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PassMedicine > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

How much of NHS’s total budget is spent on managing patients with DM?

A

8%

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2
Q

Define Diabetes Mellitus

A

Chronic conditions characterised by abnormally raised levels of blood glucose

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3
Q

How many types of DM are there and what are they?

A 
7:
T1DM
T2DM
Prediabetes
Gestational Diabetes
Maturity onset diabetes of the young (MODY)
Latent autoimmune diabetes of adults (LADA)
Other types
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4
Q

Define T1DM

A

Autoimmune disorder where the pancreatic insulin-producing beta cells of the islet of Langerhans are destroyed by T-cells. Thus resulting in absolute deficiency of insulin resulting in raised glucose levels.

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5
Q

What can poorly controlled T1DM lead to?

A

Diabetic Ketoacidosis, resulting in significant morbidity and mortality. Presents as nausea and vomiting, abdo pain, Kussmaul’s breathing, disorientation, confusion.

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6
Q

What are the main focuses of diabetes management?

A

Reducing incidence of MACROVASCULAR (ischaemic heart disease, stroke) and MICROVASCULAR (eye, nerve and kidney damage) complications

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7
Q

Define T2DM

A

Most common cause of diabetes. It is the relative deficiency of insulin due to an excess of adipose tissue ie. there is not enough insulin to go around all the excess fatty tissue, leading to raised blood glucose

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8
Q

Define Prediabetes

A

Term used for pts 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, if no lifestyle interventions are taken.

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9
Q

Define Gestational Diabetes

A

Raised blood glucose levels during pregnancy. It is important to detect this, as if left untreated, it may lead to adverse outcomes for the mother and baby

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10
Q

Define MODY

A

Maturity 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, ie. symptomatic hyperglycaemia with progression to more severe complications such as DKA.

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11
Q

Define LADA

A

LADA = Latent autoimmune diabetes of adults. Small group of pts develop autoimmune related diabetes later in life and they’re often misdiagnosed as having T2DM

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12
Q

What are less common types of DM?

A

Any pathological process which damages the insulin-producing cells of the pancreas may cause diabetes to develop. EG. chronic pancreatitis and haemochromatosis. Drugs may also cause raised glucose levels eg. glucocorticoids which commonly result in raised blood glucose levels.

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13
Q

Why do diabetes pts present with polydipsia and polyuria?

A

Polyuria and polydipsia are due to water being ‘dragged’ out of the body due to osmotic effects of excess blood glucose being excreted in the urine (glycosuria)

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14
Q

What are the 4 main investigations of blood glucose?

A
  • Bedside finger prick blood glucose monitor
  • One-off blood glucose - either fasting or non-fasting
  • HbA1c measures the amount of glycosylated haemoglobin and represents the average blood glucose over the past 2-3mths.
  • a glucose tolerance test - a fasting blood glucose is taken after which a 75g glucose load is taken. After 2hrs, a second blood glucose reading is then taken.
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15
Q

What are WHO’s diagnostic criteria?

A

Symptomatic patient:

  • fasting glucose ≥ 7mmol/l
  • random glucose ≥ 11.1mmol/l (or after 75g oral glucose tolerance test (OGTT))

In asymptomatic patients, the above criteria must be demonstrated on 2 separate occasions

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16
Q

WHO’s guidance on DM diagnosis using HbA1c

A
  • ≥ 6.5% (48mmol/mol) = DM
  • < 6.5% does not exclude DM (ie it is not as sensitive at fasting samples for detecting diabetes)
  • in asymptomatic pts, test must be repeated to confirm diagnosis

misleading HbA1c results can be caused by increased red cell turnover.

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17
Q

HbA1c and fasting glucose values for prediabetes

A

HbA1c = 42-47mmol/mol (6-6.4%)

Fasting glucose = 6.1-6.9mmol/l

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18
Q

When is insulin used?

A

For T1DM and sometimes in poorly controlled T2DM

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19
Q

How is insulin administed?

A

SC

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20
Q

What are the main side effects of INSULIN?

A

HYPOglycaemia
Weight gain
Lipodystrophy

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21
Q

How is T1DM managed?

A

SC insulin - either analogue, human sequence of porcine

either short, immediate or long-acting

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22
Q

What 6 drugs can be used in management of T2DM?

A 
Metformin
Sulfonylureas
Thiazolidinediones
DPP-4 inhibitors (-gliptins)
SGLT-2 inhibitors (-glifozins)
GLP-1 agonists (-tides)
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23
Q

What is the first-line medication for T2DM management?

A

Metformin

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24
Q

When is metformin contraindicated?

A

In pts with an eGFR of < 30ml/min

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25
Q

What are the side effects of METFORMIN?

A

Gastrointestinal upset

Lactic acidosis (does not occur very much in clinical settings)

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26
Q

What is METFORMIN’s mechanism of action?

A

It increases insulin sensitivity

Decreases hepatic gluconeogenesis

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27
Q

What is the only T2DM drug given SC?

A

GLP-1 agonists (-tides)

all others are given orally

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28
Q

Name 2 examples of sulfonylureas

A

Gliclazide

Glimepiride

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29
Q

What is SULFONYLUREAS’ mechanism of action?

A

Stimulates pancreatic beta cells to secrete insulin

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30
Q

Side effects of SULFONYLUREA

A

HYPOglycaemia
Weight gain
HYPOnatraemia

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31
Q

What is the only currently available THIAZOLIDINEDIONE?

A

Pioglitazone

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32
Q

What are the side effects of THIAZOLIDINEDIONES?

A

Weight gain

Fluid retention

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33
Q

What is the mechanism of action of THIAZOLIDINEDIONES?

A

Activate PPAR -gamma (Peroxisome proliferator-activated receptor also known as the glitazone reverse insulin resistance receptor) receptor in adipocytes to promote adipogenesis and fatty acid uptake

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34
Q

What is the mechanism of action of DPP-4 inhibitors?

A

Increases incretin levels which inhibit glucagon secretion

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35
Q

Side effects of DPP-4 inhibitors (-gliptins)

A

Generally well tolerated but increased risk of pancreatitis

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36
Q

SGLT-2 inhibitors side effects

A

UTIs

Weight loss

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37
Q

Mechanism of action of SGLT-2 inhibitors

A

Inhibits reabsorption of glucose in the kidney

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38
Q

Mechanism of action of GLP-1 agonists (-tides)

A

Incretin mimetic which inhibits glucagon secretion

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39
Q

Side effects of GLP-1 agonists

A

Nausea and Vomiting
Pancreatitis
Weight loss

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40
Q

How are drugs prescribed in T2DM?

A

METFORMIN

if HbA1c > 58mmol/mol (7.5%)
add gliptin OR sulfonylurea OR pioglitazone OR SGLT-2 inhibitor

if still >58
metformin + gliptin + sulfonylurea
OR
metformin + pioglitazone + sulfonylurea
OR
metformin + sulfonylurea + SGLT-2 inhibtor
OR
metformin + pioglitazone + SGLT-2 inhibitor
BASICALLY, all can be used together, except GLIPTINs, which only combine with sulfonylureas
OR INSULIN

IF triple therapy ‘not effective, not tolerated or contraindicated’ AND BMI > 35 ->
metformin + sulfonylurea + GLP-1 mimetic

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41
Q

How are drugs prescribed in T2DM if pt cannot tolerate metformin?

A 
GLIPTIN 
or
SULFONYLUREA
or
PIOGLITAZONE

IF HbA1c > 58mmol/mol (7.5%)
ADD another type of drugs mentioned above

If still > 58
ADD INSULIN

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42
Q

What 6 dietary advice is given to T2DM pts?

A
  1. encourage high fibre, low glycaemic index sources of carbs
  2. include low-fat dairy products and oily fish
  3. control intake of foods containing saturated fats and trans fatty acids
  4. limited substitution of sucrose-containing foods for other carbs is allowable, but care should be taken to avoid XS energy intake
  5. discourage the use of foods marketed specifically at people with diabetes
  6. initial target weight loss in an overweight person is 5-10%
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43
Q

How regularly should HbA1c should be checked?

A

Every 3-6mths until stable, then 6mths

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44
Q

NICE encourages us to consider relaxing targets on who?

A

on a case by case basis, esp for pts who are older or frail, for adults with T2DM

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45
Q

HbA1c targets are no dependent on treatment. What are they for lifestyle, metformin and drugs that may cause hypoglycaemia

A

Lifestyle: 48mmol/mol (6.5%)

Lifestyle + metformin: 48mmol/mol

Includes any drugs which may cause hypoglycaemia (eg. lifestyle + sulfonylurea): 53mmol/mol (7%)

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46
Q

What HbA1c target do you aim for in a newly T2DM diagnosed pt who wants to try lifestyle treatment first

A

48mmol/mol (6.5%)

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47
Q

What should you do if when you review a T2DM pt after 6mths on metformin and his HbA1c is 51mmol/mol (6.8%)?

A

You increase his metformin from 500mg bd (x2 a day) to 500mg tds (x3) and reinforce lifestyle factors

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48
Q

What is the target HbA1c for a T2DM pt already on one drugs but HbA1c has risen to 58mmol/mol (7.5%)

A

53mmol/mol (7%)

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49
Q

Why must you assess for cardiovascular risk in T2DM patients?

A

If they have a high risk of CVD or established CVD or Chronic Heart Failure, they should start on metformin and once that has been established, start SGLT-2 inhibitors

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50
Q

What do you do if pt cannot tolerate METFORMIN? eg due to gastrointestinal side-effects

A

Switch to modified-release metformin

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51
Q

What do you do if metformin is contraindicated?

A

If risk of CVD/ Heart failure = SGLT-2 monotherapy

If not, = DPP-4 inhibitor or Pioglitazone or Sulfonylurea. SGLT-2 may be used if certain NICE criteria are met.

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52
Q

Why should metformin be titrated up slowly when first starting the medication?

A

To minimise the possibility of gastrointestinal upset

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53
Q

When should SGLT-2 inhibitors be given in addition to metformin?

A

if pt has high risk of developing CVD eg. QRISK ≥ 10%
pt has established CVD
pt has chronic heart failure

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54
Q

What must you do to metformin before starting SGLT-2 inhibitors?

A

Metformin should be established and titrated up before SGLT-2 introduction

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55
Q

When should you continue GLP-1 mimetics?

A

Only if there is a reduction of atleast 11mmol/mol (1%) in HbA1c and weight loss of atleast 3% of initial body weight in 6mths

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56
Q

In what 2 occasions should you consider switching one of the T2DM drugs for GLP-1 mimetics if triple therapy is not effective or tolerated?

A
  • BMI ≥ 35kg/m² and specific psychological or other medical problems associated with obesity
  • BMI < 35kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
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57
Q

What is NPH insulin?

A

Neutral Protamine Hagedorn insulin, also known as isophane insulin, is an intermediate-acting insulin.

It is used by injection under the skin once to twice a day. Onset of effects is typically in 90 minutes and they last for 24 hours.

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58
Q

How does NICE recommend taking human NPH insulin?

A

take at bed-time or twice daily according to need

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59
Q

What should you do when you review an established type 2 diabetic on maximum dose metformin and her HbA1c is 55 mmol/mol (7.2%)?

A

You do not add another drug as she has not reached the threshold of 58 mmol/mol (7.5%)

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60
Q

What do you do when a type 2 diabetic is found to have an HbA1c of 62 mmol/mol (7.8%) at annual review. They are currently on maximum dose metformin?

A

You elect to add a sulfonylurea

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61
Q

What are BP targets for T2DM pts?

A

Same as for those without T2DM.

if <80y/o;

  • clinic BP <140/90mmHg
  • ABPM/ HBPM <135/85mmHg

If >80y/o

  • clinic BP <150/90mmHg
  • ABPM/HBPM <145/85mmHg
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62
Q

What is the first-line medication for hypertension in T2DM?

A

ACEi or ARBs

ARB is preferred if pt has a black African or African-Caribbean family origin

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63
Q

What are considerations for antiplatelets in T2DM?

A

They should not be offered unless pt has existing CVD

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64
Q

When can statins be offered to T2DM pts?

A

Only to pts with a 10yr cardiovascular risk > 10% (using QRISK2)
First-line statin of choice is atorvastatin 20mg on (every night)

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65
Q

What to do for primary prevention (10yr cardiovascular risk ≥ 10% OR most type 1 diabetics OR CKD if eGFR < 60ml/min/m²)

A

Atorvastatin 20mg od (if non-HDL has not fallen by ≥40% then consider titrating upto 80mg)

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66
Q

What to do for secondary prevention (known ischaemic heart disease OR cerebrovascular disease OR peripheral arterial disease)

A

Atorvastatin 80mg od (once daily)

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67
Q

In what 8 conditions may HbA1c not be used for diagnosis?

A
  • haemoglobinopathies
  • haemolytic anemias
  • untreated iron deficiency anemia
  • suspected gestational diabetes
  • children
  • HIV
  • CKD
  • people taking medication that may cause hyperglycaemia eg. corticosteroids
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68
Q

What is IFG?

A

Impaired fasting glucose is when fasting glucose is ≥ 6.1 but less than 7mmol/l

69
Q

What is IGT?

A

Impaired glucose tolerance is when fasting plasma glucose is less than 7mmol/l and OGTT 2hr value ≥ 7.8mmol/l but less than 11.1mmol/l

70
Q

What does Diabetes UK suggest about IGT and IFG?

A

‘People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’

71
Q

What is DKA?

A

Diabetic Ketoacidosis is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies

72
Q

What are the features of DKA?

A

Abdo pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
acetone-smelling breath (‘pear drops’ smell)

73
Q

What are the most common precipitating factors of DKA?

A

Infection
Missed insulin doses
MI

74
Q

American Diabetes Association 2009 diagnostic criteria for DKA

A 
Glucose > 13.8mmol/l
pH < 7.3
serum bicarbonate < 18mmol/l
anion gap > 10
ketonaemia
75
Q

Joint British Diabetes Societies (2013) diagnostic criteria for DKA

A

Glucose > 11mmol/l or known DM
pH < 7.3
bicarbonate < 15mmol/l
ketones > 3mmol/l or urine ketones ++ on dipstick

76
Q

What are the 4 main principles of management of DKA?

A
  1. Fluid replacement - initially isotonic saline, even if pt is severely acidotic.
  2. Insulin - IV infusion at 0.1 unit/kg/hour. Once blood glucose < 15mmol/l an infusion of 5% dextrose should be started
  3. correct electrolyte imbalance - Serum K+ is often high on admission, but total body K+ low, and often falls quickly following treatment with insulin, resulting in hypokalaemia, so K+ may be need to be added to replacement fluids. If rate of K+ infusion is greater than 20mmol/hr then cardiac monitoring may be required.
  4. long-acting insulin should be continued, short-acting insulin should be stopped.
77
Q

Why is a slower infusion indicated in young adults (18-25)?

A

They are at greater risk of cerebral oedema

78
Q

What are JBDS’ K+ guidelines?

A

No K+ replacement if K+ > 5.5mmol/l in first 24hr
40mmol/l of infusion solution if K+ = 3.5-5.5
Senior review as additional K+ needs to be given if K+ < 3.5mmol/l

79
Q

How is DKA resolution defined?

A

pH > 7.3
blood ketones < 0.6mmol/L
bicarbonate > 15mmol/L

80
Q

What should happen if ketonaemia and acidosis does not resolve within 24hr?

A

They should both resolve within 24hrs, if this hasn’t happened, the pt requires senior review from an endocrinologist

81
Q

What should you do if DKA resolves and ketonaemia and acidosis are resolved within 24 hrs and pt is eating and drinking

A

You should switch to SC insulin and the patient should be reviewed by the diabetes specialist nurse prior to discharge

82
Q

What are 6 complications that may occur from DKA itself or the treatment?

A

gastric stasis

thromboembolism

arrhythmias secondary to hyperkalaemia/ iatrogenic hypokalaemia

iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia

acute respiratory distress syndrome

83
Q

Who are particularly vulnerable to cerebral oedema following fluid resuscitation in DKA and what would they need? When does it occur?

A

Children and young adults.
They often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc
It usually occurs 4-12hrs following commencement of treatment but can present at any time.
If there is any suspicion a CT head and senior review should be sought

84
Q

What are the investigations for T1DM?

A
  • urine should be dipped for glucose and ketones
  • fasting and random glucose
  • HbA1c is not as useful for pts 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 pts with T1DM
  • diabetes-specific autoantibodies are useful to distinguish between T1 and T2DM
85
Q

What are the 4 antibodies used in T1DM investigation?

A
  • anti-GAD (glutamic acid decarboxylase) - present in 80% of T1DM
  • islet cell antibodies (ICA) against cytoplasmic proteins in the beta cell - present in 70-80%
  • Insulin autoantibodies (IAA) - presence in T1DM correlates strongly with age, found in over 90% of young children with T1DM but only 60% of older pts
  • Insulinoma-associated-2 autoantibodies (IA-2A)
86
Q

What are the 5 major differences between T1 and T2DM?

A

Onset age: T1 < 20yrs, but 40% > 30yrs; T2 > 40yrs, but may occur in younger obese pts

Onset speed: T1: acute - hrs-days; T2: slower - weeks-mths

Pt weight: T1: recent weight loss; T2: Obesity is strong risk factor

Features: T1: DKA; T2: Milder symptoms eg. polyuria, polydipsia

Ketonuria: T1: common; T2: rare

87
Q

What do NICE state about T1DM?

A

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
88
Q

What do NICE recommend for further tests in T1DM?

A

Consider further investigation in adults that involves measurement of C‑peptide and/or diabetes‑specific autoantibody titres if:
type 1 diabetes is suspected but the clinical presentation includes some atypical features (for example, age 50 years or above, BMI of 25 kg/m² or above, slow evolution of hyperglycaemia or long prodrome)

Conversely, for patients suspected of type 2 diabetes, if they over the age of 40 years and respond well to oral hypoglycaemic agents do not need to undergo further testing for type 1 diabetes. For those in whom there is a doubt, C-peptide levels and diabetes-specific autoantibodies are the investigations of choice.

89
Q

What is the diagnosis and next step if

a 15-year-old presents with weight loss, lethargy. Ketones and glucose found in the urine. A random serum glucose is 14 mmol/L

A

Diagnose with T1DM and no need for further investigations

90
Q

What is the diagnosis and next step if

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

A

He is the intermediate age for T1DM/T2DM, and has a risk factor for T2DM (obesity) but not clear cut -

do C-peptide levels and diabetes-specific autoantibodies

91
Q

What is the diagnosis and next step if

a 52-year-old woman (body mass index 23 kg/m²) presents with polyuria and polydipsia. Ketones are present in the urine

A

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

92
Q

What is the diagnosis and next step if

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

A

Diagnose with T2DM, no need for further investigations

93
Q

What is GLP-1?

A

Glucagon-like peptide-1 = a hormone release by the small intestine in response to an oral glucose load.

94
Q

What is the incretin effect? What is it mediated by?

A

In normal physiology an oral glucose load results in greater release of insulin that if the same load is given intravenously.

This effect is largely mediated by GLP-1 and is known to be decreased in T2DM.

95
Q

What are 2 ways in which GLP-1 levels can be increased?

A
  1. Administer an analogue eg. GLP-1 mimetics eg. exenatide

2. inhibit breakdown (dipeptidyl peptidase-4, DPP-4 inhibitors (gliptins)

96
Q

What does exenatide do? And what are its benefits over other similar drugs?

A

It is a GLP-1 mimetic so increases insulin secretion and inhibits glucagon secretion.

Typically results in weight loss, in contrast to many meds such as insulin, sulfonylureas and thiazolidinediones. They are sometimes used in combination with insulin in T2DM to minimise weight gain

97
Q

How must exenatide be given?

A

SC within 60mins before morning and evening meals. It should not be given after a meal.

98
Q

Besides Exenatide, what is another GLP-1 mimetic?

A

Liraglutide

99
Q

What is the benefit of using liraglutide over exenatide?

A

It only needs to be given once a day

100
Q

What is the benefit of using liraglutide over exenatide?

A

It only needs to be given once a day

101
Q

How can exenatide and liraglutide be combined with other drugs?

A

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.

102
Q

What has NICE said about combining exenatide with other drugs?

A

Consider adding exenatide to metformin and a sulfonylurea if:
- 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.
103
Q

How does NHS justify the ongoing prescription of GLP-1 mimetics?

A

If pt have achieved a >11mmol/mol (1%) reduction in HbA1c and 3% weight loss after 6mths to justify the ongoing prescription of GLP-1 mimetics.

104
Q

How do DPP-4 inhibitors work?

A

They increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown

105
Q

What are some benefits of DPP-4 inhibitors over other T2DM drugs?

A

Does not cause weight gain

They’re relatively well tolerated with no increased incidence of hypoglycaemia

106
Q

What are NICE guidelines on DPP-4 inhibitor use over thiazolidinediones?

A

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

107
Q

What are 2 examples of DPP-4 inhibitors?

A

Vildagliptin, sitagliptin

108
Q

How often should HbA1c be monitored? What is the target?

A

Every 3-6mths

48mmol/mol (6.5%) or lower

109
Q

How often is self-monitoring of blood glucose recommended?

A

Test at least 4x a day, including before each meal and before bed.

110
Q

When is more frequent monitoring recommended?

A

if frequency of hypoglycaemic episodes increases; during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding

111
Q

What are blood glucose targets for T1DM?

A

5-7mmol/l on waking

4-7mmol/l before meals at other times of the day

112
Q

What are the 3 types of insulin that can be offered in T1DM?

A

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

113
Q

At what BMI do NICE recommend adding metformin to insulin in T1DM?

A

BMI >= 25kg/m²

114
Q

What are the 5 things you should do if your Muslim pt with T2DM wants to fast for Ramadan?

A
  • Advise them to eat a meal containing long-acting carbs at Suhoor
  • Pts should be given a blood glucose monitor to allow them to check their glucose levels, esp if they feel unwell
  • Pts on metformin should split their dose: 1/3 at Suhoor, 2/3 at Iftar
  • Switch once-daily sulfonylureas to after sunset. For pts taking twice-daily preparations eg. gliclazide, it is recommended that a larger dose is taken after sunset
  • no adjustment needed for pts on pioglitazone
115
Q

What are the 5 advices given to diabetics when they become unwell?

A
  • Increase freq of glucose monitoring to 4hrly or more frequently.
  • encourage fluid intake aiming atleast 3L in 24hrs
  • If unable to take/ struggling to eat, may need sugary drinks to maintain carb intake
  • educate pts so they have a box of ‘sick day supplies’ that they can access if they become unwell
  • access to phone has been shown to reduce progression of ketosis to DKA.
116
Q

Should oral hypogylcaemic medications be continued even if pt is not eating much? Why?

A

Yes continue, as stress response to illness increases cortisol levels pushing blood sugars high, even without much oral intake.

117
Q

Which drug is the exception when it comes to continuing a drug even when not eating much? Why?

A

Metformin should be stopped if a pt is becoming dehydrated because of the potential impact upon renal function.

118
Q

What is the corrective dose for insulin when there is a risk of DKA

A

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).

119
Q

What are the 7 possible indications that a pt may require admission to hospital?

A
  • suspicion of underlying ilness requiring hospital treatment eg. MI
  • Inability to keep fluids down - admit if persists more than few hrs
  • persistent diarrhoea
  • significant ketosis in an insulin dependent diabetic despite additional insulin
  • blood glucose persistently > 20mmol/l despite additional insulin
  • pt unable to manage adjustments to usual diabetes management
  • lack of support at home eg. pt lives alone and is at risk of becoming unconscious
120
Q

Diabetic foot disease occurs secondary to what 2 main factors?

A
  • neuropathy: resulting in loss of protective sensation eg. not noticing a stone in shoe. Charcot’s arthropathy; dry skin
  • peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia
121
Q

What are the presentations for diabetic foot disease? (3; 10)

A
  • 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
122
Q

How often should pts be screened for diabetic foot disease?

A

at least on annually

123
Q

What does diabetic foot disease screening involve?

A
  • screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterior tibial artery pulse
  • screening for neuropathy: a 10g monofilament is used on various parts of the sole foot
124
Q

How does NICE recommend risk stratifying diabetic foot disease pts?

A
  • Low risk: no risk factors expect callus alone
  • Moderate: deformity OR neuropathy OR non-critical limb ischaemia
  • High: prev ulceration OR 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
125
Q

What are recommendations for moderate or high risk of diabetic foot disease pts?

A

All patients who are moderate or high risk (I.e. any problems other than simple calluses) should be followed up regularly by the local diabetic foot centre.

126
Q

What does peripheral neuropathy typically result in?

A

a ‘glove and stocking’ distribution, with the lower legs affected first due to the length of the sensory neurons supplying this area.

127
Q

How is diabetic peripheral neuropathy managed? (5)

A

the same way as other forms of neuropathic pain:
- 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
128
Q

How can GI autonomic neuropathy present? (3)

A
  1. Gastroparesis (condition where the stomach cannot empty in the normal way ie. partial paralysis of the stomach) - symptoms: erratic blood glucose control, bloating and vomiting
    Can be managed with metoclopramide, domperidone, or erythromycin (prokinetic agents)
  2. Chronic diarrhoea - often occurs at night
  3. Gastro-oesophageal reflux disease - caused by decreased lower oesophageal sphincter (LES) pressure
129
Q

What 5 standards need to be met if a diabetic pt on insulin wishes to hold a HGV licence?

A
  • 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
  • there are no other debarring complications of diabetes
  • to demonstrate adequate control, the Secretary of State’s Honorary Medical Advisory Panel on Diabetes Mellitus has recommended that applicants will need to have used blood glucose meters with a memory function to measure and record blood glucose levels for at least 3 months prior to submitting their application
130
Q

What form do pts on insulin who want to apply for a Group 2 (HGV) licence have to fill out?

A

VDIAB1I form

131
Q

Pts on insulin can drive (group 1 drivers) as long as they have…. (3)

A
  1. hypoglycaemic awareness
  2. not more than one episode of hypoglycaemia requiring the assistance of another person within the preceding 12 months
  3. no visual impairment
132
Q

If the pt is on what meds, will they not need to notify the DVLA?

A

Tablets or exenatide

133
Q

When do diabetics not need to inform DVLA?

A

When they are diet controlled

134
Q

What is HbA1c and how is it produced

A

Glycosylated haemoglobin is the most widely used measure of long-term glycaemic control in diabetes mellitus.

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

135
Q

What 2 things is HbA1c dependant on?

A
  • RBC lifespan

- avg blood glucose conc

136
Q

What 3 conditions can cause lower-than-expected levels of HbA1c (due to reduced RBC lifespan)?

A
  • sickle-cell anemia
  • GP6D deficiency
  • hereditary spherocytosis
137
Q

What 3 conditions can cause higher-than-expected levels of HbA1c (due to increased RBC lifespan)?

A
  • vit B12/ Folic acid deficiency
  • iron-deficiency anemia
  • splenectomy
138
Q

What is the relationship between average plasma glucose and HbA1c?

A

average plasma glucose = (2 * HbA1c) - 4.5

139
Q

What is Hyperosmolar hyperglycaemic state (HHS)? Who does it typically present in?

A

Hyperosmolar hyperglycaemic state (HHS) is a medical emergency which is extremely difficult to manage and has a significant associated mortality.

Hyperglycaemia results in osmotic diuresis, severe dehydration, and electrolyte deficiencies. HHS typically presents in the elderly with type 2 diabetes mellitus (T2DM), however the incidence in younger adults is increasing. It can be the initial presentation of T2DM.

140
Q

Which has a higher mortality? HHS or DKA?

A

HHS

141
Q

How can HHS be complicated?

A

By vascular complications eg. MI, stroke, peripheral arterial thrombosis

Seizures, cerebral oedema and central pontine myelinolysis (CPM) are uncommon but documented complications of HHS.

142
Q

How do HHS and DKA differ in terms of onset?

A

DKA presents within hours of onset.

HHS comes on over many days, and consequently the dehydration and metabolic disturbances are more extreme

143
Q

What is the pathophysiology of HHS? (3)

A
  • Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
  • Severe volume depletion results in a significant raised serum osmolarity (typically > than 320 mosmol/kg), resulting in hyperviscosity of blood.
  • Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.
144
Q

What are 4 clinical features of HHS? (12)

A
  • General: fatigue, lethargy, nausea and vomiting
  • Neurological: altered level of consciousness, headaches, papilloedema, weakness
  • Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
  • Cardiovascular: dehydration, hypotension, tachycardia
145
Q

How is HHS diagnosed? (3)

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)

Note: A precise definition of HHS does not exist, however the above 3 criteria are helpful in distinguishing between HHS and DKA. It is also important to remember that a mixed HHS / DKA picture can occur.

146
Q

How is HHS managed in 3 steps?

A
  1. Normalise the osmolality (gradually)
    - the serum osmolality is the key parameter to monitor
    - if not available it can be estimated by 2 * Na+ + glucose + urea
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)
147
Q

How much fluid is lost on avg in HHS?

A

100-200ml/kg eg. 10-22 L in an individual weighing 100kg

148
Q

Why is caution needed in fluid replacement in elderly?

A

If too rapid, rehydration may precipitate heart failure, but insufficient may fail to reverse an AKI

149
Q

What is the 1st line fluid for restoring total body fluid? WHy?

A

IV isotonic 0.9% NaCl solution

It is already relatively hypotonic compared to the serum in someone with HHS, so it is v effective at restoring normal serum osmolarity

150
Q

If serum osmolarity is not declining despite positive balance with 0.9% NaCl, then to which fluid should be switched? Why?

A

0.45% NaCl solution, as it is more hypotonic relative to the HHS pt’s serum osmolality

151
Q

What does IV fluid replacement aim to achieve?

A

a positive balance of 3-6L by 12hrs and the remaining replacement of established fluid losses within the next 12hrs.

152
Q

Why should insulin not be given initially in HHS?

A

Vigorous initial fluid replacement and this alone (without insulin) will result in a gradual decline in plasma glucose and serum osmolarity.
and
A rapid decline is potentially harmful, so insulin should NOT be used in the first instance unless there is significant ketonaemia or acidosis

153
Q

When can insulin be given initially in HHS?

A

If there is significant ketonaemia or acidosis

154
Q

What can rapid changes of serum osmolarity dangerous?

A

It can result in cardiovascular collapse and central pontine (CPM)

155
Q

Guidelines suggest that serum osmolarity, sodium and glucose levels should be plotted on a graph to permit appreciation of the rate of change. How often should they be plotted?

A

Hourly initially

156
Q

If labs don’t have access to serum osmolarity measurements, what can be done instead?

A

a calculated osmolarity can be estimated with 2Na + glucose + urea

157
Q

How does fluid replacement alone reduce osmolality?

A

It gradually lowers blood glucose

158
Q

A reduction of serum osmolarity will cause a shift of water into the intracellular space. What does this result in?

A

a rise in serum sodium (a fall in blood glucose of 5.5 mmol/L will result in a 2.4 mmol/L rise in sodium). This is not necessarily an indication to give hypotonic solutions.

159
Q

When giving fluid replacement in HHS if the inevitable rise in serum Na+ is much greater than 2.4 mmol/L for each 5.5 mmol/L fall in blood glucose, what does this suggest?

A

Insufficient fluid replacement

160
Q

When is serum Na+ rising a concern?

A

If the osmolality is not declining concurrently

161
Q

What is a safe rate of fall of plasma glucose? And what should it not exceed?

A

between 4 and 6 mmol/hr is recommended.

The rate of fall of plasma sodium should not exceed 10 mmol/L in 24 hours.

162
Q

In fluid replacement in HHS, what is the target blood glucose?

A

10-15mmol/L

163
Q

How long can it take for complete normalisation of electrolytes and osmolality?

A

upto 72hrs

164
Q

Insulin treatment prior to adequate fluid replacement can result in what?

A

Cardiovascular collapse as the water moves out of the intravascular space, with a resulting decline in intravascular volume.

165
Q

A steep decline in serum osmolarity can precipitate what?

A

central pontine myelinolysis (CPM)

166
Q

What is an indication for insulin therapy in HHS? What is the recommended insulin dose?

A

Significant ketonaemia (3β-hydroxy butyrate is more than 1 mmol/L), start insulin at time zero (eg. mixed DKA/ HHS picture), which indicates relative hypoinsulinaemia

fixed rate intravenous insulin infusion given at 0.05 units per kg per hour.

167
Q

What is the relationship of potassium with HHS?

A

Pts with HHS are potassium deplete but less acidotic than those with DKA so K+ shifts are less pronounced

168
Q

When can hyperkalaemia be present in HHS?

A

With AKI

169
Q

What are the dangers of using diuretics while in HHS?

A

Pts may be profoundly hypokalaemic. K+ should be replaced or omitted as required.

PassMedicine (5 decks)

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