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Therapeutics > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the definition of hypoglycemia in a known diabetic patient?

A

Blood glucose less than 4 mmol/L.

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2
Q

How is mild/moderate hypoglycemia characterized in diabetic patients?

A

The patient is capable of self-treatment or is conscious but requires help from someone else.

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3
Q

What characterizes severe hypoglycemia in diabetic patients?

A

The patient is semi-conscious, unconscious, or comatose and requires medical help.

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4
Q

How is hypoglycemia defined in non-diabetic patients?

A

By Whipple’s triad: plasma glucose less than 3.0 mmol/L, symptoms of hypoglycemia, and resolution of symptoms after serum glucose is corrected.

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5
Q

Neurogenic (ANS) symptoms (caused by falling glucose level)

A

shakiness
trembling
anxiety
nervousness
palpitations
clamminess
dry mouth
sweating
hunger
pallor
pupil dilatation

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6
Q

Neurogylcopenic symptoms (caused by brain neuronal glucose deprivation)

A

abnormal mentation
irritability
confusion
difficulty in thinking
difficulty speaking
ataxia
paresthesias
headaches
stupor
seizures
coma
death (if untreated)

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7
Q

Prevention of hypoglycemia

A
  1. Know and recognize signs and symptoms of hypoglycemia
  2. Take meals on a regular schedule
  3. Carry a source of carbohydrate
  4. Self monitoring of blood glucose
  5. Take regular insulin at least 30 minutes before eating
  6. Anticipate effect of exercise on blood glucose
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8
Q

How is mild/moderate hypoglycemia treated in diabetic patients?

A

Give at least 15-20 g of glucose:
- Glucose powder/tablets/glucogel
- 175 ml of fruit juice or soft drink (NOT DIET!)
- 3-4 teaspoons of sugar dissolved in water
- 2-3 Super-C sweets
- 1.5 tablespoons of honey

Repeat as necessary after 10-15 minutes.
Follow with slowly digestible carbohydrates (bread) and protein (glass of milk) for prolonged restoration of blood glucose

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9
Q

How is severe hypoglycemia treated if IV access is established?

A

Establish IV access:
- 50mL of 50% dextrose IV bolus after blood drawn.
- Measure blood glucose after 5-10 min; if still < 4.4 mmol/L, repeat 50mL of 50% dextrose.
- Follow with 10% dextrose IV infusion.

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10
Q

How is severe hypoglycemia treated if IV access cannot be established?

A
  • Glucagon 1mg IM or SC can be given (by family or friend):
  • Effective in treating hypoglycemia only if sufficient liver glycogen is present.
  • Onset of action: 10-15 min.
  • Should not be used in sulphonylurea-induced hypoglycemia as it may stimulate further insulin release.
  • Continue to establish IV access.
  • Patient is urged to eat as soon as possible once fully awake.
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11
Q

What are special considerations to remember when treating hypoglycemia?

A
  • Give thiamine prior to IV dextrose in patients with suspected alcoholism, but do not delay dextrose administration in a patient with hypoglycemia.
  • Honey or glucogel can be rubbed on the gums in patients who have lost consciousness if other medication is not readily available.
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12
Q

Which peptide hormone is produced by α-cells of the pancreas?

A

Glucagon

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13
Q

What three processes in the liver are affected by glucagon?

A

Glucagon increases glycogenolysis, increases gluconeogenesis, and decreases glycolysis

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14
Q

What is the counterregulatory hormone to insulin that increases blood glucose levels?

A

Glucagon

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15
Q

What happens to glucagon levels when carbohydrates are ingested and blood glucose increases?

A

Insulin is released, and glucagon levels decrease.

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16
Q

When does glucagon secretion occur?

A

In response to low blood glucose levels.

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17
Q

Which cells have glucagon receptors and what happens when glucagon binds to these receptors?

A

Liver cells (hepatocytes) have glucagon receptors. When glucagon binds, the liver converts glycogen into glucose and releases it into the bloodstream (glycogenolysis).

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18
Q

What process does glucagon encourage in the liver and kidney when glycogen stores become depleted?

A

Glucagon encourages gluconeogenesis, the synthesis of additional glucose.

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19
Q

What effect does glucagon have on glycolysis in the liver?

A

Glucagon turns off glycolysis, causing glycolytic intermediates to be shuttled to gluconeogenesis.

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20
Q

What is the most frequent adverse effect associated with glucagon administration?

A

Nausea (in up to 35% of cases).

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21
Q

Diagnosis of DKA

A
  1. hyperglycemia
  2. metabolic acidosis
  3. ketonaemia
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22
Q

What is the criterion for hyperglycaemia in diagnosing DKA?

A

Glucose levels greater than 13.9 mmol/L.

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23
Q

What are the criteria for metabolic acidosis in diagnosing DKA?

A

pH less than 7.3 or bicarbonate less than 18 mmol/L (high anion gap).

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24
Q

How is ketonaemia indicated in the diagnosis of DKA?

A

Blood beta-hydroxybutyrate greater than 3 mmol/L or positive ketostix.

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25
Q

Can DKA occur in both Type 1 and Type 2 diabetes mellitus?

A

Yes, DKA can occur in both Type 1 and Type 2 DM.

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26
Q

How quickly does DKA develop?

A

DKA develops acutely within days.

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27
Q

What type of metabolic acidosis is typically seen in DKA

A

High anion gap metabolic acidosis.

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28
Q

How is the anion gap calculated?

A

Anion gap = Na – (Cl + HCO3).

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29
Q

What is the normal range for the anion gap?

A

The normal anion gap range is 4 to 12.

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30
Q

What is Diabetic Ketoacidosis (DKA)?

A

DKA is a serious and potentially life-threatening complication of diabetes, primarily type 1 diabetes, but it can also occur in type 2 diabetes under certain conditions.

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31
Q

What are the key elements involved in the pathogenesis of DKA

A

The pathogenesis of DKA involves insulin deficiency, increased counter-regulatory hormones, and metabolic disturbances.

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32
Q

What role does insulin play in glucose uptake and metabolism?

A

Insulin is crucial for glucose uptake into cells and for inhibiting lipolysis (fat breakdown) and ketogenesis (ketone production)

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33
Q

How does insulin deficiency contribute to DKA?

A

In DKA, there is an absolute or relative deficiency of insulin, which can result from missed insulin doses, infection, illness, or other stressors.

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34
Q

Which counter-regulatory hormones are elevated in DKA and what do they promote?

A

Glucagon, cortisol, catecholamines, and growth hormone are elevated, promoting gluconeogenesis and glycogenolysis, leading to hyperglycemia.

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35
Q

What causes hyperglycemia in DKA and what are its effects?

A

The liver continues to produce glucose, leading to elevated blood glucose levels, causing osmotic diuresis, dehydration, and electrolyte imbalances

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36
Q

How does lipolysis contribute to DKA?

A

Due to lack of insulin, lipolysis is uninhibited, leading to the breakdown of triglycerides into free fatty acids (FFAs) and glycerol, which are converted into ketone bodies in the liver.

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37
Q

What is the result of increased ketogenesis in DKA?

A

Accumulation of ketone bodies in the blood leads to metabolic acidosis (decreased blood pH) because ketone bodies are acidic.

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38
Q

How does dehydration exacerbate DKA

A

Osmotic diuresis from hyperglycemia results in significant fluid and electrolyte losses, worsening metabolic acidosis and impairing renal function.

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39
Q

What are the common clinical manifestations of DKA?

A

Polyuria, polydipsia, dehydration, nausea, vomiting, abdominal pain, Kussmaul respirations, and fruity-smelling breath.

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40
Q

What laboratory findings are typical in DKA?

A

Hyperglycemia, ketonemia, ketonuria, metabolic acidosis, and electrolyte imbalances.

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41
Q

What is the primary trigger for DKA?

A

Absolute or relative lack of insulin.

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42
Q

What metabolic processes contribute to hyperglycemia in DKA?

A

Increased gluconeogenesis and glycogenolysis.

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43
Q

How does lipolysis lead to ketogenesis in DKA?

A

Increased breakdown of fats into free fatty acids leads to ketone production in the liver.

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44
Q

What causes metabolic acidosis in DKA?

A

Accumulation of ketone bodies causes a drop in blood pH.

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45
Q

What are the primary treatments for DKA?

A

Intravenous fluids, insulin, and electrolyte replacement.

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46
Q

How do hyperglycemia and osmotic diuresis lead to dehydration and electrolyte imbalances in DKA?

A

Osmotic diuresis caused by hyperglycemia results in significant fluid and electrolyte losses.

47
Q

What neurohormonal abnormalities are present in DKA?

A

Insulin deficiency or resistance, and elevation of counter-regulatory hormones such as glucagon, cortisol, growth hormone, and catecholamines.

48
Q

What mechanisms contribute to hyperglycemia in DKA?

A

Impaired glycolysis and glycogen synthesis, increased gluconeogenesis, and increased glycogenolysis.

49
Q

What causes an increased anion gap metabolic acidosis in DKA?

A

Accumulation of β-hydroxybutyrate (β-OHB) and acetoacetic acid. The anion gap formula is (Na+ + K+) - (Cl− + HCO3−) > 10 mEq/L.

50
Q

What causes an anion gap metabolic acidosis?

A

Anion gap metabolic acidosis is caused by the accumulation of beta-hydroxybutyrate (β-OHB) and acetoacetic acid.

51
Q

How is the anion gap calculated, and what is the threshold for metabolic acidosis?

A

The anion gap is calculated using the formula

An anion gap greater than 10 mEq/L indicates metabolic acidosis.

52
Q

What happens to total body and serum potassium levels in anion gap metabolic acidosis?

A

Total body potassium is low, while serum potassium can be normal or raised.

53
Q

Why is total body potassium low despite normal or raised serum levels?

A

Urinary losses occur due to glucose osmotic diuresis and excretion of potassium ketoacid anion salts.

54
Q

What is the role of the H+/K+ exchange mechanism in acidosis?

A

In acidosis, H+ ions are shifted intracellularly in exchange for K+ as a buffering mechanism, increasing serum potassium while intracellular potassium is low.

55
Q

Why is it important to understand the potassium balance when treating with insulin therapy

A

Insulin therapy shifts potassium into cells, risking severe hypokalemia if not monitored properly.

56
Q

What usually happens to serum sodium levels in anion gap metabolic acidosis?

A

Serum sodium levels are usually low.

57
Q

What is pseudohyponatremia, and how is it related to anion gap metabolic acidosis?

A

Pseudohyponatremia is a false low sodium reading, where serum sodium decreases by approximately 1.6 mmol/L for each 5.6 mmol/L increase in serum glucose.

58
Q

What causes the sodium diuresis with ketones?

A

Electrolyte-free urine loss due to sodium diuresis with ketones contributes to low serum sodium levels.

59
Q

How does the intracellular fluid shift cause dilutional hyponatremia?

A

The ICF shift leads to dilutional (hyperosmolar) hyponatremia due to the osmotic effect of high blood glucose.

60
Q

How do you correct the plasma sodium value for blood glucose?

A

A rough guide is to divide the glucose level by 3 and add it to the sodium value.

61
Q

What causes dehydration in anion gap metabolic acidosis?

A

Dehydration is due to osmotic diuresis, where the body loses water through urine due to high blood glucose levels.

62
Q

Precipitants of DKA

A

The “Eight I’s” mnemonic for the main causes of hyperglycemia is:

  1. Infection: pancreatitis, pneumonia and UTI
  2. Infarction: MI
  3. Infraction: patient noncompliant with therapy
  4. Infant: pregnancy
  5. Ischemia: CVA
  6. Illegal: drugs
  7. Iatrogenic: prescription drug interactions e.g. steroids
  8. Idiopathic: new onset of type 1 diabetes or other causes
63
Q

DKA- special investigations

A
  1. CXR
  2. ECG
  3. Urine dipstick
  4. Full blood count
  5. U and E
  6. ABG or VBG
64
Q

DKA- CXR

A

signs of infection

65
Q

DKA- ECG

A

Hypokalemia
Hyperkalemia
Myocardial infarction (silent MI in diabetics

66
Q

DKA- Urine dipstick

A

Ketones
Leukocytes
Nitrates

67
Q

DKA- Full blood count

A

Leukocytosis (even without infection)

68
Q

DKA- U and E

A

Urea & creatinine frequently increased due to dehydration
Potassium

69
Q

DKA- differential diagnosis

A
  1. lactic acidosis
  2. starvation ketosis
  3. alcoholic ketoacidosis
  4. hyperuraemic acidosis
70
Q

DKA- Lactic acidosis

A

Serum glucose and ketones should be normal

Serum lactate concentration > 5mmol/L

71
Q

DKA- starvation ketosis

A

Blood glucose is usually normal or low

Arterial pH is normal

72
Q

DKA- Alcoholic ketoacidosis

A

Serum and urine ketones are present

Usually, patient is normoglycemic or hypoglycemic

73
Q

DKA- hyperuraemic acidosis

A

pH and anion gap are usually only mildly abnormal

74
Q

What is the initial fluid replacement strategy for DKA?

A

Start with 0.9% NaCl IV, 15–20 mL/kg in the first hour (1 – 1.5 L), then 5-15 mL/kg/hour (200 – 500 mL/hour), ensuring not to exceed 50 mL/kg in the first 4 hours.

75
Q

How should fluid replacement continue over the next 48 hours in DKA treatment?

A

Continue fluid replacement at ±5 mL/kg/hour.

76
Q

When should you switch to 0.45% NaCl?

A

Switch to 0.45% NaCl if Na+ is greater than 140 mmol/L.

77
Q

When should you switch to 5% Dextrose or 5% Dextrose in NaCl 0.9%?

A

Switch to 5% Dextrose or 5% Dextrose in NaCl 0.9% when plasma glucose is less than 14 mmol/L and ketones are still present.

78
Q

What general measures should be taken for a DKA patient?

A

Insert large bore IV lines in both arms, protect the airway, and insert an NGT if the patient is unconscious. Monitor urine output

79
Q

What is the average fluid deficit in DKA, and how should it be replaced?

A

The average fluid deficit is 5 – 10 L. Aim to replace 50% of the deficit in the first 12 hours and the remainder over the next 12 – 16 hours using normal saline or Ringer’s lactate

80
Q

What should be checked before starting potassium replacement in DKA treatment?

A

Check serum potassium (K+) on ABG.

81
Q

When should potassium be withheld initially in DKA treatment?

A

Withhold potassium if serum K+ is markedly raised or if there are ECG features of hyperkalemia

82
Q

When should potassium replacement be initiated in DKA treatment?

A

Initiate potassium immediately if K+ is low/normal, ECG is normal, and the patient is passing urine.

83
Q

What should be done if K+ is less than 3.5 mmol/L before starting insulin infusion?

A

Start potassium replacement before starting the insulin infusion.

84
Q

What should always be checked before starting insulin therapy in DKA?

A

Always check potassium (K+) levels before starting insulin.

85
Q

How should insulin be administered in DKA treatment?

A

Administer an IV infusion of short-acting regular human insulin (actrapid), mixing 50 units in 200 mL 0.9% NaCl (4 mL = 1 unit insulin), with an initial infusion rate of 0.1 unit/kg/hour (5 – 7 units/hour or 20 – 28 mL/hour).

86
Q

What should be done if glucose does not fall by 3 mmol/L in the first hour?

A

Double the insulin infusion rate hourly until a steady reduction of 3-4 mmol/L per hour is achieved.

87
Q

How should insulin infusion be adjusted when glucose levels fall below 14 mmol/L?

A

Reduce the insulin infusion rate to 1 - 2 units/hour.

88
Q

How often should HGT be monitored during DKA treatment?

A

Monitor HGT hourly.

89
Q

When should you switch from IV insulin to SC insulin in DKA treatment?

A

Switch when the patient is fully conscious and able to eat, pH is greater than 7.3, bicarbonate is greater than 18 mmol/L, blood glucose is less than 15 mmol/L, and serum ketones are less than 1 mmol/L. Ensure an overlap of 1-2 hours between IV insulin and the SC regimen.

90
Q

Is there a role for IV sodium bicarbonate in the treatment of DKA?

A

No, there is no proven role for IV sodium bicarbonate in the treatment of DKA, and it could cause harm

91
Q

What is Hyperosmolar Hyperglycemic State (HHS)?

A

HHS, also known as Hyperosmolar Non-Ketotic Hyperglycemia (HONK), is a serious complication of type 2 diabetes characterized by extreme hyperglycemia, hyperosmolarity, and dehydration without significant ketosis or acidosis

92
Q

What type of insulin deficiency is present in HHS?

A

There is a relative rather than absolute deficiency of insulin in HHS

93
Q

How does this relative insulin deficiency affect blood glucose levels and ketogenesis?

A

The available insulin is insufficient to adequately control blood glucose levels but is enough to prevent significant ketogenesis.

94
Q

What leads to severe hyperglycemia in HHS?

A

Severe hyperglycemia results from increased hepatic glucose production (via gluconeogenesis and glycogenolysis) and decreased glucose utilization due to relative insulin deficiency.

95
Q

What causes osmotic diuresis in HHS?

A

Extremely high blood glucose levels exceed the renal threshold for glucose reabsorption, leading to glucosuria (glucose in urine) which causes osmotic diuresis

96
Q

What are the consequences of osmotic diuresis in HHS?

A

Osmotic diuresis leads to significant loss of water and electrolytes in the urine, contributing to severe dehydration.

97
Q

What causes hyperosmolarity in HHS?

A

Severe hyperglycemia and dehydration lead to increased plasma osmolality

98
Q

How does hyperosmolarity affect cells in HHS?

A

Elevated osmolality pulls water out of cells, causing cellular dehydration and contributing to neurological symptoms.

99
Q

Why is significant ketosis and acidosis not prominent in HHS?

A

The residual insulin activity in HHS is sufficient to inhibit lipolysis and ketogenesis.

100
Q

What electrolyte imbalances are common in HHS?

A

Electrolyte imbalances, particularly sodium and potassium, are common due to osmotic diuresis.

101
Q

How does dehydration affect sodium levels in HHS?

A

Dehydration often leads to hypernatremia (high sodium levels) due to water loss.

102
Q

What are common precipitating factors for HHS?

A

Common precipitating factors for HHS include infections, medications (e.g., corticosteroids, thiazides), poor diabetes management, acute illness, or other stressors that increase insulin requirements.

103
Q

How is serum osmolarity calculated?

A

2(Na + K) + glucose + urea

104
Q

What is the normal range for serum osmolarity?

A

The normal range for serum osmolarity is 275 - 285 mOsm/L.

105
Q

What does an elevated serum osmolarity indicate in the context of HHS?

A

Elevated serum osmolarity indicates severe hyperglycemia and dehydration, contributing to the hyperosmolar state in HHS.

106
Q

Why is it important to calculate serum osmolarity in patients with suspected HHS?

A

Calculating serum osmolarity is important to assess the severity of dehydration and hyperosmolarity, which are key features of HHS and guide the treatment strategy.

107
Q

Over what time frame does HHS typically occur?

A

HHS occurs over days to weeks.

108
Q

Which population is most commonly affected by HHS?

A

HHS is most commonly seen in elderly patients with type 2 diabetes.

109
Q

What is the typical blood glucose level in HHS?

A

Blood glucose levels are typically greater than 40 mmol/L in HHS.

110
Q

What is the typical serum osmolarity in HHS?

A

Serum osmolarity is typically greater than 320 mOsm/kg in HHS.

111
Q

What is a distinguishing feature of dehydration in HHS?

A

Severe dehydration occurs with little or no ketoacidosis in HHS.

112
Q

What is the usual pH level in patients with HHS?

A

The pH level is usually greater than 7.20 in HHS.

113
Q

What is the typical serum bicarbonate level in HHS?

A

Serum bicarbonate levels are typically greater than 18 mEq/L in HHS.

114
Q

What neurological symptoms are commonly seen in HHS?

A

Patients with HHS may experience altered mental status, ranging from obtundation and stupor to coma.

Therapeutics (15 decks)

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