Diabetic Ketoacidosis

Question 1

What is the clinical diagnosis of hypoglycaemia?

1 - <2mmol/L
2 - <4mmol/L
3 - <6mmol/L
4 - <8mmol/L

Answer 1

• <4mmol/L
• below 4 we drop to the floor

Question 2

How many people worldwide are estimated to be affected by hypoglycaemia?

1 - 100,000
2 - 4.5 million
3 - 460 million
4 - 4.6 billion

Answer 2

3 - 460 million

Question 3

When a patients blood glucose drops <4mmol/L the autonomic system attempt to increase the bodies blood glucose levels through sympathetic stimulation. What 2 key hormones are released and which gland releases them?

1 - insulin from beta cells in pancreas
2 - cortisol from zona fasiculitis of adrenal gland
3 - adrenalin from chromaffin cells in adrenal cortex
4 - glucagon from alpha cells in pancreas

Answer 3

3 - adrenalin from chromaffin cells in adrenal cortex
4 - glucagon from alpha cells in pancreas

- pancreas = glucagon

Question 4

Which of the following are common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia?

1 - shaking/trembling
2 - pallor
3 - sweating
4 - all of the above

Answer 4

4 - all of the above

• patients can also describe anxiety, tiredness, hunger, headaches, blurred vision, palpitations and lips/tongue tingling

Question 5

What does the term neuroglycopaenic mean?

1 - excessive glucose sin the brain
2 - excessive glucose being stored in the brain
3 - lack of glucose supply to the brain
4 - all of the above

Answer 5

3 - lack of glucose supply to the brain

- means that the patient is unaware that their blood glucose is becoming hypoglycaemic

Question 6

Neuroglycopaenic refers to low blood glucose to the brain. We can see symptoms in patients such as slurred speech, slower reactions, disorientation, seizures/fitting, coma, low concentration, dizziness, confusion and aggression or irritability. What level does the glucose drop below to typically see these levels?

1 - <2mmol/L
2 - <2.8mmol/L
3 - <4mmol/L
4 - <4.8mmol/L

Answer 6

2 - <2.8mmol/L

Question 7

Hypoglycaemia Unawareness is when a patient is unaware that their blood has dropped, before they appreciate this. This is generally because they experience symptoms associated with neuroglycopenia before the autonomic response (adrenalin and glucagon) is able to mobilise glucose.

• sympathetic activity is reduced due to cellular adaptation to hypoglycaemia
• leads to hypoglycaemia-associated autonomic failure
• chronically low glucose in liver and glucagon in pancreas

What % of patients with T1DM experience hypoglycaemia unawareness?

1 - 4%
2 - 14%
3 - 40%
4 - 90%

Answer 7

3 - 40%

Question 8

Which of the following are common causes for patients to become hypoglycaemia?

1 - increased/decreased carbohydrate intake
2 - excessive exercise
3 - medication (insulin, GLP-1)
4 - alcohol
5 - age and duration of diabetes
6 - impaired renal function
7 - pregnancy/breast feeding
8 - all of the above

Answer 8

8 - all of the above

Question 9

In a patient who consumes excessive alcohol, this can be followed by hypoglycaemia. Why is this?

1 - alcohol results in decreased insulin secretion
2 - alcohol elicits insulin release
3 - alcohol inhibits glycogenesis
4 - alcohol increases glycogenolysis

Answer 9

2 - alcohol elicits insulin release

• carbohydrates in sugar elicit large insulin spike
• lack of food means insulin causes all glucose in blood to be absorbed
• low glucose in blood causing hypoglycaemia

Question 10

If a patients is hypoglycaemic (<4mmol/L), we can give them the immediate 20g of quick/rapid acting carbohydrates (if they can swallow). How can we check to see if this has improved the patients hypoglycaemia?

1 - perform ABG
2 - ask the patient how they feel
3 - perform capillary blood glucose
4 - complete GCS

Answer 10

3 - perform capillary blood glucose

• 10-15 minutes following 20g glucose

- if still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates

Question 11

If a patients is hypoglycaemic (<4mmol/L), we can give them the immediate 20g of quick/rapid acting carbohydrates (if they can swallow), and monitor after 10-15 minutes using a capillary blood glucose. If the patient is still <4mmol/L, we can repeat this. If the patient is still <4mmol/L, what can we do next in hospital and at home?

1 - home = administer glucagon
2 - home = repeat above again
3 - hospital = administer glucagon
4 - hospital = administer IV dextrose

Answer 11

1 - home = administer glucagon
4 - hospital = administer IV dextrose

• once patient is stable we can administer slow releasing carbohydrates
• patients can also be given intramuscular injection of glucagon at home if unconscious

Question 12

Which of the following are examples of 20g of fast acting carbohydrates?

1 - 200 ml pure fruit juice e.g. orange
2 - 120ml of original Lucozade®
3 - 6-7 Dextrosol® tablets (or 5 Glucotabs®)
4 - 3 – 4 Jelly babies
5 - 200mls coke
6 - Glucojuice is equivalent of 15g of carbs
7 - all of the above

Answer 12

7 - all of the above

Question 13

If a diabetic patient is suspected of being hypoglycaemia and arrives at hospital, which of the following is most important to check initially?

1 - ABC
2 - capillary blood glucose
3 - ABG/VBG
4 - all of the above

Answer 13

1 - ABC

• then assess blood glucose and GCS

Question 14

If a patient is confirmed as being hypoglycaemic and they are taking insulin, would we continue with the insulin or stop it?

Answer 14

• stop the insulin
• DO NOT STOP if patient is T1DM

Question 15

If a patient is at home, is unconscious, unable to swallow and confirmed as being hypoglycaemic, they may be given a subcutaneous or intramuscular injection of glucagon. What should the patients blood glucose be after 10 minutes following the glucagon administration?

1 - >4 mmol/L
2 - 3.5-5/7 mmol/L
3 - 5-7 mmol/L
4 - >8 mmol/L

Answer 15

2 - 3.5-5/7 mmol/L

• can then administer slow acting carbohydrates

Question 16

If a patient is at home, is unconscious, unable to swallow and confirmed as being hypoglycaemic, they may be given a subcutaneous or intramuscular injection of glucagon. Which of the following groups of patients might be less responsive to glucagon injections?

1 - chronically malnourished
2 - depleted glycogen stores
3 - severe liver disease (low glycogen stores and/or metabolism)
4 - all of the above

Answer 16

4 - all of the above

Question 17

Dextrose is provided to patient intravenously when patients are hypoglycaemic. What is the recommended dose for a patient who is hypoglycaemic and requires dextrose administration?

1 - 5% dextrose (100m IV)
2 - 10% dextrose (100m IV)
3 - 20% dextrose (100m IV)
4 - 40% dextrose (100m IV)

Answer 17

3 - 20% dextrose (100m IV)

• once recovered (>4 hours), provide with 20g of slow acting carbohydrates

Question 18

Dextrose is provided to patient intravenously when patients are hypoglycaemic. The recommended dose for a patient who is hypoglycaemic and requires dextrose administration is as follows:

• 20% dextrose (100m IV)
• once recovered (4 hours), provide with 20g of slow acting carbohydrates

Why can it be dangerous to administer 50% dextrose?

1 - phlebitis(skin irritation)
2 - thrombosis (blood clot) at injection site
3 - overcorrection and hyperglycaemia
4 - all of the above

Answer 18

4 - all of the above

Question 19

Ketone bodies are a group of carbon-containing molecules produced by liver mitochondria using a 2-carbon molecule during states of low energy intake, such as fasting and exercise. What molecule does this come from?

1 - oxolacetate
2 - acetyl-CoA
3 - SCFA
4 - pyruvate

Answer 19

2 - acetyl-CoA

Question 20

Ketones bodies are produced in the mitochondria in the liver from acetyl-CoA. they can enter the blood and be taken up by tissues. They are then used in mitochondria to create ATP. If there are excessive levels of ketones in the blood this can cause metabolic acidosis. Why is this?

1 - ketones donate protons
2 - ketones take up free protons
3 - ketones are neutralised by HCO3-
4 - all of the above

Answer 20

1 - ketones donate protons

• CO2 and H2O = H2CO3 (carbonic anhydrase) = H+ and HCO3-
• essentially misbalances the above equation

Question 21

Diabetic ketoacidosis (DKA) can occur due to increased sympathetic activity which stimulates the alpha cells in the pancreas to release glucagon and raise blood glucose in preparation of the fight or flight response. However, the rise in blood glucose is not matched by insulin levels, so glucose cannot be absorbed. This can result in ketone body production for energy, but high levels can be very dangerous. What is the incidence of DKA in 10,000 of the diabetic population?

1 - 4.6 - 8.0
2 - 46 - 80
3 - 460 - 800
4 - 4600 - 8000

Answer 21

2 - 46 - 80

Question 22

The incidence of diabetic ketoacidosis that occurs in 10,000 of the diabetic population is 46-80. What is the mortality rate?

1 - 0.4 - 1%
2 - 4 - 10%
3 - 24 - 44%
4 - >50%

Answer 22

2 - 4 - 10%

Question 23

Are chronic or newly diagnosed diabetic patients more likely to have DKA?

Answer 23

• those with new onset diabetes

Question 24

Which of the following must be present to diagnose a patient with DKA?

1 - hyperglycaemia (>11mmol/L) or known diabetes
2 - ketonaemia (>3mmol/L)
3 - HCO3- (<15mmol/L) or venous pH < 7.3
4 - all of the above

Answer 24

4 - all of the above

• urine ketones can be >+2 as well
  -patients typically urinate a lot more

- >11mmol/L

Question 25

In diabetic ketoacidosis why is it important to be aware of euglycaemic?

Answer 25

• if on SGLT-2 patients can pass glucose through urine
• glucose appears normal (euglycaemic)
• patient still has no insulin so remains in DKA

- BUT ketonaemia and acidosis are present

Question 26

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which 2 of the following occur in adipose tissue?

1 - increased lipolysis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

Answer 26

1 - increased lipolysis
- fatty acid breakdown from TAG
- increased FFA in the blood

3 - decreased adipogenesis
- reduced adipocyte differentiation

Question 27

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which 2 of the following occur in the liver?

1 - increased lipolysis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

Answer 27

2 - increased gluconeogenesis
- protein and lipids used for energy

4 - decreased glycogenolysis
- glucose is not stored as glycogen

Question 28

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. What 2 things occur in the skeletal muscle?

1 - decreased protein synthesis
2 - increased gluconeogenesis
3 - decreased adipogenesis
4 - decreased glycogenolysis

Answer 28

1 - decreased protein synthesis

4 - decreased glycogenolysis
- glucose is not stored as glycogen

Question 29

The pathophysiology of ketoacidosis is complex and includes a number of factors which are based around insulin deficiency. Which of the following hormones are secreted in an attempt to correct the problem?

1 - cortisol
2 - growth hormone
3 - catecholamines
4 - glucagon
5 - all of the above

Answer 29

5 - all of the above

• cortisol = increased gluconeogenesis in an attempt to increase blood glucose
• growth hormone (opposite affect of insulin, so more glucose in blood)
• catecholamines (signal increase release of glucagon)
• glucagon (increase glucose release into blood)

Question 30

A lack of Insulin is generally what causes hyperglycaemia. Will this causes a hyper or hypo-osmolar concentration of glucose?

Answer 30

• hyper-osmolarity due to high glucose concentration

Question 31

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, what is this called?

1 - glycosuria
2 - polyuria
3 - dysuria
4 - osmoluria

Answer 31

1 - glycosuria

Question 32

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to 2 major effects on the patient, both linked with 2 much fluid leaving the body as urine. What are these 2 effects?

1 - dehyrdation
2 - ketonaemia
3 - lipoaemia
4 - electrolyte losses

Answer 32

1 - dehyrdation

4 - electrolyte losses
- lost in urine

2 - electrolyte loss

Question 33

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria. This can then lead to dehydration and electrolyte loss. How does hyperglycaemia cause electrolyte loss?

1 - hyperglycaemia induces hyponatraemia
2 - hyperglycaemia induces hypernatraemia
3 - hyperglycaemia induces hypokalaemia
4 - hyperglycaemia induces hyperkalaemia

Answer 33

1 - hyperglycaemia induces hyponatraemia

• high blood glucose increases extracellular fluid due to osmosis
• high extracellular fluid causes hyponatraemia
• diuresis is increased to reduce extracellular fluid and glucose
• electrolytes and glucose are lost

Question 34

Insulin deficiency causes hyperglycaemia, which in turn can lead to increased glucose to be present in the urine, called glycosuria, which can then lead to dehydration and electrolyte loss. Long term what effect can this have on renal function?

1 - increased eGFR
2 - damaged renal tubules
3 - decreased eGFR
4 - no effect

Answer 34

2 - damaged renal tubules

- impaired renal function or even failure

Question 35

The effects of insulin deficiency and hyperglycaemia can have a number of detrimental effects, culminating in diabetic ketoacidosis, as seen in the image. What does the ultimately lead to?

1 - liver damage
2 - shock and CV collapse
3 - brain damage
4 - renal failure

Answer 35

2 - shock and CV collapse

- most diabetic patients die of heart complications

Question 36

Which of the following are common signs of diabetic ketoacidosis?

1 - polyuria
2 - polydipsia (abnormal thirst
3 - nausea and abdominal pain
4 - ketone breath
5 - Kussmaul breathing
6 - lethargy
7 - confusion
8 - coma
9 - all of the above

Answer 36

9 - all of the above

• ketone breath = acetate causes pear drop sweets or nail varnish
• Kussmaul breathing = deep and laboured breathes to remove CO2 and lower pH

Question 37

There are the 3 main ketone bodies that cause diabetic ketoacidosis. Which of the following is NOT one of these?

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone
4 - butyrate

Answer 37

4 - butyrate

Question 38

At normal level the ratio of acetoacetate to β-hydroxybutyrate is 1:1. However, during diabetic ketoacidosis, what does this ratio reach?

1 - acetoacetate to β-hydroxybutyrate is 10:10
2 - acetoacetate to β-hydroxybutyrate is 5:10
3 - acetoacetate to β-hydroxybutyrate is 1:10
4 - acetoacetate to β-hydroxybutyrate is 10:1

Answer 38

3 - acetoacetate to β-hydroxybutyrate is 1:10

Question 39

The 3 main ketone bodies that cause diabetic ketoacidosis are

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone

No enzyme is required for the conversion of acetoacetate to acetone, but what enzyme is responsible for the conversion of acetoacetate to β-hydroxybutyrate?

Answer 39

• D-beta-hydroxybutyrate dehydrogenase

Question 40

When trying to measure if a patient has diabetic ketoacidosis, what is the main ketone measured in clinical practice?

1 - acetoacetate
2 - β-hydroxybutyrate
3 - acetatone

Answer 40

1 - acetoacetate

- BUT β-hydroxybutyrate is a better marker and kits are becoming available

Question 41

In a patient with diabetic ketoacidosis (DKA), increased ketone bodies reduces pH as protons are donated. To counter this H+ can enter cells down a concentration gradient in exchange for what electrolyte?

1 - Na+
2 - K+
3 - Ca2+
4 - Mg2+

Answer 41

2 - K+

• this can initially cause hyperkalaemia
• insulin is also required for Na+/K+ ATPase, so without insulin K+ cannopt re-enter the cells

Question 42

In a patient with diabetic ketoacidosis (DKA), increased ketone bodies reduces pH as protons are donated. H+ enter cells and K+ leaves in an attempt to reduce pH, causing hyperkalaemia. Excess K+ is then lost in the urine causing hypokalaemia. How can K+ levels in DKA be addressed?

1 - address K+ depletion
2 - wait and see approach
3 - increase insulin secretion
4 - all of the above

Answer 42

1 - address K+ depletion
- return electrolyte balance between intra and extracellular space

Question 43

In a patient with diabetic ketoacidosis (DKA), there is metabolic acidosis as patients ketone bodies donate protons (H+) that reduces plasma pH. Why can this cause Kussmaul breathing (deep and laboured breathes)?

1 - reduces CO2 inspiration
2 - reduces O2 inspiration
3 - reduces H+ uptake in cells
4 - all of the above

Answer 43

1 - reduces CO2 inspiration
- less CO2 means pH will start to rise

• CO2 and H2O = H2CO3 (carbonic anhydrase) = H+ and HCO3-
• purpose is to remove excessive H+

Question 44

In a patient with diabetic ketoacidosis (DKA), initially hyperkalaemia occurs as K+ leaves the cell in exchange for H+. The excessive K+ in the blood (initially hyperkalaemia) is then excreted in urine, resulting hypokalaemia. Treating DKA needs to address hypokalaemia and excessive H+ (normally through breathing). What one other major thing needs to be addressed when treating a patient?

1 - provide quick release glucose
2 - provide fluids
3 - provide GCS assessment
4 - all of the above

Answer 44

2 - provide fluids
- addresses dehydration and reduces the risk of cardiovascular collapse

• 0.9% saline
• 100ml/kg (70kg male = 100x7 = 7L)

Question 45

Based on the glasgow coma scale, what would be classed as severe diabetic ketoacidosis?

1 - <15
2 - <12
3 - <8
4 - <4

Answer 45

2 - <12
- score ranges from 3 to 15
- 3 is no response and 15 is all responses are maximum

Question 46

Based on the blood pH, what would be classed as severe diabetic ketoacidosis?

1 - <9
2 - <7.1
3 - <6.1
4 - <5

Answer 46

2 - <7.1

- bicarb = <5

Question 47

In a patient with severe diabetic ketoacidosis, which of the following may be a sign of shock?

1 - low BP (due to polyuria)
2 - organ failure (kidney disease)
3 - low potassium
4 - all of the above

Answer 47

4 - all of the above

Question 48

When managing a patient with diabetic ketoacidosis what must we assess 1st?

1 - ABC
2 - capillary blood glucose
3 - ABG/VBG
4 - all of the above

Answer 48

1 - ABC

Question 49

When managing a patient with diabetic ketoacidosis (DKA), would we need to do a blood culture?

Answer 49

• yes
• infection could be a precipitating cause of DKA

- administer broad spectrum antibodies if infection

Question 50

When managing a patient with diabetic ketoacidosis (DKA), we would administer fluids based on the patients BP through a cannula. What would we measure to assess the effectiveness of this?

1 - urine output
2 - glucose
3 - ABG/VBG
4 - lactate

Answer 50

3 - ABG/VBG
- assess venous blood gas whilst administering fluids and check K+

Question 51

When managing a patient with diabetic ketoacidosis (DKA), one fluid will help address fluid levels and electrolytes. What would be administered through a second cannula?

1 - glucagon
2 - insulin
3 - dextrose
4 - cortisol

Answer 51

2 - insulin
- amount is based on the patients weight

Question 52

The aim of management in a patient with diabetic ketoacidosis is reduce ketones, glucose, whilst increasing bicarbonate and K+ levels. What are the levels that we would want each of the following to change by:

• ketones
• bicarbonate
• glucose
• potassium

Answer 52

• ketones = reduction of 0.5mmol/l/h
• bicarbonate = increase of 3mmol/L/h
• glucose= reduction of 3mmol/L/h
• potassium = maintain normal range

Question 53

In a patient with diabetic ketoacidosis they will be administered with insulin to reduce the hyperglycaemia. in addition to insulin, what else is administered alongside and when would it be administered?

1 - glucagon
2 - insulin
3 - dextrose
4 - cortisol

Answer 53

3 - dextrose

• patients may overshoot with insulin administration
• avoid hypoglycaemia at 10% with blood glucose <14mmol/L
• administer at 125ml/hour

NO K+ ADDED AT THIS STAGE

Question 54

Using the standard treatment approach for diabetic ketoacidosis, how long should it take for ketonaemia and acidosis to be corrected?

1 - <6 hours
2 - <12 hours
3 - <24 hours
4 - <48 hours

Answer 54

4 - <48 hours

Question 55

In a patient with diabetic ketoacidosis, which of the following can affect the treatment?

1 - cerebral oedema
2 - hypo/hyperkaelaemia
3 - hypoglycaemia
4 - pulmonary oedema (due to fluid administration)
5 - all of the above

Answer 55

5 - all of the above