Diabetes Mellitus Flashcards
(114 cards)
1
Q
What is the definition of hypoglycemia in a known diabetic patient?
A
Blood glucose less than 4 mmol/L.
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.
3
Q
What characterizes severe hypoglycemia in diabetic patients?
A
The patient is semi-conscious, unconscious, or comatose and requires medical help.
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.
5
Q
Neurogenic (ANS) symptoms (caused by falling glucose level)
A
shakiness
trembling
anxiety
nervousness
palpitations
clamminess
dry mouth
sweating
hunger
pallor
pupil dilatation
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)
7
Q
Prevention of hypoglycemia
A
- Know and recognize signs and symptoms of hypoglycemia
- Take meals on a regular schedule
- Carry a source of carbohydrate
- Self monitoring of blood glucose
- Take regular insulin at least 30 minutes before eating
- Anticipate effect of exercise on blood glucose
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
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.
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.
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.
12
Q
Which peptide hormone is produced by α-cells of the pancreas?
A
Glucagon
13
Q
What three processes in the liver are affected by glucagon?
A
Glucagon increases glycogenolysis, increases gluconeogenesis, and decreases glycolysis
14
Q
What is the counterregulatory hormone to insulin that increases blood glucose levels?
A
Glucagon
15
Q
What happens to glucagon levels when carbohydrates are ingested and blood glucose increases?
A
Insulin is released, and glucagon levels decrease.
16
Q
When does glucagon secretion occur?
A
In response to low blood glucose levels.
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).
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.
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.
20
Q
What is the most frequent adverse effect associated with glucagon administration?
A
Nausea (in up to 35% of cases).
21
Q
Diagnosis of DKA
A
- hyperglycemia
- metabolic acidosis
- ketonaemia
22
Q
What is the criterion for hyperglycaemia in diagnosing DKA?
A
Glucose levels greater than 13.9 mmol/L.
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).
24
Q
How is ketonaemia indicated in the diagnosis of DKA?
A
Blood beta-hydroxybutyrate greater than 3 mmol/L or positive ketostix.
25
Can DKA occur in both Type 1 and Type 2 diabetes mellitus?
Yes, DKA can occur in both Type 1 and Type 2 DM.
26
How quickly does DKA develop?
DKA develops acutely within days.
27
What type of metabolic acidosis is typically seen in DKA
High anion gap metabolic acidosis.
28
How is the anion gap calculated?
Anion gap = Na – (Cl + HCO3).
29
What is the normal range for the anion gap?
The normal anion gap range is 4 to 12.
30
What is Diabetic Ketoacidosis (DKA)?
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.
31
What are the key elements involved in the pathogenesis of DKA
The pathogenesis of DKA involves insulin deficiency, increased counter-regulatory hormones, and metabolic disturbances.
32
What role does insulin play in glucose uptake and metabolism?
Insulin is crucial for glucose uptake into cells and for inhibiting lipolysis (fat breakdown) and ketogenesis (ketone production)
33
How does insulin deficiency contribute to DKA?
In DKA, there is an absolute or relative deficiency of insulin, which can result from missed insulin doses, infection, illness, or other stressors.
34
Which counter-regulatory hormones are elevated in DKA and what do they promote?
Glucagon, cortisol, catecholamines, and growth hormone are elevated, promoting gluconeogenesis and glycogenolysis, leading to hyperglycemia.
35
What causes hyperglycemia in DKA and what are its effects?
The liver continues to produce glucose, leading to elevated blood glucose levels, causing osmotic diuresis, dehydration, and electrolyte imbalances
36
How does lipolysis contribute to DKA?
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.
37
What is the result of increased ketogenesis in DKA?
Accumulation of ketone bodies in the blood leads to metabolic acidosis (decreased blood pH) because ketone bodies are acidic.
38
How does dehydration exacerbate DKA
Osmotic diuresis from hyperglycemia results in significant fluid and electrolyte losses, worsening metabolic acidosis and impairing renal function.
39
What are the common clinical manifestations of DKA?
Polyuria, polydipsia, dehydration, nausea, vomiting, abdominal pain, Kussmaul respirations, and fruity-smelling breath.
40
What laboratory findings are typical in DKA?
Hyperglycemia, ketonemia, ketonuria, metabolic acidosis, and electrolyte imbalances.
41
What is the primary trigger for DKA?
Absolute or relative lack of insulin.
42
What metabolic processes contribute to hyperglycemia in DKA?
Increased gluconeogenesis and glycogenolysis.
43
How does lipolysis lead to ketogenesis in DKA?
Increased breakdown of fats into free fatty acids leads to ketone production in the liver.
44
What causes metabolic acidosis in DKA?
Accumulation of ketone bodies causes a drop in blood pH.
45
What are the primary treatments for DKA?
Intravenous fluids, insulin, and electrolyte replacement.
46
How do hyperglycemia and osmotic diuresis lead to dehydration and electrolyte imbalances in DKA?
Osmotic diuresis caused by hyperglycemia results in significant fluid and electrolyte losses.
47
What neurohormonal abnormalities are present in DKA?
Insulin deficiency or resistance, and elevation of counter-regulatory hormones such as glucagon, cortisol, growth hormone, and catecholamines.
48
What mechanisms contribute to hyperglycemia in DKA?
Impaired glycolysis and glycogen synthesis, increased gluconeogenesis, and increased glycogenolysis.
49
What causes an increased anion gap metabolic acidosis in DKA?
Accumulation of β-hydroxybutyrate (β-OHB) and acetoacetic acid. The anion gap formula is (Na+ + K+) - (Cl− + HCO3−) > 10 mEq/L.
50
What causes an anion gap metabolic acidosis?
Anion gap metabolic acidosis is caused by the accumulation of beta-hydroxybutyrate (β-OHB) and acetoacetic acid.
51
How is the anion gap calculated, and what is the threshold for metabolic acidosis?
The anion gap is calculated using the formula
An anion gap greater than 10 mEq/L indicates metabolic acidosis.
52
What happens to total body and serum potassium levels in anion gap metabolic acidosis?
Total body potassium is low, while serum potassium can be normal or raised.
53
Why is total body potassium low despite normal or raised serum levels?
Urinary losses occur due to glucose osmotic diuresis and excretion of potassium ketoacid anion salts.
54
What is the role of the H+/K+ exchange mechanism in acidosis?
In acidosis, H+ ions are shifted intracellularly in exchange for K+ as a buffering mechanism, increasing serum potassium while intracellular potassium is low.
55
Why is it important to understand the potassium balance when treating with insulin therapy
Insulin therapy shifts potassium into cells, risking severe hypokalemia if not monitored properly.
56
What usually happens to serum sodium levels in anion gap metabolic acidosis?
Serum sodium levels are usually low.
57
What is pseudohyponatremia, and how is it related to anion gap metabolic acidosis?
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
What causes the sodium diuresis with ketones?
Electrolyte-free urine loss due to sodium diuresis with ketones contributes to low serum sodium levels.
59
How does the intracellular fluid shift cause dilutional hyponatremia?
The ICF shift leads to dilutional (hyperosmolar) hyponatremia due to the osmotic effect of high blood glucose.
60
How do you correct the plasma sodium value for blood glucose?
A rough guide is to divide the glucose level by 3 and add it to the sodium value.
61
What causes dehydration in anion gap metabolic acidosis?
Dehydration is due to osmotic diuresis, where the body loses water through urine due to high blood glucose levels.
62
Precipitants of DKA
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
DKA- special investigations
1. CXR
2. ECG
3. Urine dipstick
4. Full blood count
5. U and E
6. ABG or VBG
64
DKA- CXR
signs of infection
65
DKA- ECG
Hypokalemia
Hyperkalemia
Myocardial infarction (silent MI in diabetics
66
DKA- Urine dipstick
Ketones
Leukocytes
Nitrates
67
DKA- Full blood count
Leukocytosis (even without infection)
68
DKA- U and E
Urea & creatinine frequently increased due to dehydration
Potassium
69
DKA- differential diagnosis
1. lactic acidosis
2. starvation ketosis
3. alcoholic ketoacidosis
4. hyperuraemic acidosis
70
DKA- Lactic acidosis
Serum glucose and ketones should be normal
Serum lactate concentration > 5mmol/L
71
DKA- starvation ketosis
Blood glucose is usually normal or low
Arterial pH is normal
72
DKA- Alcoholic ketoacidosis
Serum and urine ketones are present
Usually, patient is normoglycemic or hypoglycemic
73
DKA- hyperuraemic acidosis
pH and anion gap are usually only mildly abnormal
74
What is the initial fluid replacement strategy for DKA?
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
How should fluid replacement continue over the next 48 hours in DKA treatment?
Continue fluid replacement at ±5 mL/kg/hour.
76
When should you switch to 0.45% NaCl?
Switch to 0.45% NaCl if Na+ is greater than 140 mmol/L.
77
When should you switch to 5% Dextrose or 5% Dextrose in NaCl 0.9%?
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
What general measures should be taken for a DKA patient?
Insert large bore IV lines in both arms, protect the airway, and insert an NGT if the patient is unconscious. Monitor urine output
79
What is the average fluid deficit in DKA, and how should it be replaced?
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
What should be checked before starting potassium replacement in DKA treatment?
Check serum potassium (K+) on ABG.
81
When should potassium be withheld initially in DKA treatment?
Withhold potassium if serum K+ is markedly raised or if there are ECG features of hyperkalemia
82
When should potassium replacement be initiated in DKA treatment?
Initiate potassium immediately if K+ is low/normal, ECG is normal, and the patient is passing urine.
83
What should be done if K+ is less than 3.5 mmol/L before starting insulin infusion?
Start potassium replacement before starting the insulin infusion.
84
What should always be checked before starting insulin therapy in DKA?
Always check potassium (K+) levels before starting insulin.
85
How should insulin be administered in DKA treatment?
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
What should be done if glucose does not fall by 3 mmol/L in the first hour?
Double the insulin infusion rate hourly until a steady reduction of 3-4 mmol/L per hour is achieved.
87
How should insulin infusion be adjusted when glucose levels fall below 14 mmol/L?
Reduce the insulin infusion rate to 1 - 2 units/hour.
88
How often should HGT be monitored during DKA treatment?
Monitor HGT hourly.
89
When should you switch from IV insulin to SC insulin in DKA treatment?
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
Is there a role for IV sodium bicarbonate in the treatment of DKA?
No, there is no proven role for IV sodium bicarbonate in the treatment of DKA, and it could cause harm
91
What is Hyperosmolar Hyperglycemic State (HHS)?
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
What type of insulin deficiency is present in HHS?
There is a relative rather than absolute deficiency of insulin in HHS
93
How does this relative insulin deficiency affect blood glucose levels and ketogenesis?
The available insulin is insufficient to adequately control blood glucose levels but is enough to prevent significant ketogenesis.
94
What leads to severe hyperglycemia in HHS?
Severe hyperglycemia results from increased hepatic glucose production (via gluconeogenesis and glycogenolysis) and decreased glucose utilization due to relative insulin deficiency.
95
What causes osmotic diuresis in HHS?
Extremely high blood glucose levels exceed the renal threshold for glucose reabsorption, leading to glucosuria (glucose in urine) which causes osmotic diuresis
96
What are the consequences of osmotic diuresis in HHS?
Osmotic diuresis leads to significant loss of water and electrolytes in the urine, contributing to severe dehydration.
97
What causes hyperosmolarity in HHS?
Severe hyperglycemia and dehydration lead to increased plasma osmolality
98
How does hyperosmolarity affect cells in HHS?
Elevated osmolality pulls water out of cells, causing cellular dehydration and contributing to neurological symptoms.
99
Why is significant ketosis and acidosis not prominent in HHS?
The residual insulin activity in HHS is sufficient to inhibit lipolysis and ketogenesis.
100
What electrolyte imbalances are common in HHS?
Electrolyte imbalances, particularly sodium and potassium, are common due to osmotic diuresis.
101
How does dehydration affect sodium levels in HHS?
Dehydration often leads to hypernatremia (high sodium levels) due to water loss.
102
What are common precipitating factors for HHS?
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
How is serum osmolarity calculated?
2(Na + K) + glucose + urea
104
What is the normal range for serum osmolarity?
The normal range for serum osmolarity is 275 - 285 mOsm/L.
105
What does an elevated serum osmolarity indicate in the context of HHS?
Elevated serum osmolarity indicates severe hyperglycemia and dehydration, contributing to the hyperosmolar state in HHS.
106
Why is it important to calculate serum osmolarity in patients with suspected HHS?
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
Over what time frame does HHS typically occur?
HHS occurs over days to weeks.
108
Which population is most commonly affected by HHS?
HHS is most commonly seen in elderly patients with type 2 diabetes.
109
What is the typical blood glucose level in HHS?
Blood glucose levels are typically greater than 40 mmol/L in HHS.
110
What is the typical serum osmolarity in HHS?
Serum osmolarity is typically greater than 320 mOsm/kg in HHS.
111
What is a distinguishing feature of dehydration in HHS?
Severe dehydration occurs with little or no ketoacidosis in HHS.
112
What is the usual pH level in patients with HHS?
The pH level is usually greater than 7.20 in HHS.
113
What is the typical serum bicarbonate level in HHS?
Serum bicarbonate levels are typically greater than 18 mEq/L in HHS.
114
What neurological symptoms are commonly seen in HHS?
Patients with HHS may experience altered mental status, ranging from obtundation and stupor to coma.
