Acute Complications of Diabetes Flashcards
What does hypoglycaemia mean?
- hypo = low
- glyc = glucose
- aemia = blood
What is the clinical diagnosis of hypoglycaemia?
- <4mmol/L
How many people worldwide are estimated to be affected by hypoglycaemia?
- 460 million
When a patients blood glucose drops <4mmol/L what systems combine to try and increase the bodies blood glucose levels?
- autonomic
- sympathetic activity
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?
- adrenal gland (medulla) = adrenalin
- pancreas = glucagon
What are the 3 most common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia?
- shaking/trembling
- pallor
- sweating
3 of the most common signs that we as clinicians can see in a patient who is experiencing hypoglycaemia are:
1 - shaking/trembling
2 - pallor
3 - sweating
What are 7 other symptoms a patient may describe?
- anxiety
- tiredness
- hunger
- headaches
- blurred vision
- palpitations
- lips/tongue tingling
What does the term neuroglycopaenic mean?
- low 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. What blood glucose level would we expect to see more neurological issues developing?
- 2.8mmol/L
Neuroglycopaenic refers to low blood glucose to the brain, which is when blood glucose drops below 2.8mmol/L. What are some of the most common later signs of hypoglycaemia?
- slurred speech
- sower reactions
- disorientation
- seizures/fitting
- coma
- low concentration
- dizziness
- confusion
- aggression or irritable
What is Hypoglycaemia Unawareness?
- patient is unaware that their blood glucose is dangerously low
- Neuroglycopenia symptoms occur before autonomic symptoms (brain is affected before the adrenal gland and adrenalin can have an effect to warn the body and try to mobilise glucose, generally in people have had multiple hypos)
Hypoglycaemia Unawareness is when a patient is unaware that their blood glucose is dangerously low and then neuroglycopenia symptoms occur before autonomic symptoms. What % of patients with T1DM experience this?
- aprox 40%
Hypoglycaemia Unawareness is when a patient is unaware that their blood glucose is dangerously low and then neuroglycopenia symptoms occur before autonomic symptoms, which occurs in aprox 40% of T1DM patients. What 3 things must have happened for this to occur?
- 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 are some of the most common causes that cause hypoglycaemia in patients?
- increased/decreased carbohydrate intake (alcohol)
- too much exercise
- mismanaged medication (insulin, GLP-1)
- alcohol
- age and duration of diabetes
- hypoglycaemia unawareness
- impaired renal function
- pregnancy/breast feeding
How can excessive alcohol cause hypoglycaemia?
- alcohol contains a lot of sugar which causes the body to produce excessive insulin
- if food is not consumed alongside patients will have too much insulin and blood glucose drops
If a patients has been identified as being hypoglycaemia (<4mmol/L), what would the immediate treatment be if the patient is conscious and able to swallow?
- give 20g quick/rapid acting carbohydrates
If a patients has been identified as being hypoglycaemia (<4mmol/L), the immediate treatment be if the patient is conscious and able to swallow, we would give the patient 20g of quick/rapid acting carbohydrates. How would we assess if the patients blood glucose has risen above 4mmol/L and if it has not what would we do next?
- perform capillary blood glucose (CBG) after 10-15 minutes
- if still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates
If a patients has been identified as being hypoglycaemia (<4mmol/L), the immediate treatment be if the patient is conscious and able to swallow, we would give the patient 20g of quick/rapid acting carbohydrates. We would then take a capillary blood glucose (CBG) after 10-15 minutes to assess if the blood glucose has risen >4mmol/L. If still <4mmol/L give the patient an additional 20g of quick/rapid acting carbohydrates. If you assess the CBG again after 10-15 minutes and the patients blood glucose is still <4mmol/L, what would then next immediate treatment option be?
- hospital = intravenous dextrose (essentially a simple sugar)
- home = glucagon injection administered
Once we are happy that a patient is no longer hypoglycaemic (>4mmol/L), how would we treat the patient?
- provide slow releasing carbohydrates
- 10-20 grams (food such as toast, biscuits)
What are a few simple examples of 20g of fast acting carbohydrates?
- 200 ml pure fruit juice e.g. orange
- 120ml of original Lucozade®
- 6-7 Dextrosol® tablets (or 5 Glucotabs®)
- 3 – 4 Jelly babies
- 200mls coke
- Glucojuice is equivalent of 15g of carbs
If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, what would a family/friend need to do?
- call 999 and ask for help as this is a medical emergency
If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, what 2 things must we check?
- ABCs
- Airway, Breathing and Circulation
- temperature (patients may become hypothermic)
If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, and we have checked their ABCs, what would be really important to measure to assess their consciousness?
- glasgow coma scale (GCS)
If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and has been brought into hospital, we have checked their ABCs, assessed their consciousness using the Glasgow Coma Scale, what do we need to do to assess if they are actually hypoglycaemia?
- assess blood glucose
- check to see if <4mmol/L
If a diabetic patient is suspected of being hypoglycaemia and unconscious at home, and is in hospital, what would we want to do with insulin and dextrose?
- insulin = if patient is taking insulin this would be stopped immediately (unless T1DM)
- dextrose = patient would receive intravenous dextrose to raise blood glucose
If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, what can a family/friend or on site clinical team member do?
- administer subcutaneous or intramuscular injection of glucagon
If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, what can a family/friend or on site clinical team member do?
- administer subcutaneous or intramuscular injection of glucagon
If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, and a family/friend or on site clinical team member has administered subcutaneous or intramuscular injection of glucagon, what should the normal response in blood glucose be within 10 minutes?
- 3.5-5.7 mmol/L
If a patient is at home, is unconscious, unable to swallow and confirmed to being hypoglycaemic, a family/friend or on site clinical team member can administered subcutaneous or intramuscular injection of glucagon. Which 3 groups of patients might be less responsive to glucagon injections?
- chronically malnourished
- depleted glycogen stores
- severe liver disease (low glycogen stores and/or metabolism)
If a patient is at home and has become hypoglycaemic and been administered with a glucagon injection and their blood glucose has risen to within 3.5-5.7 mmol/L, what must they then do?
- administer slow acting carbohydrates
- patient must be able to swallow safely
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?
- 20% dextrose
- given in 100ml over 10-15 minutes
- 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
- given in 100ml over 10-15 minutes
- once recovered (4 hours), provide with 20g of slow acting carbohydrates
Why can it be dangerous to administer 50% dextrose?
- 50% is hypertonic and may cause the following:
1 - phlebitis(skin irritation)
2 - thrombosis (blood clot) at injection site
3 - overcorrection and hyperglycaemia
Dextrose is provided to patient intravenously when patients are hypoglycaemic. Insulin is normally stopped to allow blood glucose to rise following the administration of dextrose. However, when would we never stop insulin administration?
- in T1DM patient
What is diabetic ketoacidosis?
- excessive levels of ketone bodies in the blood
- ketones are carbon molecules of energy produced by mitochondria of the liver produced when glycogen/glucose levels are low
- can donate their protons in blood, causing metabolic acidosis
When does diabetic ketoacidosis occur?
- stressor increases sympathetic tone and signals pancreas to secretes glucagon, raising blood glucose
- blood glucose levels increase, but no insulin
- high blood glucose causes cause polyuria
- body produces ketones from fatty acids for energy, but too much is acidic and dangerous
Insulin deficiency can cause hyperglycaemia. What effect does this have on the concentration of solutes in the blood and what is this called?
- 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?
- 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 - dehydration
2 - 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?
- hyperglycaemia draw fluid from intra to extracellular space to dilute blood glucose
- movement of H2O from intra to extracellular space causes hyponatraemia
- the body therefore has too much extracellular fluid and attempt to remove it via diuresis
- diuresis means glucose and electrolytes will be loss in the urine in an attempt to reduce blood volume and hyperglycaemia
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?
- damage to renal tubules
- impaired renal function or even failure
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
At normal level the ratio of acetoacetate to β-hydroxybutyrate is 1:1. However, during diabetic ketoacidosis, what does this ratio reach?
- acetoacetate to β-hydroxybutyrate is 1:10
In a patient with diabetic ketoacidosis (DKA) there are multiple aspects that need to be addressed. One aspect is to address low K+ concentrations. There are 2 mechanisms explaining why K+ concentrations increase in DKA, initially causing hyperkalaemia, what are these 2 mechanisms?
- cells posses a H+ (enter the cell) / K+ (leave the cell) cation exchanger
- DKA causes high ketone bodies causing increased H+ osmolality in plasma
- 1st mechanism = H+ moves down concentration gradient into cells and K+ leaves the cell
- 2nd mechanism = insulin activates Na+/K+ pump, no insulin means K+ cannot enter the cell
ULTIMATELY CAUSES HYPerKALAEMIA initially and then HYPOKALAEMIA AS K+ LOST IN THE URINE
In a patient with Hyperosmolar Hyperglycaemia State (HHS) what is the pathway for shock and cardiovascular failure?
- patient presents with HSS so hyperglycaemia and hyperosmolality state
- glycosuria occurs follow by loss of electrolytes (Na+, K+ and phosphates)
- dehydration occurs due to loss of fluids
- renal failure occurs
- shock and cardiovascular failure
