Diabetes

Question 1

Ix T1DM (5 things)

Answer 1

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

Question 2

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

Answer 2

true

Question 3

Antibodies in T1DM

Answer 3

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)

Question 4

Diagnostic criteria for type 1 diabetes mellitus

Answer 4

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.

Question 5

T1DM
Age of onset  
Speed of onset
Weight of patient
Fetaures
Ketonuria

Answer 5

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

Question 6

T2DM
Age of onset  
Speed of onset
Weight of patient
Fetaures
Ketonuria

Answer 6

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

Question 7

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:

Answer 7

ketosis
rapid weight loss
age of onset below 50 years
BMI below 25 kg/m²
personal and/or family history of autoimmune disease

Question 8

In terms of diagnosing T1DM, NICE recommend the following on who may need further tests:

Answer 8

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

Question 9

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

Answer 9

T1DM, no need for further investigations

Question 10

Which investigations for following patient:

a 38-year-old obese man presents with polyuria. A random glucose is 12.5 mmol/L

Answer 10

Intermediate age for T1DM/T2DM, a risk factor for T2DM (obesity) but not clear cut - do C-peptide levels and diabetes-specific autoantibodies

Question 11

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

Answer 11

age atypical for T1DM but other features consistent - do C-peptide levels and diabetes-specific autoantibodies

Question 12

Which investigations for following patient:

a 59-year-old obese man presents with polyuria. A random serum glucose is 12.0 mmol/L

Answer 12

T2DM, no need for further investigations

Question 13

The diagnosis of type 2 diabetes mellitus can be made by

Answer 13

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.

Question 14

In 2011 WHO released supplementary guidance on the use of HbA1c on the diagnosis of diabetes:

Answer 14

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

Question 15

it should be remembered that misleading HbA1c results can be caused by

Answer 15

increased red cell turnover

Question 16

Conditions where HbA1c may not be used for diagnosis:

Answer 16

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)

Question 17

A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies

Answer 17

Impaired fasting glucose (IFG)

Question 18

Impaired glucose tolerance (IGT) is defined as

Answer 18

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

Question 19

It is now estimated that 8% of the total NHS budget is now spent on managing patients with diabetes mellitus.

Answer 19

true

Question 20

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).

Answer 20

tru

Question 21

The main focus of diabetes management now is

Answer 21

reducing the incidence of macrovascular (ischaemic heart disease, stroke) and microvascular (eye, nerve and kidney damage) complications.

Question 22

What is T1DM

Answer 22

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

Question 23

What is T2DM

Answer 23

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.

Question 24

What is Prediabetes

Answer 24

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

Question 25

What is Gestational diabetes

Answer 25

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

Question 26

What i sMaturity onset diabetes of the young (MODY)

Answer 26

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

Question 27

What is Latent autoimmune diabetes of adults (LADA)

Answer 27

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

Question 28

Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. Examples include

Answer 28

chronic pancreatitis and haemochromatosis.

Question 29

Drugs may also cause raised glucose levels. A common example is

Answer 29

glucocorticoids which commonly result in raised blood glucose levels

Question 30

Remember that the polyuria and polydipsia are due to

Answer 30

water being 'dragged' out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).

Question 31

There are 4 main ways to check blood glucose:

Answer 31

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

Question 32

The principle of managing diabetes mellitus are as follows:

Answer 32

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

Question 33

The principle of managing T1 diabetes mellitus are as follows:

Answer 33

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

Question 34

The principle of managing T2 diabetes mellitus are as follows:

Answer 34

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

Question 35

Insulin Mechanism: Route: Main side effects:

Answer 35

Direct replacement for endogenous insulin Subcutaneous Hypoglycaemia, Weight gain, Lipodystrophy Used in all patients with T1DM and some patients with poorly controlled T2DM

Question 36

What is first line in T2DM?

Answer 36

Metformin

Question 37

Metformin Mechanism: Route: Main side effects & considerations?

Answer 37

Increases insulin sensitivity & Decreases hepatic gluconeogenesis Oral Gastrointestinal upset, Lactic acidosis Cannot be used in patients with an eGFR of < 30 ml/min

Question 38

``` Sulfonylureas Mechanism: Route: Main side effects: Examples: ```

Answer 38

Stimulate pancreatic beta cells to secrete insulin Oral Hypoglycaemia, Weight gain, Hyponatraemia Examples include gliclazide and glimepiride

Question 39

``` Thiazolidinediones Mechanism: Route: Main side effects: Examples: ```

Answer 39

Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake Oral Weight gain, Fluid retention Only currently available thiazolidinedione is pioglitazone

Question 40

``` DPP-4 inhibitors Mechanism: Route: Main side effects: Examples: ```

Answer 40

Increases incretin levels which inhibit glucagon secretion Oral Generally well tolerated but increased risk of pancreatitis (-gliptins)

Question 41

``` SGLT-2 inhibitors Mechanism: Route: Main side effects: Examples: ```

Answer 41

Inhibits reabsorption of glucose in the kidney Oral Urinary tract infection (-gliflozins)

Question 42

``` GLP-1 agonists (-tides) Mechanism: Route: Main side effects: Examples: ```

Answer 42

Incretin mimetic which inhibits glucagon secretion Subcutaneous Nausea and vomiting, Pancreatitis (-tides)

Question 43

Which diabetes meds result in weight loss

Answer 43

SGLT-2 inhibitors (-gliflozins) | GLP-1 agonists (-tides)

Question 44

What is glucagon-like peptide-1 (GLP-1),

Answer 44

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.

Question 45

What is the incretin effect

Answer 45

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 and is known to be decreased in T2DM. in t2dm insulin resistance and insufficient B-cell compensation occur

Question 46

example of a glucagon-like peptide-1 (GLP-1) mimetic.

Answer 46

exenatide | Liraglutide

Question 47

Examples of Dipeptidyl peptidase-4 (DPP-4) inhibitors

Answer 47

Vildagliptin, sitagliptin

Question 48

Key points of GLP-1 mimetics?

Answer 48

ne 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. Exenatide must be given by subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal. Liraglutide is the other GLP-1 mimetic currently available. One the main advantages of liraglutide over exenatide is that it only needs to be given once a day. Both exenatide and liraglutide may be combined with metformin and a sulfonylurea. Standard release exenatide is also licensed to be used with basal insulin alone or with metformin. Please see the BNF for a more complete list of licensed indications.

Question 49

Consider adding exenatide to metformin and a sulfonylurea if:

Answer 49

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.

Question 50

NICE like patients to have achieved a > 11 mmol/mol (1%) reduction in HbA1c and ?% weight loss after 6 months to justify the ongoing prescription of GLP-1 mimetics.

Answer 50

3%

Question 51

The major adverse effect of GLP-1 mimetics is

Answer 51

nausea and vomiting. The Medicines and Healthcare products Regulatory Agency has issued specific warnings on the use of exenatide, reporting that is has been linked to severe pancreatitis in some patients.

Question 52

Key points DPP-4 inhibitors?

Answer 52

dipeptidyl peptidase-4, DPP-4 inhibitors increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown oral preparation trials to date show that the drugs are relatively well tolerated with no increased incidence of hypoglycaemia do not cause weight gain

Question 53

NICE guidelines on DPP-4 inhibitors

Answer 53

NICE suggest that a DPP-4 inhibitor might be preferable to a thiazolidinedione if further weight gain would cause significant problems, a thiazolidinedione is contraindicated or the person has had a poor response to a thiazolidinedione

Question 54

NICE updated its guidance on the management of type 2 diabetes mellitus (T2DM) in 2015. there is more flexibility in the second stage of treating patients (i.e. after metformin has been started) - you now have a choice of 4 oral antidiabetic agents, what are these

Answer 54

sulfonylurea gliptin pioglitazone SGLT-2 inhibitor

Question 55

Dietary advice T2DM

Answer 55

encourage high fibre, low glycaemic index sources of carbohydrates include low-fat dairy products and oily fish control the intake of foods containing saturated fats and trans fatty acids limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake discourage the use of foods marketed specifically at people with diabetes initial target weight loss in an overweight person is 5-10%

Question 56

HBA1C targets in T2DM

Answer 56

Lifestyle 48 mmol/mol (6.5%) Lifestyle + metformin 48 mmol/mol (6.5%) Includes any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea) 53 mmol/mol (7.0%) Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%) 53 mmol/mol (7.0%)

Question 57

a patient is newly diagnosed with T2DM and wants to try lifestyle treatment first. You agree a target of ? you review a patient 6 months after starting metformin. His HbA1c is 51 mmol/mol (6.8%) What next?

Answer 57

48 mmol/mol (6.5%) | You increase his metformin from 500mg bd to 500mg tds and reinforce lifestyle factors

Question 58

Outline mx T2DM for someone who tolerates metformin?

Answer 58

metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy OR insulin therapy should be considered

Question 59

Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide) in T2DM

Answer 59

if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagonlike peptide1 (GLP1) mimetic if: BMI >= 35 kg/m² and specific psychological or other medical problems associated with obesity or BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities 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

Question 60

Outline mx T2DM for someone who Cannot tolerate metformin or contraindicated AND HbA1c rises to 48 mmol/mol (6.5%)

Answer 60

if the HbA1c rises to 48 mmol/mol (6.5%) on lifestyle interventions, consider one of the following: sulfonylurea gliptin pioglitazone

Question 61

Outline mx T2DM for someone who Cannot tolerate metformin or contraindicated AND if the HbA1c has risen to 58 mmol/mol (7.5%)

Answer 61

one of the following combinations should be used: gliptin + pioglitazone gliptin + sulfonylurea pioglitazone + sulfonylurea if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy

Question 62

starting insulin in t2dm

Answer 62

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

Question 63

bp targets are the same in T2DM patients as everyone else

Answer 63

true

Question 64

mx hypertension t2dm?

Answer 64

ACE inhibitors or angiotensin II receptor blockers (ARB) are first-line an ARB is preferred if the patient has a black African or African–Caribbean family origin

Question 65

mx lipids t2dm?

Answer 65

following the 2014 NICE lipid modification guidelines only patients with a 10-year cardiovascular risk > 10% (using QRISK2) should be offered a statin. The first-line statin of choice is atorvastatin 20mg on

Question 66

T2DM pts should be offered antiplatelets

Answer 66

Antiplatelets | should not be offered unless a patient has existing cardiovascular disease

Question 67

The long-term management of type 1 diabetics is an important and complex process requiring the input of many different clinical specialties and members of the healthcare team.

Answer 67

true

Question 68

A diagnosis of type 1 diabetes can still reduce the life expectancy of patients by 13 years and the micro and macrovascular complications are well documented.

Answer 68

true

Question 69

T1DM HbA1c | should be monitored HOW OFTEN

Answer 69

every 3-6 months

Question 70

T1DM adults should have a target of HbA1c level of

Answer 70

48 mmol/mol (6.5%) or lower. NICE do however recommend taking into account factors such as the person's daily activities, aspirations, likelihood of complications, comorbidities, occupation and history of hypoglycaemia

Question 71

How often should patients self-monitor blood glucose? T1DM

Answer 71

recommend testing at least 4 times a day, including before each meal and before bed more frequent monitoring is recommended if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding

Question 72

Blood glucose targets in T1DM?

Answer 72

5-7 mmol/l on waking and | 4-7 mmol/l before meals at other times of the day

Question 73

Insulin regime of T1DM?

Answer 73

offer multiple daily injection basal–bolus insulin regimens, rather than twice‑daily mixed insulin regimens, as the insulin injection regimen of choice for all adults twice‑daily insulin detemir is the regime of choice. Once-daily insulin glargine or insulin detemir is an alternative offer rapid‑acting insulin analogues injected before meals, rather than rapid‑acting soluble human or animal insulins, for mealtime insulin replacement for adults with type 1 diabetes

Question 74

When should you add metformin in T1DM

Answer 74

considering adding metformin if the BMI >= 25 kg/m²

Question 75

Type 2 diabetes mellitus is more common in people of which ethnicity?

Answer 75

Asian ethnicity

Question 76

ound 79% of Muslim patients with type 2 diabetes mellitus fast Ramadan

Answer 76

true

Question 77

If a patient with type 2 diabetes mellitus does decide to fast what advice do u give

Answer 77

they should try and and eat a meal containing long-acting carbohydrates prior to sunrise (Suhoor) patients should be given a blood glucose monitor to allow them to check their glucose levels, particularly if they feel unwell for patients taking metformin the expert consensus is that the dose should be split one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar) expert consensus also recommends switching once-daily sulfonylureas to after sunset. For patients taking twice-daily preparations such as gliclazide it is recommended that a larger proportion of the dose is taken after after sunset no adjustment is needed for patients taking pioglitazone

Question 78

people with diabetes who used insulin can not hold a HGV licence.

Answer 78

false Until recently people with diabetes who used insulin could not hold a HGV licence. The DVLA changed the rules in October 2011.

Question 79

DVLA rules for diabetes? | (and also apply to patients using other hypoglycaemic inducing drugs such as sulfonylureas)?

Answer 79

there has not been any severe hypoglycaemic event in the previous 12 months the driver has full hypoglycaemic awareness the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving the driver must demonstrate an understanding of the risks of hypoglycaemia here are no other debarring complications of diabetes

Question 80

From a practical point of view patients on insulin who want to apply for a Group 2 (HGV) licence need to complete a

Answer 80

VDIAB1I form.

Question 81

if on insulin then patient can drive a car as long as

Answer 81

hey have hypoglycaemic awareness, not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months and no relevant visual impairment. Drivers are normally contacted by DVLA

Question 82

if on tablets or exenatide no need to notify DVLA.

Answer 82

true If tablets may induce hypoglycaemia (e.g. sulfonylureas) then there must not have been more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months

Question 83

if diet controlled alone then no requirement to inform DVLA

Answer 83

true

Question 84

The following are key messages that should be given to all patients with diabetes if they become unwell:

Answer 84

Increase frequency of blood glucose monitoring to four hourly or more frequently Encourage fluid intake aiming for at least 3 litres in 24hrs If unable to take struggling to eat may need sugary drinks to maintain carbohydrate intake It is useful to educate patients so that they have a box of 'sick day supplies' that they can access if they become unwell Access to a mobile phone has been shown to reduce progression of ketosis to diabetic ketoacidosis

Question 85

Possible indications that a patient might require admission to hospital would include: (7 things)

Answer 85

Suspicion of underlying illness requiring hospital treatment eg myocardial infarction Inability to keep fluids down - admit if persisting more than a few hours Persistent diarrhoea Significant ketosis in an insulin dependent diabetic despite additional insulin Blood glucose persistently >20mmol/l despite additional insulin Patient unable to manage adjustments to usual diabetes management Lack of support at home e.g. a patient who lives alone and is at risk of becoming unconscious

Question 86

Sick day rules If a patient is taking oral hypoglycaemic medication then what are the key points

Answer 86

they should be advised to continue taking their medication even if they are not eating much. Remember that the stress response to illness increases cortisol levels pushing blood sugars high even without much oral intake. The possible exception is with metformin, which should be stopped if a patient is becoming dehydrated because of the potential impact upon renal function.

Question 87

Sick day rules If a patient is on insulin what are the key points?

Answer 87

If a patient is on insulinas per, they must not stop it due to the risk of diabetic ketoacidosis. ensure that they are checking their blood sugars frequently. check their ketone levels and if these are raised and blood sugars are also raised they may need to give corrective doses of insulin. The corrective dose to be given varies by patient, but a rule of thumb would be total daily insulin dose divided by 6 (maximum 15 units).

Question 88

Diabetic foot disease is an important complication of diabetes mellitus which should be screen for on a regular basis. How is this done?

Answer 88

All patients with diabetes should be screened for diabetic foot disease on at least an annual basis screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot

Question 89

Diabetic foot disease occurs due to?

Answer 89

neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot's arthropathy, dry skin peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia

Question 90

Presentations of diabetic foot disease?

Answer 90

neuropathy: loss of sensation ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication complications: calluses, ulceration, Charcot's arthropathy, cellulitis, osteomyelitis, gangrene

Question 91

How do you risk stratify for diabetic foot disease?

Answer 91

Low risk • no risk factors except callus alone Moderate risk deformity or • neuropathy or • non-critical limb ischaemia. High risk previous ulceration or • previous amputation or • on renal replacement therapy or • neuropathy and non-critical limb ischaemia together or • neuropathy in combination with callus and/or deformity or • non-critical limb ischaemia in combination with callus and/or deformity.

Question 92

Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:

Answer 92

first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin if the first-line drug treatment does not work try one of the other 3 drugs tramadol may be used as 'rescue therapy' for exacerbations of neuropathic pain topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia) pain management clinics may be useful in patients with resistant problems

Question 93

Diabetes typically leads to what type of neuropathy?

Answer 93

sensory loss and not motor loss in peripheral neuropathy. Painful diabetic neuropathy is a common problem in clinical practice.

Question 94

How can diabetes affect the GI system?

Answer 94

Gastrointestinal autonomic neuropathy Gastroparesis symptoms include erratic blood glucose control, bloating and vomiting management options include metoclopramide, domperidone or erythromycin (prokinetic agents) Chronic diarrhoea often occurs at night Gastro-oesophageal reflux disease caused by decreased lower esophageal sphincter (LES) pressure

Question 95

Diabetic ketoacidosis (DKA) may be a complication of existing type ? diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type ? diabetes mellitus may also develop DKA.

Answer 95

Diabetic ketoacidosis (DKA) may be a complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA.

Question 96

Pathophysiology | DKA

Answer 96

caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.

Question 97

Features of dka

Answer 97

abdominal pain polyuria, polydipsia, dehydration Kussmaul respiration (deep hyperventilation) Acetone-smelling breath ('pear drops' smell)

Question 98

Diagnostic criteria of DKA?

Answer 98

glucose > 11 mmol/l or known diabetes mellitus pH < 7.3 bicarbonate < 15 mmol/l ketones > 3 mmol/l or urine ketones ++ on dipstick

Question 99

mx DKA

Answer 99

fluid replacement insulin - long-acting insulin should be continued, short-acting insulin should be stopped correction of electrolyte disturbance

Question 100

Describe fluid replacement in DKA

Answer 100

most patients with DKA are deplete around 5-8 litres | isotonic saline is used initially, even if the patient is severely acidotic

Question 101

Describe insulin mx in DKA

Answer 101

an intravenous infusion should be started at 0.1 unit/kg/hour once blood glucose is < 15 mmol/l an infusion of 5% dextrose should be started

Question 102

Describe correction of electrolyte disturbance in dka

Answer 102

serum potassium is often high on admission despite total body potassium being low this often falls quickly following treatment with insulin resulting in hypokalaemia potassium may therefore need to be added to the replacement fluids if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required

Question 103

JBDS potassium guidelines

Answer 103

Potassium level in first 24 hours (mmol/L) Over 5.5 Nil Potassium replacement in mmol/L of infusion solution 3.5-5.5 40 Potassium replacement in mmol/L of infusion solution Below 3.5 Senior review as additional potassium needs to be given

Question 104

DKA resolution is defined as: | Key points of discharge?

Answer 104

pH >7.3 and blood ketones < 0.3 mmol/L both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn't happened the patient requires senior review from an endocrinologist if the above criteria are met and the patient is eating and drinking switch to subcutaneous insulin the patient should be reviewed by the diabetes specialist nurse prior to discharge

Question 105

Complications may occur from DKA itself or the treatment:

Answer 105

gastric stasis thromboembolism arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia acute respiratory distress syndrome acute kidney injury

Question 106

Who is at high risk of CE and how to mx this

Answer 106

children/young adults following fluid resuscitation in DKA monitor for headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment If there is any suspicion a CT head and senior review should be sought

Question 107

The level of HbA1c is dependant on

Answer 107

red blood cell lifespan | average blood glucose concentration

Question 108

what is hba1c

Answer 108

HbA1c is produced by the glycosylation of haemoglobin at a rate proportional to the glucose concentration

Question 109

Lower-than-expected levels of HbA1c

Answer 109

(due to reduced red blood cell lifespan) Sickle-cell anaemia GP6D deficiency Hereditary spherocytosis

Question 110

Higher-than-expected levels of HbA1c | due to increased red blood cell lifespan

Answer 110

Vitamin B12/folic acid deficiency Iron-deficiency anaemia Splenectomy

Question 111

HbA1c should be checked every

Answer 111

3-6 months until stable, then 6 monthly'.

Question 112

HbA1c is generally thought to reflect the blood glucose over the previous '

Answer 112

3 months' although there is some evidence it is weighed more strongly to glucose levels of the past 2-4 weeks