyperaldosteronism, Cushing’s Syndrome,
Hypertonic dialysis, Hypertonic Sodium Bicarbonate,
Sodium Chloride tablets

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13
Q

Hypernatraemia

Diabetes Insipidus

A

(differential = psychogenic polydipsia)
– dilute urine (Urine osmolality <300)
Polydipsia and polyuria – not always hypernatraemic
Impaired release of ADH (Cranial DI)

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14
Q

Hypernatraemia - Diabetes Insipidus

Causes

A

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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15
Q

Hypernatraemia - Diabetes Insipidus

Treatment

A

Generally - free water

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16
Q

Hyponatraemia

A

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

17
Q

Hyponatraemia - causes

A

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

18
Q

Hyponatraemia - investigations

A

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.

19
Q

Hypovolaemic hypernatraemia

A

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

20
Q

Euvolaemic hyponatraemia

A

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

21
Q

Hyponatraemia - 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

22
Q

SIADH management

A

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

23
Q

Hypervolaemic hyponatraemia

A

CCF, Nephrotic syndrome, Liver cirrhosis

Treatment – fluid restrict and consider furosemide

24
Q

Correcting hyponatraemia too quickly

A

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

25
Q

Treatment of hyponatraemia - acute

A

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

26
Q

Treatment of hyponatraemia - chronic

A

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

27
Q

Hyperkalaemia

Causes

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 – Hyperkalaemic periodic paralysis, Gordon’s
syndrome
 Artifact Hyperkalaemia – haemolysis, leucocytosis,
thrombocytosis

28
Q

Hyperkalaemia

Hyporeninaemic hypoaldosteronism

A 
Hyporeninaemic Hypoaldosteronism (Type IV RTA)
Hypochloraemic acidosis in about 50%, hyperkalaemia,
typically with increased age and reduced eGFR classically in diabetes nephropathy, acute GN (nephritis), TIN/sickle cell, NSAIDs, CNIs, lupus nephritis
29
Q

Hyperkalaemia

Hypertensive with increased ECF

A

Often hypertensive with increased extra-cellular fluid
volume (renin often down-regulated by fluid overload)
Treat – low K diet, loop diuretic if overloaded

30
Q

Hyperkalaemia

ECG changes

A 
  Tented T waves
  Prolonged QRS
  Slurring of ST segment
  Loss of P waves
  Asystole
31
Q

Treatment of hyperkalaemia

A
  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
32
Q

Hypokalaemia

Symptoms

A

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

33
Q

Hypokalaemia

Causes

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.

34
Q

Hypokalaemia

ECG changes

A

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

35
Q

Hypokalaemia

Treatment

A

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

Y3 - Medicine (12 decks)

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