Type 2 Diabetes Flashcards
What is type 2
In Type 2 Diabetes Mellitus, pancreatic beta cell production of insulin becomes insufficient due to insulin resistance.
Onset is usually in adults and there is often a strong family history.
What are the causes
Causes include a combination of environmental and genetic factors, poor diet, lack of exercise and obesity.
What is required for a diagnosis
If symptomatic one of the following results is sufficient:
Random blood glucose =11.1mmol/l
Fasting plasma glucose =7mmol/l
2 hour glucose tolerance =11.1mmol/l
HbA1C =48mmol/mol (6.5%)
If the patient is asymptomatic two results are required from different days.
What would the random glucose be in a positive result
11.1
What would the fasting glucose be
7
What would be shown after the 2 hour glucose tolerance test
11,1
What would be a positive HbA1C result
48mmol/mol
What is gastroparesis
Gastroparesis is a recognised gastro-intestinal complication of diabetes, related to poor glycaemic control.
Gastroparesis is caused by nerve damage to the autonomic nervous system.
What happens in gastroparesis
Vagus nerve damage -l ead to delayed gastric emptying, offensive egg smelling burps due to bacterial overgrowth, early satiety, abnormal stomach wall movements and morning nausea
What is the management for gastroparesis
Treatment includes the use of motility agents such as metoclopramide or domperidone, tight glycaemic control, antibiotics such as Erythromycin to kill off the bacterial overgrowth and botox injections to relax the gastric outflow obstruction. Else gastric pacemakers
What happens in autonomic neuropathy
Postural or orthostatic hypotension is defined as a fall in systolic blood pressure by 20mmHg or more after changing position or posture, typically from lying to standing.
What are the treatments of autonomic nueropathy
Increased dietary salts
Use of fludrocortisone or miodrine to increase the presence of salt retaining hormones
raising bed head position to retrain baroreceptors and ted stocking use
How does peripheral artery disease manifest
If the circulation is compromised then this can manifest itself in several ways including foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).
What has to be done if patient found with critical ischaemia
need to be urgently seen by a multi-disciplinary specialist diabetic foot team which includes a vascular surgeon.
What are the risks to the foot
high risk of diabetic foot ulceration and subsequent infection.
Once an infected diabetic ulcer sets in, it can be very difficult to treat and may take a very long time to treat and heal.
How to manage a diabetic foot
Management requires multi-disciplinary input with consideration to good glycaemic and blood pressure control, stopping smoking, improving the circulation (potentially with angioplasty or bypass surgery), debridement of the wound, the use of larvae therapy (maggots) and antibiotics.
When to use antibiotics
Targeted to organism especially if deep ulceration and if osteomyelitis is suspected
How to diagnose osteomyelitis
MRI is the imaging modality of choice to diagnose osteomyelitis as it does not reliably show up on plain X-rays.
What organisms cause diabetic foot infections
Gram positive organisms e.g. such as Staphylococcus aureus, Enterococcus, and gram-negative organisms like Pseudomonas aeruginosa, Escherichia coli, Klebsiella species, Proteus species and anaerobes.
How to screen for sexual dysfunction
Low testosterone (hypogonadism) can be primary (testicular failure) or secondary (pituitary) and needs to be screened for using a 9AM testosterone blood test (this is the peak time of release because of diurnal hormone secretion patterns) and gonadotrophins (LH and FSH).
Why may ED be present
Nerve damage in neuropathy, blood vessel damage in vascular disease and psychological problems such as depression all also contribute to ED, given that having an erection is a complex physiological process.
why are there cardiac complications
Hyperglycaemia, which characterises diabetes, in combination with free fatty acids in the blood can change the makeup of blood vessels, and this can lead to cardiovascular disease.
The lining of the blood vessels may become thicker, and this in turn can impair blood flow.
What advice is given to patients
Patient education is integral to ensure patients take steps to avoid further progression of their disease and associated complications. This involves diet advice, encouraging regular physical activity and smoking cessation advice.
How often should you measure HbA1c
3-6 month intervals.
What is the initial management
Initial drug treatment is usually metformin. Pioglitazone, DPP‑4 inhibitors, sulphonylureas or SGLT-2 inhibitors may be options for some patients who cannot take metformin.
What is the management after monotherapy
Dual Therapy
Following initial management, consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).
What to do if dual therapy is insufficient
Triple Therapy
metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
If dual therapy has not controlled drug glucose, triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.
What are the side effects of metformin
Gastrointestinal upset
What is the mechanism of action for metformin
the centre of metformin’s mechanism of action is the alteration of the energy metabolism of the cell. Metformin exerts its prevailing, glucose-lowering effect by inhibiting hepatic gluconeogenesis and opposing the action of glucagon.
When is SGLT given
should also be given in addition to metformin if any of the following apply:
the patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
the patient has established CVD
the patient has chronic heart failure
What should happen before SGLT -2 inhibitors are introduced
metformin should be established and titrated up before introducing the SGLT-2 inhibitor
When may DPP-4 inhibitors, pitogliatzone or a sulfonylurea preferred over SGLT -2 when metformin is contraindicated
if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure:
When is a second drug added
titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)
How is T2DM managed when HbA1c target is 48 mmol/mol (6.5%)
Lifestyle (+/- metformin) depending on patient preference
What to do if metformin is not tolerated
Switch to modified release metformin
What is the suffix for SGLT-2 INHIBITORS
-Liflozin
What to do if triple therapy is ineffective
Consider switching one of the drugs for a GLP-1 mimetic
When should GLP-1 be added to insulin
Under specialist care
When can you continue GLP-1 therapy
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
What should be done before starting insulin
metformin should be continued. In terms of other drugs NICE advice: ‘Review the continued need for other blood glucose-lowering therapies’
NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need
Which fast acting insulin analogues may be used
Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.
What are the long acting insulin analogues
Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).
What is the incretin effect
In normal physiology an oral glucose load results in a greater release of insulin than if the same load is given intravenously - this known as the incretin effect. This effect is largely mediated by GLP-1 (a type of incretin) and is known to be decreased in T2DM.
What are the purpose of Glucagon like mimetic e.g. Exenatide/liraglutide
Increasing GLP-1 levels, these drugs increase insulin secretion and inhibit glucagon secretion.
What are the benefits of GLP-1
One of the major advances of GLP-1 mimetics is that they typically result in weight loss, in contrast to many medications such as insulin, sulfonylureas and thiazolidinediones. They are sometimes used in combination with insulin in T2DM to minimise weight gain.
What do DPP-4 inhibitors do - gliptins
Inhibit breakdown of GLP-1
When must exenatide given
subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal.
What is the advantage of liraglutide
Only has to be given once a day
When should exenatide be considered to be added to metformin and a sulfonylurea
BMI >= 35 kg/m² in people of European descent and there are problems associated with high weight, or
BMI < 35 kg/m² and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities.
What are the adverse effects of GLP-1 mimetics
Nausea + vomiting in some cases pancreatitis
When is a DPP-4 preferred over a thiazolidinedione
NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems
When is a DPP-4 preferred over a thiazolidinedione
NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems
