Week 1 Flashcards
What is type 1 diabetes?
The autoimmune system destroys beta cells of the pancreas causing insulin deficiency. Commonly occurs between 9 months and 14yrs.
What is type 2 diabetes?
Insulin resistance where muscle, fat and liver cells stop responding to insulin after long term high blood glucose and uptake of glucose into these cells stops.
What is hyperglycaemia?
What is the pathophysiology?
High blood glucose.
When the beta cells of the pancreas don’t produce insulin or the cells that store glucose stop responding to insulin, glucose storage decreases and glucose stays in the blood.
What is gestational diabetes?
Diabetes that occurs during pregnancy. Pathology is largely unknown.
What are 4 contributing factors that lead to type 2 diabetes?
- Obesity
- Sedentary lifestyle
- Hypertension
- Elevated blood triglycerides
Name 6 signs/symptoms of hyperglycaemia.
Diuretic, thirsty, dry skin,
Hungry, fatigued, blurry vision.
A patient presents with excessive urination, is excessively thirsty, frequently hungry and tired. Their BGL is 11mmol/L.
What are they presenting with and how will you treat them?
Hyperglycaemia.
1. Treat presenting symptoms
2. Assess dehydration, perfusion and ketones
3. Provide IV, fluid and oxygen
What is diabetic ketoacidosis?
An absolute insulin deficiency more common in type 1 diabetics. Glucose can’t enter cells so fatty acids are broken down for cellular energy. The byproduct is organic acids (ketones, H+ and acetone) causing acidosis. High BGL, ketosis and metabolic acidosis.
What are the 4 key clinical features of DKA?
- Kissmaul breathing
- Vomiting
- BGL >13mmol/L
- Fruity, sweet smelling breath (acetone)
Patient is a 25 y/o male presenting with BGL 15, kussmaul breathing, fruity breath, uncontrolled vomiting and ALOC.
What is your differential?
How will you treat it (4)?
Diabetic ketoacidosis.
1. Assess dehydration status:
dry mouth, skin turgor, hypotension and ALOC
2. Manage airways
3. IV fluids 250ml (reassess every 250ml)
4. Transport
What is HHS?
How does it work?
hyperosmolar hyperglycaemic state,
A relative insulin deficiency. Blood glucose is high and cellular glucose is low causing hyperglycaemia, hyperosmolarity and severe dehydration but there is a sufficient amount of insulin available to prevent fatty acid break down and consequential acidosis.
Presents with BGL >33mmol/L and commonly in type 2 diabetics.
10 y/o female presents with severe dehydration, hypotension, tachycardia, hemiparesis, aphasia and a BGL 34mmol/L.
What is your differential?
How will you treat this patient?
Hyperosmolar hyperglycaemic state.
1. Assess dehydration status
(Dry mouth, turgor, hypotension, ALOC)
2. Manage airways
3. IV fluids 10-20ml/kg, TMD 60ml/kg
(Reassess every 10ml/kg)
4. Transport
What is hypoglycaemia?
How does it work?
Low blood glucose.
BGL <4mmol/L inhibits insulin and stimulates glucagon from pancreatic alpha cells. Glucagon stimulates the breakdown of glycogen to glucose for energy. The SNS releases adrenaline/noradrenaline to further increase blood glucose levels.
What are the 2 key physiological consequences of low blood glucose levels?
- Decreased neurological function
- Increased sympathetic activity
Where is hypoglycaemia commonly seen?
Name 2 reasons why they may have hypoglycaemia.
Type 1 diabetics.
1. Inject insulin but don’t eat afterwards.
2. Inject excessive insulin (accidental or intentional)
25 y/o female presents with tachycardia, cool, pale, sweaty appearance, ALOC with a BGL 3mmol/L. IV access possible.
What is your differential?
How will you treat this patient?
Hypoglycaemia.
1. Manage airway
2. IV glucose 10%
(15g/150ml, repeat 10g/100ml every 5 mins to achieve >4mmol/L)
3. Reassess for transport
18 y/o male presents unconscious, tachycardic, cool, pale, sweaty with a BGL 2.5. IV access not possible.
What is your differential?
How will you treat this patient?
Hypoglycaemia
1. Manage airways
2. IM glucagon
(1mg single dose)
3. Transport
What is Graves’ disease?
Autoimmune thyroid disease.
An antibody, thyroid stimulating immunoglobulin (TSI) binds to the TSH receptor on the thyroid causing excessive T3, T4 production. This causes a significant increase in metabolism.
What is hyperthyroidism?
What 2 conditions can cause it?
An increase in T3, T4 hormones from the thyroid gland causing an increase in metabolism.
- Graves’ disease
- Thyroid tumour
If a patient with pre-existing hyperthyroidism experiences surgery, trauma, infection or ingests thyroxine, what are they at risk of?
What are the signs/symptoms?
Thyroid storm.
Metabolism goes into overdrive.
- fever
- tachycardia
- vomiting/diahrrea
- confusion, ALOC, seizures or death
What is adrenocortical insufficiency?
Why is this significant?
The adrenal gland isn’t producing enough aldosterone or cortisol.
Aldosterone is crucial for BP maintenance and cortisol is crucial for stress management.
What 3 conditions can cause adrenal insufficiency?
- Primary AI - Addisons disease (autoimmune attack)
- Secondary AI- (ACTH) isn’t released from pituitary gland to act on adrenal gland for hormone release.
- Sudden stop of exogenous steroid use leaving the body cortisol deficient.
If a patient with adrenocortical insufficiency undergoes sudden stress or abrupt cessation of exogenous steroids, what are they at risk of?
Addisonian crisis.
What is Addisonian crisis?
A life threatening, acute onset of adrenocortical insufficiency.
Caused by physical or psychological stress or a sudden cessation of exogenous steroids.
The body doesn’t have the aldosterone or cortisol to cope with it.
