Diabetic Ketoacidosis Flashcards
What is the clinical diagnosis of hypoglycaemia?
1 - <2mmol/L
2 - <4mmol/L
3 - <6mmol/L
4 - <8mmol/L
- <4mmol/L
- below 4 we drop to the floor
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
3 - 460 million
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
3 - adrenalin from chromaffin cells in adrenal cortex
4 - glucagon from alpha cells in pancreas
- pancreas = glucagon
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
4 - all of the above
- patients can also describe anxiety, tiredness, hunger, headaches, blurred vision, palpitations and lips/tongue tingling
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
3 - lack of glucose supply to the brain
- means that the patient is unaware that their blood glucose is becoming hypoglycaemic
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
2 - <2.8mmol/L
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%
3 - 40%
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
8 - all of the above
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
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
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
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
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
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
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
7 - all of the above
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
1 - ABC
- then assess blood glucose and GCS
If a patient is confirmed as being hypoglycaemic and they are taking insulin, would we continue with the insulin or stop it?
- stop the insulin
- DO NOT STOP if patient is T1DM
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
2 - 3.5-5/7 mmol/L
- can then administer slow acting carbohydrates
f 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
4 - all of the above
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)
3 - 20% dextrose (100m IV)
- once recovered (>4 hours), provide with 20g of slow acting carbohydrates
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
4 - all of the above
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
2 - acetyl-CoA
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
1 - ketones donate protons
- CO2 and H2O = H2CO3 (carbonic anhydrase) = H+ and HCO3-
- essentially misbalances the above equation
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
2 - 46 - 80
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%
2 - 4 - 10%
Are chronic or newly diagnosed diabetic patients more likely to have DKA?
- those with new onset diabetes
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
4 - all of the above
- urine ketones can be >+2 as well
-patients typically urinate a lot more - > 11mmol/L
A lack of Insulin is generally what causes hyperglycaemia. Will this causes a hyper or hypo-osmolar concentration of glucose?
- hyper-osmolarity due to high glucose concentration
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
1 - glycosuria
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
1 - dehyrdation
4 - electrolyte losses
- glucose is osmotic so fluid follows, and electrolyte as well
- lost in urine
- electrolyte loss
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
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
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
2 - damaged renal tubules
- impaired renal function or even failure
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
2 - shock and CV collapse
- most diabetic patients die of heart complications
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
3 - acetoacetate to β-hydroxybutyrate is 1:10
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?
- D-beta-hydroxybutyrate dehydrogenase
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+
2 - K+
- this can initially cause hyperkalaemia
- insulin is also required for Na+/K+ ATPase, so without insulin K+ cannopt re-enter the cells
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
1 - address K+ depletion
- return electrolyte balance between intra and extracellular space
