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DMod3 Pt6 Endocrine Disease > DM3 Pt6-3 Diabetic ketoacidosis > Flashcards

DM3 Pt6-3 Diabetic ketoacidosis Flashcards

1
Q

What is diabetic ketoacidosis (DKA)?

A

DKA is an emergency complication of untreated or poorly controlled diabetes mellitus, characterized by the accumulation of ketones in the bloodstream.

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2
Q

How are ketone bodies generated in diabetic ketoacidosis?

A

Free fatty acids (FFAs) released from adipose tissue are metabolized by the liver into acetoacetate and ß-hydroxybutyrate, leading to ketone production.

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3
Q

What role does insulin deficiency play in DKA?

A

Insulin deficiency increases lipolysis and FFA mobilization, which leads to ketone production and eventually ketoacidosis.

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4
Q

What is the effect of insulin resistance in DKA?

A

Insulin resistance, caused by increased glucose counter-regulatory hormones, leads to greater FFA mobilization and protein catabolism, worsening hyperglycaemia and ketogenesis.

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5
Q

What hormones increase during DKA, contributing to insulin resistance?

A

Adrenaline, noradrenaline, glucagon, cortisol, and growth hormone increase, causing insulin resistance and promoting ketogenesis.

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6
Q

How do increased ketones affect the body in DKA?

A

Ketones initially provide energy but eventually rise above the renal threshold, leading to osmotic diuresis and the loss of water and electrolytes, resulting in hypovolaemia and acidosis.

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7
Q

Why do diabetic ketoacidotic cats often have concurrent disorders?

A

Conditions like pancreatitis, infection, or other endocrinopathies increase glucose counter-regulatory hormones, exacerbating DKA.

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8
Q

What happens when ketones rise above the renal threshold in DKA?

A

Excess ketones are excreted in the urine, causing osmotic diuresis and loss of positively charged ions like sodium, potassium, calcium, and magnesium.

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9
Q

What is the consequence of osmotic diuresis in DKA?

A

Osmotic diuresis leads to severe dehydration, electrolyte imbalance, and hypovolaemia, which worsen tissue perfusion and metabolic acidosis.

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10
Q

What is the effect of metabolic acidosis in DKA?

A

The production of H+ ions from ketones causes metabolic acidosis, leading to vomiting, diarrhoea, dehydration, and further electrolyte losses, worsening the condition.

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11
Q

Why does DKA cause increased blood glucose and ketones?

A

Reduced glomerular filtration rate (GFR) leads to reduced excretion of glucose and ketones, further increasing their levels in the bloodstream.

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12
Q

What is the ultimate outcome of untreated DKA in cats?

A

Untreated DKA leads to severe dehydration, metabolic acidosis, cellular dehydration, and eventually death.

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13
Q

In what type of cats does DKA most commonly occur?

A

DKA most commonly occurs in cats with undiagnosed diabetes mellitus, or in treated cats receiving inadequate insulin doses.

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14
Q

What concurrent conditions are often associated with DKA in cats?

A

Infectious, inflammatory, or endocrine disorders often occur concurrently with DKA.

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15
Q

What is the difference between diabetic ketosis (DK) and diabetic ketoacidosis (DKA)?

A

In DK, cats are ketonuric but still bright and eating, while in DKA, cats have severe metabolic acidosis and are very ill or moribund.

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16
Q

Why might classic signs of diabetes mellitus, like PUPD, go unnoticed in cats?

A

Cats that go outdoors may drink and urinate outside, making it difficult for owners to observe polyuria, polydipsia, and weight loss.

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17
Q

What systemic signs may appear as ketosis and acidosis worsen?

A

Lethargy, anorexia, and vomiting become more pronounced as ketosis and acidosis worsen.

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18
Q

What are common physical findings in cats with DKA?

A

Dehydration, depression, weakness, tachypnoea, vomiting, and sometimes a strong acetone odor on the breath.

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19
Q

How is diabetes mellitus diagnosed in cats?

A

Diagnosis is based on appropriate clinical signs, persistent fasting hyperglycaemia, glycosuria, and elevated serum fructosamine.

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20
Q

What are the classic signs of diabetes mellitus in cats?

A

Polyuria, polydipsia, polyphagia, and weight loss are classic signs of diabetes mellitus.

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21
Q

Why is a thorough history and physical exam essential in DKA cases?

A

Managing any concurrent disease is critical to improving the outcome in cats with DKA.

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22
Q

What breath odor might indicate DKA in cats?

A

A strong odor of acetone on the breath may indicate DKA.

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23
Q

What distinguishes diabetic ketosis from diabetic ketoacidosis (DKA)?

A

Diabetic ketosis involves elevated serum ketones and ketonuria without acidosis, while DKA involves both ketones and metabolic acidosis.

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24
Q

What are the clinical signs of diabetic ketosis?

A

Cats with diabetic ketosis are usually bright and eating, but show elevated serum ketones and ketonuria.

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25
Q

How are serum ketones and ketonuria detected in diabetic cats?

A

Urine dipsticks detect acetone and acetoacetate, but may not detect beta-hydroxybutyrate, especially in cases of severe acidosis or tissue hypoxia.

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26
Q

What type of ketone may be missed by urine dipsticks, particularly in severe cases?

A

Beta-hydroxybutyrate may be missed by urine dipsticks in severe acidosis, hypovolaemia, or tissue hypoxia.

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27
Q

What is the typical treatment approach for diabetic ketosis?

A

Cats with diabetic ketosis usually stabilize as normal diabetic patients with close monitoring, without the need for aggressive therapy.

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28
Q

What additional signs appear with diabetic ketoacidosis (DKA)?

A

In DKA, systemic signs like lethargy, anorexia, vomiting, and metabolic acidosis occur.

29
Q

How is metabolic acidosis confirmed in diabetic ketoacidosis (DKA)?

A

Blood gas analysis confirms the presence of metabolic acidosis in DKA cases.

30
Q

What is required for the treatment of diabetic ketoacidosis (DKA)?

A

DKA requires intensive emergency treatment due to the severity of metabolic acidosis and systemic illness.

31
Q

What two key findings does urinalysis help identify in DKA patients?

A

Glycosuria and ketonuria.

32
Q

Why should a urine culture be performed in DKA cases?

A

A concurrent UTI is a common contributing cause of DKA.

33
Q

What does azotaemia indicate in DKA patients?

A

Azotaemia is common in DKA and can help differentiate between pre-renal and renal azotaemia.

34
Q

Why should urine output be closely monitored in DKA patients?

A

Oliguric or anuric renal failure is a potential complication of DKA.

35
Q

What is the typical blood glucose level in cats with DKA?

A

Blood glucose is normally about 25 mmol/L but can range from 10 mmol/L to >50 mmol/L.

36
Q

Why is it important not to drop blood glucose too rapidly in DKA patients?

A

Rapid decreases in blood glucose can cause cerebral oedema due to sudden plasma osmolality changes.

37
Q

What acid-base imbalance is present in DKA patients?

A

Metabolic acidosis, with venous pH values <7.0 being life-threatening.

38
Q

What electrolyte imbalance is common in DKA, and why does it occur?

A

Hyponatraemia, due to excessive sodium loss from osmotic diuresis caused by glycosuria and ketonuria.

39
Q

What is the relationship between hyperglycaemia and sodium concentration in DKA?

A

For every 5 mmol/L increase in serum glucose, the plasma sodium concentration decreases by about 1.6 mmol/L.

40
Q

Why do DKA patients often have a marked potassium deficiency?

A

Potassium shifts from cells into ECF due to intracellular dehydration and acidosis, combined with urinary potassium losses.

41
Q

What is the most common complication of severe hypophosphataemia in DKA treatment?

A

Haemolytic anaemia is the most common complication of severe hypophosphataemia.

42
Q

What complications can hypomagnesaemia cause in DKA patients?

A

Lethargy, anorexia, neuromuscular signs, and cardiac dysrhythmias.

43
Q

What enzyme is most useful for diagnosing pancreatitis in DKA cats?

A

Feline PLI (pancreatic lipase immunoreactivity) is the most useful test for pancreatitis in cats.

44
Q

Why should systolic blood pressure be monitored in DKA patients?

A

Hypotension is common due to hypovolaemia, and fluid therapy should be adjusted to maintain systolic BP above 100 mmHg.

45
Q

What role does an ECG play in DKA management?

A

ECGs help detect cardiac dysrhythmias caused by severe electrolyte and acid-base imbalances in DKA patients.

46
Q

How should mild diabetic ketosis (ketonuria +/++) be treated?

A

Follow the same protocol as for non-ketotic diabetics, with close monitoring of ketosis. Alternatively, short-acting insulin every 8 hours may be given until ketonuria resolves.

47
Q

What are the key goals in treating diabetic ketoacidosis (DKA)?

A
  1. Provide adequate insulin to stop ketone production; 2. Restore water and electrolyte balance; 3. Correct acidosis; 4. Identify any underlying disease; 5. Provide carbohydrate substrate when required.
48
Q

Why should fluid and electrolyte imbalances be corrected slowly in DKA treatment?

A

Rapid changes can cause harm, such as cerebral oedema, so abnormal parameters should be corrected over 36-48 hours.

49
Q

What initial fluid therapy is recommended for DKA?

A

0.9% normal saline, with rehydration over 24 hours and potassium/phosphate supplementation as needed.

50
Q

When is potassium supplementation required during DKA treatment?

A

Potassium is supplemented based on serum potassium concentrations; if unavailable, add 30-40 mEq KCl to each liter of fluids, but do not exceed 0.5 mEq/kg/hr.

51
Q

When should phosphate supplementation be provided in DKA treatment?

A

If serum phosphate concentration is <0.5mmol/L or if haemolytic anaemia develops.

52
Q

When should dextrose supplementation be initiated during DKA treatment?

A

When blood glucose approaches 12.5-15 mmol/L to allow ongoing insulin therapy without hypoglycaemia.

53
Q

What insulin therapy is used for DKA treatment?

A

Regular (neutral) crystalline insulin is used, starting after fluid therapy, with intermittent i/m, i/v techniques, or continuous i/v infusion.

54
Q

What is the target blood glucose reduction during DKA insulin therapy?

A

Blood glucose should decrease by less than 0.5 mmol/L per hour, targeting 12.5-15 mmol/L.

55
Q

What is the role of bicarbonate therapy in DKA?

A

Bicarbonate therapy is rarely required as acidosis usually resolves with fluids and insulin, but may be used if plasma bicarbonate <12 mEq/L.

56
Q

Why is bicarbonate therapy risky in DKA patients?

A

It can worsen hypokalaemia, impair oxygen delivery, cause sodium overload, rebound alkalosis, paradoxical CSF acidosis, and delay reductions in lactate/ketones.

57
Q

What concurrent conditions should be treated during DKA management?

A

Infections (use broad-spectrum antibiotics), pancreatitis (aggressive fluids, anti-emetics, analgesia), and discontinue glucocorticoid therapy safely.

58
Q

What type of fluid therapy is used for DKA cats?

A

0.9% saline at 2 times maintenance rate, adjusted for hydration status. Fluid boluses may be needed.

59
Q

How is potassium supplementation managed in DKA cats?

A

Add 30-40 mEq KCl (potassium chloride) to 1 litre of fluids if serum potassium levels are unknown. Do not exceed 0.5 mEq/kg/hr.

60
Q

When is phosphate supplementation required for DKA cats?

A

Phosphate supplementation is required if serum phosphate levels are low. Administer at 0.01-0.03 mmol/kg/hr in 0.9% saline.

61
Q

What type of insulin is used in DKA treatment?

A

Regular (neutral) insulin is used, with an initial dose of 0.2 U/kg i/v or i/m, then 0.1 U/kg every hour.

62
Q

What is the target blood glucose reduction in DKA treatment?

A

The goal is to reduce blood glucose by 3-4 mmol/L per hour until it is less than 14 mmol/L.

63
Q

When should dextrose saline be started in DKA treatment?

A

Begin 5% dextrose saline infusion when blood glucose is below 14 mmol/L.

64
Q

What is the frequency of monitoring blood glucose during DKA treatment?

A

Blood glucose should be measured every 1-2 hours initially, with insulin therapy adjusted accordingly.

65
Q

How often should hydration status and vital signs be checked in DKA cats?

A

Hydration, respiration, and pulse should be checked every 2-4 hours, with fluid adjustments as needed.

66
Q

What parameters should be monitored every 6-12 hours in DKA treatment?

A

Serum electrolyte levels, acid/base status, and bicarbonate therapy should be monitored and adjusted every 6-12 hours.

67
Q

What complications can arise from DKA treatment?

A

Hypoglycaemia, hypokalaemia, hypophosphataemia, haemolytic anaemia, hypernatraemia, oliguria, hypotension, cerebral oedema, and paradoxical cerebral acidosis.

68
Q

What is the prognosis for cats with DKA?

A

With careful treatment and monitoring, many DKA patients recover and become stable diabetics, though severe underlying disease or complications can result in death.

DMod3 Pt6 Endocrine Disease (6 decks)

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