Type 2 Diabetes Flashcards

1
Q

What is type 2

A

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.

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2
Q

What are the causes

A

Causes include a combination of environmental and genetic factors, poor diet, lack of exercise and obesity.

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3
Q

What is required for a diagnosis

A

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.

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4
Q

What would the random glucose be in a positive result

A

11.1

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5
Q

What would the fasting glucose be

A

7

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6
Q

What would be shown after the 2 hour glucose tolerance test

A

11,1

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7
Q

What would be a positive HbA1C result

A

48mmol/mol

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8
Q

What is gastroparesis

A

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.

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9
Q

What happens in gastroparesis

A

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

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10
Q

What is the management for gastroparesis

A

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

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11
Q

What happens in autonomic neuropathy

A

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.

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12
Q

What are the treatments of autonomic nueropathy

A

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

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13
Q

How does peripheral artery disease manifest

A

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).

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14
Q

What has to be done if patient found with critical ischaemia

A

need to be urgently seen by a multi-disciplinary specialist diabetic foot team which includes a vascular surgeon.

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15
Q

What are the risks to the foot

A

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.

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16
Q

How to manage a diabetic foot

A

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.

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17
Q

When to use antibiotics

A

Targeted to organism especially if deep ulceration and if osteomyelitis is suspected

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18
Q

How to diagnose osteomyelitis

A

MRI is the imaging modality of choice to diagnose osteomyelitis as it does not reliably show up on plain X-rays.

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19
Q

What organisms cause diabetic foot infections

A

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.

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20
Q

How to screen for sexual dysfunction

A

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).

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21
Q

Why may ED be present

A

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.

22
Q

why are there cardiac complications

A

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.

23
Q

What advice is given to patients

A

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.

24
Q

How often should you measure HbA1c

A

3-6 month intervals.

25
Q

What is the initial management

A

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.

26
Q

What is the management after monotherapy

A

Dual Therapy

Following initial management, consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).

27
Q

What to do if dual therapy is insufficient

A

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.

28
Q

What are the side effects of metformin

A

Gastrointestinal upset

29
Q

What is the mechanism of action for metformin

A

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.

30
Q

When is SGLT given

A

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

31
Q

What should happen before SGLT -2 inhibitors are introduced

A

metformin should be established and titrated up before introducing the SGLT-2 inhibitor

32
Q

When may DPP-4 inhibitors, pitogliatzone or a sulfonylurea preferred over SGLT -2 when metformin is contraindicated

A

if the patient doesn’t have a risk of CVD, established CVD or chronic heart failure:

33
Q

When is a second drug added

A

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%)

34
Q

How is T2DM managed when HbA1c target is 48 mmol/mol (6.5%)

A

Lifestyle (+/- metformin) depending on patient preference

35
Q

What to do if metformin is not tolerated

A

Switch to modified release metformin

36
Q

What is the suffix for SGLT-2 INHIBITORS

A

-Liflozin

37
Q

What to do if triple therapy is ineffective

A

Consider switching one of the drugs for a GLP-1 mimetic

38
Q

When should GLP-1 be added to insulin

A

Under specialist care

39
Q

When can you continue GLP-1 therapy

A

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

40
Q

What should be done before starting insulin

A

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

41
Q

Which fast acting insulin analogues may be used

A

Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.

42
Q

What are the long acting insulin analogues

A

Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).

43
Q

What is the incretin effect

A

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.

44
Q

What are the purpose of Glucagon like mimetic e.g. Exenatide/liraglutide

A

Increasing GLP-1 levels, these drugs increase insulin secretion and inhibit glucagon secretion.

45
Q

What are the benefits of GLP-1

A

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.

46
Q

What do DPP-4 inhibitors do - gliptins

A

Inhibit breakdown of GLP-1

47
Q

When must exenatide given

A

subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal.

48
Q

What is the advantage of liraglutide

A

Only has to be given once a day

49
Q

When should exenatide be considered to be added to metformin and a sulfonylurea

A

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.

50
Q

What are the adverse effects of GLP-1 mimetics

A

Nausea + vomiting in some cases pancreatitis

51
Q

When is a DPP-4 preferred over a thiazolidinedione

A

NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems

51
Q

When is a DPP-4 preferred over a thiazolidinedione

A

NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems