what are the acute complications of diabetes mellitus
- hypoglycaemia
- hyperglycaemia in very unwell patients
- diabetic ketoacidosis - type 1 DM
- hyperosmolar hyperglycaemic state/syndrome - type 2 DM
complications of Type 1 and 2 DM
what is hypoglycaemia
- defined as a BGL <4mmoI/L
- can be fatal
causes - medication overdose
- not eating enough carbohydrates or skippin meals
- excess alcohol consumption
- excessive exercise
- malnutrition
clinical manifestations
hypoglycaemia
- BGL <4mmoI/L
- sweating
- pale
- hunger
- dizziness
- anxiety
- seizures
- coma
- death
- vision changes
hypoglycaemia - management
- if the person is unconciouss, drowsy - do not give them food
- medical emegrency
- check BGL <4mmoI/L
- eat 15-20g of fast acting carbohydrates
complications of hyperglycaemia
- acutely unwell
- stress mehcanism
- impaired insulin function
- hyperglycaemia
what is diabetic ketoacidosis (DKA)
- medical condition
- related to hyperglycaemia
- due to lack of insulin leading to glucose build up in blood
risk factors of DKA
- new diagnosis
- acute stress or illness
- omission of inuslin
- lack of access to medical care
DKA clinical manifestations
lab markers
* BGL >11mmoI/L
* ketones present in blood and urine
symptoms
* sunken eyes
* dry skin
* headache
* polyuria
* polydipsia
* abdo pain
DKA management
- correction of dehydration
- reverse ketosis
- acid base and electrolyte corrections
complications
hyperosmolar hyperglycaemic state (HHS)
- complications arising from T2D seen at initial presentation
- severe dehydration
- high serum osmality
- very unwell
risk factor/ causes of HHS
- elderly - reduced thirst or fluid intake
- poorly controlled t2d
- infection and illness
- drugs that reduce insulin action
clinical manifestations of HHS
lab markers
* BGL >30mmoI/L
* ketones can be present/ absent
symptoms
* polyuria +
* polydispia +
* sunken eyes
* coma
* seizures
* abdo pain
* weakness
* cramps
* dry skin
HHS management
- correction of dehydration
- reverse hyperglycaemia
- acid base and electrolyte corrections
whats the normal fasting BGL range
4-6 mmoI/L
what causes type 1 diabetes
- autoimmune destruction of the beta cells
- genetics
- envrionmental factors - drugs, viruses
- non immune mediated diabetes - secondary to other conditons (pancreas_
whats the pathophysiology of T1D
- genetic factors or viral infections cause
- immune response against beta cells which cause
- beta cell destruction
- lack of insulin released
- GLUT - 4s are not activated
- glucose unable to be taken up by cells leads to either
- hyperglycaemia which leads to T1D OR
- release of glucagon which leads to
- liver continuing to release glucose which leads to hyperglycaemia which leads to T1D
clinical manifestations of T1D
- 3 P’s (polyphagia, polyuria, polydispia)
- fatigue
- weight loss
- blurred vision
- confusion
- abdo pain
- nausea/ vomitting
- coma
treatment of T1D
- insulin is the only teatment option for T1DM
- protein based molecule
risk factors of T2D
- genetic factors/ family history
- overweight/ obese
- sedentary lifestyle
- age 35> + overweight
- history of gestational diabetes
pathophysiology of T2D
- characterised by insulin resistance
- decreased insulin production
- increased insulin resistance at the cell
- decrease beta cell responsiveness
what is the inflammatory response
- response is rapid
- limit the extent of injury
- destroy contaminating infectious microorganisms
- initate the immune response
- begin healing process
homeostaitic role in PGs, TXA2 and COX
- COX enzymes are required to produce the mediators thromboxanes and prostaglandins
- thromboxanes - involved in blood clotting function
- PGI2- initate platlet activation
what causes hypoglycaemia
- excess alcohol consumption
- exercise
- insulin overdose
