Type 1 Diabetes and Hypo management Flashcards
what are the symptoms of T1DM
weight loss, excessive thirst, polyuria, fatigue
can also be headache, anxiety, muscle spasm
what are GAD autoantibodies
antibody often seen in T1DM, destroys GAD cells (in pancrease) which produce the enzyme glutamate decarboxylase
what is T1DM
autoimmune beta cell destruction leading to absolute insulin deficiency
what is type two DM
progressive sensory defect on the background on insulin resistance
what is gestational DM
diabetes diagnosed in 2nd/3rd trimester that is not clearly overt diabetes
what are the two types of monogenic diabetes
neonatal DM and MODY
give an example of an endocrine pancreas disease that can cause diabetes
cystic fibrosis
what can induce diabetes
drugs (HIV treatment, organ transplant) or chemical
what cell mediates T1DM
T cells
what is the onset of T1DM like
prolonged, months to years
what causes T1DM
genetic susceptibility and environmental factors
how long before symptoms begin
need to have lost 80-90% of beta cells before marked hyperglycaemia occurs
what other autoimmune conditions is T1DM associated with
thyroid, coeliac (1:20 will have T1DM), addisons, pernicious anaemia, vitiligo
what is LADA
latent autoimmune diabetes of adulthood
what is the presentation of LADA
slowly progressive disease onset, non obese, no FHx T2DM, age >35 at onset, mild insulin resistance, low C peptide, HLA gene positive (GAD)
what does a positive GAD mean
80% of + will be insulin dependent in 6 years
75-84% of recent onset T1DM will be GAD +
what does C peptide show
how much insulin is being produced, low= low
what is the incidence of T1DM in scotland
1 in 25, 3rd in the world
what is polyglandular endocrinopathy type 2
autoimmune conditions that causes T1DM along with (any/all of):
- addisons disease
- hypothyroidism
- hypogonadism
- vitiligo
- coeliac
(not linked to a gene)
what is polyglandular endocrinopathy type 1
(autosomal recessive) mild immune deficiency with T1DM, addisons, hypothyroidism, hypogonadism, vitiligo, coeliac PLUS there may also be: -alopecia -pernicious anaemia -hypoparathyroidism
what is the difference in histology between T1DM and T2DM
T1DM- lymphocytic infiltrate attacking islets
T2DM- amyloid deposition in islet
what are the islet autoantibodies
IA-2, IA-2beta, GAD65, ZnT8
how many newly diagnosed cases will have positive antibodies - what can cause them to vary
70-80%
age, ethnicity, gender, quality of assay
what autoantibodies are most commonly tested
IA-2, GAD, Znt8
what gene is associated with T1DM
chromosome 6, HLA DR3, DR4 and DQ
how does insulin deficiency affect protein metabolism
increase protein catabolism =
increased AA in plasma
urinary nitrogen loss
how does insulin deficiency affect lipid metabolism
increased lipolysis =
increased plasma FFA
ketogenesis
ketonuria
what is the function of insulin
released in response to carbohydrate, suppresses glycolysis and stimulate glycogenesis and lipogenesis
is insulin anabolic or catabolic
anabolic- insulin deficiency a catabolic state
what are the features of insulin deficiency
accelerated starvation, hyperglycaemia, hepatic gluconeogenesis, lipolysis, protein catabolism, reduced glucose storage
what happens to the alpha and delta cells when beta cells destroyed
are dysregulated
what are the symptoms of diabetic ketoacidosis
vomiting, abdominal pain, altered consciousness,
acidotic beathing, pH
<7.3, urine ketones +++, dehydrated, coma/death
what is the classical presentation of T1DM
acute onset, presents with DKA or severe symptoms, pre-school and peri-puberty (can present at any age), non obese, insulin dependant, FHx uncommon
what are the BM diagnosis guidelines
a random venous plasma glucose concentration ≥ 11.1 mmol/l or
a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
two hour plasma glucose concentration ≥ 11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).
An HbA1c of 48mmol/mol (6.5%) is recommended as the cut off point for diagnosing diabetes
what are the long acting, background insulins
glargine and determir
what are the mealtime insulins
aspart, lispro and gulisine
why do you need more insulin to achieve homeostasis in T2DM
as patients will all be hyper insulinaemic (too much insulin compared to glucose)
what can cause glucose variability even with correct insulin dosages
injection- failure to mix insulin, accuracy of device, leak from injection site
external factors- exercise and temp will increase absorption
tissue- injection into muscle (will increase absorption), lipohypertrophy, blood supply
carb delivery- meal constituents, gastroparesis (delayed stomach emptying- increased fat in the meal)
what is DAFNE
dose adjustment for normal eating
what does high glucose over time cause
micro (retinopathy, nephropathy, neuropathy) and macro (heart, stroke and peripheral limb ischaemia) vascular disease
how do you evaluate metabolic control
glycated haemoglobin (HbA1c)
what is HbA1c
formed by non enzymatic glycation of haemoglobin on exposure to glucose- shows how much glucose has been in blood over past 6-8 weeks
what can HbA1c vary with
haemolytic anaemia, blood loss, pregnancy
what are the markers for HbA1C
42 and above pre-diabetes
48 and above diabetes
75 and above high risk of complications
goal for diabetics 52
how do you monitor blood glucose
BM, urine, implanted devices (freestyle libre)
what resp condition is made in diabetes
cystic fibrosis
what is DIDMOAD or wolfram syndrome
Diabetes Insipidus Diabetes Mellitus Optic Atrophy Deafness Neurological anomalies
what is bardet biedl syndrome
Often very obese Polydactyly Hypogonadal Visual impairment Hearing impairment Mental retardation Diabetes
Consanguineous parents
what is the treatment foe T1DM
insulin, DAFNE
what are the prandial insulins
insulin analogues- insulin aspart, lispor, gluisine
soluble insulin- actrapid, humulin S
what are the basal insulins
insulatard, humulin I, glargine, determir
what can happen if there is repeated insulin injections at the same site
lipohypertrophy, insulin absorption poor, problems with hypo and hyperglycaemia
what happens if you inject insulin into subcutaneous oedema
delays insulin absorption
what happens when you inject insulin into muscle
is absorbed too quickly, can cause hypoglycemia
what is the concentration of the vast majority of insulin in hospital
100 units per millilitre
should all insulin be kept in the fridge
opened ‘in-use’ insulin devices are stable at room temperature for one month
in use devices should not be kept in the fridge in hospital to avoid cross infection
unopened vials/ devices should be stores in the fridge
what is hypoglycaemia
a BG less than 4 millimoles per litre
what medications can cause hypos
sulphonylureas- gliclazide, glipizide, glimepiride, glibenclamide
insulin
what hormones are released in the body in response to hypoglycaemia
adrenaline, glucagon, cortisol, growth hormone
aimed to release glucose from the liver
when in hypglycaemia can glucose release be impaired
if patients are: malnourished have had repeated hypoglycaemia have severe liver disease excessive alcohol consumption
what causes the symptoms of hypos
the activation of the autonomic nervous system
what are the symptoms of a hypo
trembling anxiety palpitations numbness and tingling around lips/finger tips irritability hunger pale and sweaty feel vulnerable or afraid
what are the neuroglycopenic symptoms of a hypo
when the brain becomes short of glucose (usually at 2mmol/L or lower)
- weakness
- concentration and coordination difficulties
- vision problems
- slurred speech
- loss of consciousness
- seizure
what is the treatment for hypos
if patient can swallow- 15-20g of fast acting carbohydrates:
- glucose tablets
- glucose gel if drowsy but can swallow (squeezed between teeth and gums
unconscious patients:
- stop insulin IV
- IV glucose
- subcutaneous/ IM glucagon
in treating hypos who should you avoid giving fruit juice to
patients with renal failure
when might glucagon be ineffective
undernourish patients or those with severe liver disease, repeated hypos
or those who have had an OHA induced hypo
how is glucagon stored and administerd
in fridge
subcutaneously/ IM/ IV
adult (>25kg) dose 1mg, child 500 micrograms
how do you prevent the recurrence of hypos
think what caused it
check BG every 15 mins after treatment
if BG still under 4 mmol/L give more glucose
after initial 20 grams of more complex carbs should be given to those who can swallow (bread, biscuits) or IV infusion if they cant swallow
what is the target BG range for inpatients
6-12mmol/l
what must quick acting insulins always be given with
carbohydrates- cover snacks, meal times with carbs
what are the types of quick acting insulins
rapid acting analogue, short acting (soluble) insulin)
give examples of rapid acting insulin analogues
humalog, novorapid, apidra
what is the action of onset and duration of rapid acting analogues
immediate onset, peak at 2 hours, last 4 hours
what is the action of onset and duration of short acting soluble insulin
30 mins before effect, peak at 4 hours, lasts 8 hours
give examples of short acting soluble insulin
actrapid, humulin S, insuman rapid
give examples of intermediate acting insulin- how long do they last
insulatard, humulin I, ismuman basal (last 16 hours)
give examples of long acting analogue insulin - how long do they last
lantus and levemir basal insulin (last 24 hours
what is in fix mix insulin
rapid acting analgoue intermediate mixture
short acting- intermediate mixture
name 5 bolus insulins
novorapid, humalog, humulin S, aprida, actrapid
what effect does acute kidney injury have on insulin duration
reduces insulin secretion- effects will last longer
how much change in insulin is recommended to improve BG control
+/- 10%
whatever time you measure BG to be high or low, increase the dosage of the previous meal in the next day (high at lunch, increase breakfast dose, low at breakfast reduce basal dose)
what insulin at not at standard concentration
tresiba, humalog, toujeo, humunlin R
what are the indications for IV insulin
acute illness
DKA
HHS
unable to take oral/ fasting patients
is IV insulin good for people who are eating and drinking
not generally suitable
how long is IV insulins half life
approx 5 mins
what can prolonged IV insulin cause
cannula related complications (infection), electrolyte abnormalities (hyponatraemia)
what separate infusions are given with IV insulin (through same cannula)
Iv glucose and potassium
insulin in solution of sodium chloride
different fluids for different clinical needs
patients switching to IV insulin should continue what
subcutaneous long acting basal insulin if they already take it
after how long must all IV insulin solutions be discarded
24 hours
how often do you monitor BG in IV insulin
hourly
when can you switch from IV insulin to subcutaneous
when patient is stable and 30- 60 mins after short acting (and long acting basal if not already still on that) has been given
queck BG 4 times daily after stopping IV insulin
when can you restart oral medication from IV insulin
after patient is tolerating food and clinically stable
what else should be measured when on IV glucose
daily urea and electrolytes
