Diabetes Flashcards
Ix T1DM (5 things)
urine should be dipped for glucose and ketones
fasting glucose and random glucose
HbA1c is not as useful for patients with a possible or suspected diagnosis of T1DM as it may not accurately reflect a recent rapid rise in serum glucose
C-peptide levels are typically low in patients with T1DM
diabetes-specific autoantibodies are useful to distinguish between type 1 and type 2 diabetes
The symptoms and signs in a new diagnosis of type 1 diabetes mellitus (T1DM) are typically those seen in diabetic ketoacidosis although the diagnosis is usually over a longer time frame
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Antibodies in T1DM
Antibodies to glutamic acid decarboxylase (anti-GAD) Present in around 80% of patients with T1DM
Islet cell antibodies (ICA, against cytoplasmic proteins in the beta cell) Present in around 70-80% of patients with T1DM
Insulin autoantibodies (IAA) Presence in T1DM correlates strongly with age, found in over 90% of young children with T1DM but only 60% of older patients
Insulinoma-associated-2 autoantibodies (IA-2A)
Diagnostic criteria for type 1 diabetes mellitus
If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
T1DM Age of onset Speed of onset Weight of patient Fetaures Ketonuria
Age of onset: Typically < 20 years, however, 40% > 30 years
Speed of onset: More acute, hours-days
Weight of patient: Recent weight loss typical
Features of DKA
Ketonuria Common
T2DM Age of onset Speed of onset Weight of patient Fetaures Ketonuria
Age of onset Typically > 40 years
however, may occur in younger, obese patients
Speed of onset Slower, weeks-months
Weight of patient Obesity is strong risk factor and recent weight loss is rare
Features Milder symptoms e.g. polyuria, polydipsia
Ketonuria rare
Diagnose type 1 diabetes on clinical grounds in adults presenting with hyperglycaemia, bearing in mind that people with type 1 diabetes typically (but not always) have one or more of:
ketosis rapid weight loss age of onset below 50 years BMI below 25 kg/m² personal and/or family history of autoimmune disease
In terms of diagnosing T1DM, NICE recommend the following on who may need further tests:
Consider further investigation - C‑peptide and/or diabetes‑specific autoantibody titres if:
type 1 diabetes is suspected but the clinical presentation includes some atypical features
age 50 years or above
BMI of 25 kg/m² or above
slow evolution of hyperglycaemia or long prodrome
Which investigations for following patient:
a 15-year-old presents with weight loss, lethargy. Ketones and glucose found in the urine. A random serum glucose is 14 mmol/L
T1DM, no need for further investigations
Which investigations for following patient:
a 38-year-old obese man presents with polyuria. A random glucose is 12.5 mmol/L
Intermediate age for T1DM/T2DM, a risk factor for T2DM (obesity) but not clear cut - do C-peptide levels and diabetes-specific autoantibodies
Which investigations for following patient:
a 52-year-old woman (body mass index 23 kg/m²) presents with polyuria and polydipsia. Ketones are present in the urine
age atypical for T1DM but other features consistent - do C-peptide levels and diabetes-specific autoantibodies
Which investigations for following patient:
a 59-year-old obese man presents with polyuria. A random serum glucose is 12.0 mmol/L
T2DM, no need for further investigations
The diagnosis of type 2 diabetes mellitus can be made by
either a plasma glucose or a HbA1c sample. Diagnostic criteria vary according to whether the patient is symptomatic (polyuria, polydipsia etc) or not.
If the patient is symptomatic:
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
In 2011 WHO released supplementary guidance on the use of HbA1c on the diagnosis of diabetes:
a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)
in patients without symptoms, the test must be repeated to confirm the diagnosis
it should be remembered that misleading HbA1c results can be caused by
increased red cell turnover
Conditions where HbA1c may not be used for diagnosis:
haemoglobinopathies
haemolytic anaemia, untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
people taking medication that may cause hyperglycaemia (for example corticosteroids)
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies
Impaired fasting glucose (IFG)
Impaired glucose tolerance (IGT) is defined as
fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies
OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
It is now estimated that 8% of the total NHS budget is now spent on managing patients with diabetes mellitus.
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Before the advent of insulin therapy untreated type 1 diabetes would usually result in death. Poorly treated type 1 diabetes mellitus can still result in significant morbidity and mortality (as a result of diabetic ketoacidosis).
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The main focus of diabetes management now is
reducing the incidence of macrovascular (ischaemic heart disease, stroke) and microvascular (eye, nerve and kidney damage) complications.
What is T1DM
Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system
This results in an absolute deficiency of insulin resulting in raised glucose levels
Patients tend to develop T1DM in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis
What is T2DM
This is the most common cause of diabetes in the developed world. It is caused by a relative deficiency of insulin due to an excess of adipose tissue. In simple terms there isn’t enough insulin to ‘go around’ all the excess fatty tissue, leading to blood glucose creeping up.
What is Prediabetes
This term is used for patients who don’t yet meet the criteria for a formal diagnosis of T2DM to be made but are likely to develop the condition over the next few years. They, therefore, require closer monitoring and lifestyle interventions such as weight loss
What is Gestational diabetes
Some pregnant develop raised glucose levels during pregnancy. This is important to detect as untreated it may lead to adverse outcomes for the mother and baby
What i sMaturity onset diabetes of the young (MODY)
A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
What is Latent autoimmune diabetes of adults (LADA)
The majority of patients with autoimmune-related diabetes present younger in life. There are however a small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM
Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. Examples include
chronic pancreatitis and haemochromatosis.
Drugs may also cause raised glucose levels. A common example is
glucocorticoids which commonly result in raised blood glucose levels
Remember that the polyuria and polydipsia are due to
water being ‘dragged’ out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).
There are 4 main ways to check blood glucose:
a finger-prick bedside glucose monitor
a one-off blood glucose. This may either be fasting or non-fasting
a HbA1c. This measures the amount of glycosylated haemoglobin and represents the average blood glucose over the past 2-3 months
a glucose tolerance test. In this test, a fasting blood glucose is taken after which a 75g glucose load is taken. After 2 hours a second blood glucose reading is then taken
The principle of managing diabetes mellitus are as follows:
drug therapy to normalise blood glucose levels
monitoring for and treating any complications related to diabetes
modifying any other risk factors for other conditions such as cardiovascular disease
The principle of managing T1 diabetes mellitus are as follows:
patients always require insulin to control the blood sugar levels. This is because there is an absolute deficiency of insulin with no pancreatic tissue left to stimulate with drugs
different types of insulin are available according to their duration of action
The principle of managing T2 diabetes mellitus are as follows:
the majority of patients with type 2 diabetes are controlled using oral medication
the first-line drug for the vast majority of patients is metformin
second-line drugs include sulfonylureas, gliptins and pioglitazone.
if oral medication is not controlling the blood glucose to a sufficient degree then insulin is used
Insulin
Mechanism:
Route:
Main side effects:
Direct replacement for endogenous insulin
Subcutaneous
Hypoglycaemia, Weight gain, Lipodystrophy
Used in all patients with T1DM and some patients with poorly controlled T2DM
What is first line in T2DM?
Metformin
Metformin
Mechanism:
Route:
Main side effects & considerations?
Increases insulin sensitivity & Decreases hepatic gluconeogenesis
Oral
Gastrointestinal upset, Lactic acidosis
Cannot be used in patients with an eGFR of < 30 ml/min
Sulfonylureas Mechanism: Route: Main side effects: Examples:
Stimulate pancreatic beta cells to secrete insulin Oral
Hypoglycaemia, Weight gain, Hyponatraemia
Examples include gliclazide and glimepiride
Thiazolidinediones Mechanism: Route: Main side effects: Examples:
Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
Oral
Weight gain, Fluid retention
Only currently available thiazolidinedione is pioglitazone
DPP-4 inhibitors Mechanism: Route: Main side effects: Examples:
Increases incretin levels which inhibit glucagon secretion Oral Generally well tolerated but increased risk of pancreatitis
(-gliptins)
SGLT-2 inhibitors Mechanism: Route: Main side effects: Examples:
Inhibits reabsorption of glucose in the kidney Oral Urinary tract infection
(-gliflozins)
GLP-1 agonists (-tides) Mechanism: Route: Main side effects: Examples:
Incretin mimetic which inhibits glucagon secretion
Subcutaneous
Nausea and vomiting, Pancreatitis
(-tides)
Which diabetes meds result in weight loss
SGLT-2 inhibitors (-gliflozins)
GLP-1 agonists (-tides)
What is glucagon-like peptide-1 (GLP-1),
hormone released by the small intestine in response to an oral glucose load
Increasing GLP-1 levels, either by the administration of an analogue (glucagon-like peptide-1, GLP-1 mimetics, e.g. exenatide) or inhibiting its breakdown (dipeptidyl peptidase-4 ,DPP-4 inhibitors - the gliptins), is therefore the target of two recent classes of drug.
