Metabolic & Diabetes Flashcards
Why is hyponatraemia dangerous?
Fluid shifts-> cerebral oedema
Drowsy
Fitting
Respiratory arrest
How much sodium is in normal saline?
0.9%
150mg
Why does lactic acidosis occur?
Lack of tissue perfusion
Anaerobic respiration
Build up of lactate
Define hypoglycaemia
Blood glucose<4mmol/l
Mild: if pt self treats
Severe: if 3rd party is involved
Early symptoms of hypoglycaemia
Adrenergic effects: Sweating Tachycardia Palpitations Pallor Hunger Restlessness
Late symptoms of hypoglycaemia
Neuroglycopenic effects: Confusion Slurred speech Drowsiness Numbness of nose/lips/fingers Anxiety Blurred vision
Risk factors for hypoglycaemia
- Reduced intake (eg hospital food, fasting in Ramadan)
- Increased exercise/physiotherapy
- Over dosed insulin (wrong vol, stat doses, IV insulin without glucose)
- Insulin given without meals
- Problems with monitoring
- Recovery from acute illness
- Major amputation
- Discontinuation of long term steroids
- Renal dysfunction
Treatment of hypoglycaemia
Sugar! (avoid fatty foods)
Recheck blood glucose after 10 mins (x3)
If still low then 10% dextrose infusion 150-200ml or IM glucagon
If severe hypoglycaemia and blood glucose is less than 2.2, what needs to be investigated?
Whether cause is an insulinoma, insulin poisoning or fasting alcoholic ketoacidosis Insulin levels (raised in insulinoma/insulin poisoning) C-peptide (raised in insulinoma) 3-OH butyrate (raised in fasting ketosis)
What does the DVLA need to know about diabetics?
- If lorry/bus drivers are taking oral meds or insulin for diabetes
- If drivers are on insulin
- If there is any impairment of consciousness with hypoglycaemia
- If there are any episodes of severe hypoglycaemia in the last 12 months
- If hypoglycaemia occurs when driving.
Define DKA
Diabetic ketoacidosis T1DM insulin deficiency -Hyperglycaemia (>11mmol/L) -Metabolic acidosis (ph<7.3, low bicarb) -Ketonaemia (ß-OHbutyrate>3mmol/l in blood, ++ in urine)
Treatment of DKA
- Replace fluids (500ml normal saline over 15 mins, 500ml normal saline over 45mins)
- Replace and correct electrolyte abnormalities (K+!)
- Replace insulin (50 units made up to 50ml with saline, infused at 0.1 units/kg/hour) after 1 hr of fluids
- Gradually reduce serum glucose concentration (3mmol/l/hr)
- Gradually correct ketosis (0.5mmol/L/hr)
- Identify treatment of co-morbid precipitants and give LMWH prophylactically
- Ensure long acting regime is still given on time
Define HHS
HHS (Hyperosmolar Hyperglycaemic State) • Hypovolaemia • Hyperglycaemia (>30mmol/l) • Raised osmolarity (>320mmol/kg) • Ketones are not present (<3mmol/l) • Acidosis is not present (ph>7.3, bicarb>15mmol/l)
Treatment of HHS
- Normalise osmolarity (glucose and sodium and urea)
- Replace fluids (1L normal saline)
- Monitor and replace electrolytes
- Normalise blood glucose (5mmol/hr primarily due to rehydration)
- LMWH prophylactically
What can initiate RAAS?
Sodium down, potassium up or hypotension-> juxtaglomerular cells -> RAAS
How does aldosterone act?
Aldosterone works at distal convoluted tubule, sodium and water reabsorption (in exchange for either K+ or H+)
What acts in opposition to aldosterone?
Spironolactone
ANP (Atrial Natriuretic Peptide)
What is the 1st step when you see a low sodium on a blood test result?
Check osmolality
Is it really low?
If the osmolality of a hyponatraemic sample is increased or normal, what would this indicate?
Increased osmolality: Hyperglycaemia/mannitol
Normal osmolality: Lipaemia/hyperproteinaemia
If the osmolality of a hyponatraemic sample is low, what next?
Assess extracellular fluid volume
Increased/normal/decreased
Hyponatraemia with decreased osmolality and increased ECF volume indicates what?
Na and H20 excess- oedema 2º hyperaldosteronism CCF Hepatic failure (lack of albumin produced) Nephrotic syndrome (albumin lost)
Hyponatraemia with decreased osmolality and normal ECF volume indicates what?
H20 excess
Acutely: increased intake and reduced output
Chronic: Impaired excretion
SIADH (urine osmolality>plasma osmolality)
Hyponatraemia with decreased osmolality and decreased ECF volume indicates what?
True Na depletion Renal failure GI loss (diarrhoea) Cutaneous loss (fever/sweating) Look at urine osmolality and Na: are kidneys working and concentrating urine?
How do you calculate osmolality?
2(Na+K+) + urea + glucose
What happens in hyperosmolality?
• Thirst from hypothalamus
• ADH from posterior pituitary
• Redistribution of water from ICF to ECF
ADH reabsorbs free water in collecting duct, concentrated urine.
What needs to be normal to diagnose SIADH?
Normal renal, thyroid and adrenal function
Treatment of SIADH
Fluid restrict slowly
Na should rise
Name 5 causes of SIADH
- Lung disease (TB, pneumonia, empyema, tumours, COPD)
- CNS disease (Mass, Guillain Barre, subarachnoid haemorrhage)
- Drug induced (Nicotine, phenothiazines, tricyclics)
- Tumours (pancreatic, uterine, leukaemia)
- Pain, opiates, nausea
Name 5 causes of a hypokalaemic blood test?
- Drip arm contamination (urea and creatinine also really low)
- Decreased intake (eg tea and toast diet of elderly/anorexia/alcoholism)
- Increased losses (diuretics, vomiting, diarrhoea, aldosterone excess, renal)
- Redistribution (alkalosis correction so K+ goes into cells)
- Glucose infusion, insulin
What does a hypokalaemic ECG show?
Wide inverted t waves, u waves
5 causes of hyperkalaemia on blood test
- Kidney failure (creatinine and urea raised too?)
- Lysis of cells in sample (delay in transport, haemolysis from traumatic venipuncture)
- Increased intake (combined with chronic renal failure/iatrogenic from TPN feeding)
- Decreased losses (Potassium sparing diuretic, kidney injury, aldosterone deficiency due to Addison’s or ACEi or angiotensin receptor blockers)
- Redistribution (acidosis correction to K+ comes out of cells)
