Diabetes - COPIED Flashcards
Type I defined
autoimmune condition causing destruction of the pancreatic B cells resulting in absolute insulin deficiency.
(70-90% of cells must be destroyed before symptoms)
What are the EM physiological side effects of type I diabetes causing hypoglycaemia? (3)
>>> sugar in blood, none in cells.
Breakdown of fats and proteins; ketones and acidosis
leads to dehydration, Potassium loss and acidosis.
Dehydration because water follows excretion of sugar (osmotic diuresis)
what could be triggers for hypoglycaemia attacks?
infections; UTI, pneumonia
physiological stressors including cold, status epilepticus.
What is a big danger of px with long-standing diabetes and neuropathy?
MI or abdominal conditions such as infection or pancreatitis may be painless. Maybe osteomyelitis in the feet..
Tests for diabetes
Blood glucose
urine or blood test for ketones
pH (venous fine)
Symptoms of hypoglycaemia
confusion, sweating, fatigue and feeling dizzy.
maybe pale, weak, blurred vision, tachycardia, unconsciousness
EM tx of hypoglycaemia
50ml of glucose 50% if IV access available.
otherwise 1 mg glucagon
(as PAs 10% glucose IV okay)
non-emergency; dextrose, then more complex carbohydrates.
What is Kussmaul breathing?
Deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure.
What is diagnosis of DKA based on?
Diabetic ketoacidosis is a serious complication of Type I DM.
Diagnosis based on
diabetes (blood glucose >11 mmol/L)
ketones (urine or blood)
acidosis (pH <7.30 venous blood)
Diagnositic symptoms of DKA?
polydipsia
weight loss
dehydration
+ Kussmaul breathing
Tx for DKA
(Sickness and vomiting, abdominal pain, muscular weakness)
500ml then another 500ml then another 500ml (saline). MUST ensure patient is rehydrated before giving insulin. 0.1units per kilo per hour.
As sugar moves into cells (insulin taking effect) potassium follows therefore px becomes hypokalaemic. Normal potassium 3.5 to 5.
Watch urine output to check hydration.
Red flag; peds until 22-23 yr old. Can die from cerebral oedema; therefore don’t give insulin until properly hydrated.
Why rehydrate gradually with DKA?
to avoid rapid intracellular osmotic/ sodium shifts that may cause fatal CNS oedema.
Remember: with DKA and polydipsia, rapid fluid shift from intracellular compartments.
What factors cause cause a hypoglycaemic attack?
Too high a dose of medication (insulin or hypo causing tablets)
Delayed meals
Exercise
Alcohol
Obese px; type I or type II diabetes more likely?
type II
What is HONK?
hyperosmolar non-ketotic coma
induced by prolonged hyperglycaemia and dehydration and hypernatraemia.
* require careful management with fluid replacement and small doses of insulin to restore euvolaemia and euglycaemia.
Px advise for type II diabetes to reduce risk?
lose weight
stop smoking
- these are additional risk factors for hypertension and CV disease, both common in type II diabetes.
What’s the most prevalent cause of death for diabetic patients
coronary artery disease
(diabetic px after develop hypertension, dyslipidemia, and a decline in HDL, and a rise in triglyceride levels)
What is glipizide?
SE: weight gain
Can be combined with metformin for better control.
Sulfonylurea drug; increases the secretion of insulin and secondarily decreases the secretion of glucagon.
‘hypoglycaemic drug’
What the the two groups of antidiabetic drugs?
hypoglycaemic agents
antihyperglycaemic agents
What is an inherent problem with Sulfonylurea drugs?
Since they increase insulin secretion, can lead to hypoglycaemic episode if px skips or delays meals.
Alcohol increases hypoglycaemic effect.
Examples of 2nd generation sulfonylurea drugs (3)
glimepiride
glipizide
glyburide
What are sulfonylureas and meglitinides examples of?
hypoglycaemic drugs
Name the two meglitinides drugs that are short-acting and are useful for patients whose meal schedules vary.
Repaglinide
Nateglinide
How does metformin (biguanide drug) work?
NB> stop if acidosis suspected due to rare effect of lactic acidosis.
increases insulin receptor affinity in peripheral tissues.
1st line drug for type 2 diabetes. Can be used alone or in combo.
DOES NOT; stimulate insulin secretion, or cause hypoglycaemia, or weight gain.
DIARRHOEA common in 30% of px.
What is pramlintide acetate?
Analogue of amylin.
Amylin; co-secreted with insulin. It slows gastric emptying and reduces appetite.
Subcutaneous at mealtimes for type I and 2 diabetes. SE; nausea, vomiting, anorexia, headache.
What are the first line drugs for type 2 diabetes?
metformin
sulfonylureas
meglitinides
What is the management of type II Diabetes?
Patient education: reduce risk factors -
smoking, sedentary life style, hypertension, dyslipidaemia, and obesity.
Discuss dietary advice. Encourage exercise.
HbA1c testing until glucose levels stabilised.
Drug tx: standard-release metformin. Consider dual therapy if ineffective, or triple therapy.
BP: Aim for 140/80 and below
What is glipizide?
SE: weight gain
Can be combined with metformin for better control.
Sulfonylurea drug; increases the secretion of insulin and secondarily decreases the secretion of glucagon.
‘hypoglycaemic drug’
What the the two groups of antidiabetic drugs?
hypoglycaemic agents
antihyperglycaemic agents
What is an inherent problem with Sulfonylurea drugs?
Since they increase insulin secretion, can lead to hypoglycaemic episode if px skips or delays meals.
Alcohol increases hypoglycaemic effect.
Examples of 2nd generation sulfonylurea drugs (3)
glimepiride
glipizide
glyburide
What are sulfonylureas and meglitinides examples of?
hypoglycaemic drugs
Name the two meglitinides drugs that are short-acting and are useful for patients whose meal schedules vary.
Repaglinide
Nateglinide
How does metformin (biguanide drug) work?
NB> stop if acidosis suspected due to rare effect of lactic acidosis.
increases insulin receptor affinity in peripheral tissues.
1st line drug for type 2 diabetes. Can be used alone or in combo.
DOES NOT; stimulate insulin secretion, or cause hypoglycaemia, or weight gain.
DIARRHOEA common in 30% of px.
MCQ - important facts about Metformin
MOA, adverse effects, contraindications
Mechanism of action
- increases insulin sensitivity
- decreases hepatic gluconeogenesis
- may also reduce gastrointestinal absorption of carbohydrates
Adverse effects
gastrointestinal upsets are common (nausea, anorexia, diarrhoea), intolerable in 20%
lactic acidosis* with severe liver disease or renal failure (rare but important to know for exams)
Contraindications**
chronic kidney disease: NICE recommend that the dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)
metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration, iodine-containing x-ray contrast media: there is an increasing risk of provoking renal impairment due to contrast nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter
**metformin is now sometimes used in pregnancy, for example in women with polycystic ovarian syndrome
