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Acute Care > Metabolic & Diabetes > Flashcards

Metabolic & Diabetes Flashcards

1
Q

Why is hyponatraemia dangerous?

A

Fluid shifts-> cerebral oedema
Drowsy
Fitting
Respiratory arrest

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2
Q

How much sodium is in normal saline?

A

0.9%

150mg

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3
Q

Why does lactic acidosis occur?

A

Lack of tissue perfusion
Anaerobic respiration
Build up of lactate

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4
Q

Define hypoglycaemia

A

Blood glucose<4mmol/l
Mild: if pt self treats
Severe: if 3rd party is involved

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5
Q

Early symptoms of hypoglycaemia

A 
Adrenergic effects:
Sweating
Tachycardia
Palpitations
Pallor
Hunger
Restlessness
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6
Q

Late symptoms of hypoglycaemia

A 
Neuroglycopenic effects:
Confusion
Slurred speech
Drowsiness
Numbness of nose/lips/fingers
Anxiety
Blurred vision
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7
Q

Risk factors for hypoglycaemia

A
  • 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
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8
Q

Treatment of hypoglycaemia

A

Sugar! (avoid fatty foods)
Recheck blood glucose after 10 mins (x3)
If still low then 10% dextrose infusion 150-200ml or IM glucagon

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9
Q

If severe hypoglycaemia and blood glucose is less than 2.2, what needs to be investigated?

A 
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)
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10
Q

What does the DVLA need to know about diabetics?

A
  • 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.
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11
Q

Define DKA

A 
Diabetic ketoacidosis
T1DM insulin deficiency
-Hyperglycaemia (>11mmol/L)
-Metabolic acidosis (ph<7.3, low bicarb)
-Ketonaemia (ß-OHbutyrate>3mmol/l in blood, ++ in urine)
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12
Q

Treatment of DKA

A
  • 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
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13
Q

Define HHS

A 
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)
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14
Q

Treatment of HHS

A
  1. Normalise osmolarity (glucose and sodium and urea)
  2. Replace fluids (1L normal saline)
  3. Monitor and replace electrolytes
  4. Normalise blood glucose (5mmol/hr primarily due to rehydration)
  5. LMWH prophylactically
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15
Q

What can initiate RAAS?

A

Sodium down, potassium up or hypotension-> juxtaglomerular cells -> RAAS

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16
Q

How does aldosterone act?

A

Aldosterone works at distal convoluted tubule, sodium and water reabsorption (in exchange for either K+ or H+)

17
Q

What acts in opposition to aldosterone?

A

Spironolactone

ANP (Atrial Natriuretic Peptide)

18
Q

What is the 1st step when you see a low sodium on a blood test result?

A

Check osmolality

Is it really low?

19
Q

If the osmolality of a hyponatraemic sample is increased or normal, what would this indicate?

A

Increased osmolality: Hyperglycaemia/mannitol

Normal osmolality: Lipaemia/hyperproteinaemia

20
Q

If the osmolality of a hyponatraemic sample is low, what next?

A

Assess extracellular fluid volume

Increased/normal/decreased

21
Q

Hyponatraemia with decreased osmolality and increased ECF volume indicates what?

A 
Na and H20 excess- oedema
2º hyperaldosteronism
CCF
Hepatic failure (lack of albumin produced)
Nephrotic syndrome (albumin lost)
22
Q

Hyponatraemia with decreased osmolality and normal ECF volume indicates what?

A

H20 excess
Acutely: increased intake and reduced output
Chronic: Impaired excretion
SIADH (urine osmolality>plasma osmolality)

23
Q

Hyponatraemia with decreased osmolality and decreased ECF volume indicates what?

A 
True Na depletion
Renal failure
GI loss (diarrhoea)
Cutaneous loss (fever/sweating)
Look at urine osmolality and Na: are kidneys working and concentrating urine?
24
Q

How do you calculate osmolality?

A

2(Na+K+) + urea + glucose

25
Q

What happens in hyperosmolality?

A

• Thirst from hypothalamus
• ADH from posterior pituitary
• Redistribution of water from ICF to ECF
ADH reabsorbs free water in collecting duct, concentrated urine.

26
Q

What needs to be normal to diagnose SIADH?

A

Normal renal, thyroid and adrenal function

27
Q

Treatment of SIADH

A

Fluid restrict slowly

Na should rise

28
Q

Name 5 causes of SIADH

A
  • 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
29
Q

Name 5 causes of a hypokalaemic blood test?

A
  • 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
30
Q

What does a hypokalaemic ECG show?

A

Wide inverted t waves, u waves

31
Q

5 causes of hyperkalaemia on blood test

A
  • 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)

Acute Care (11 decks)

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