Diabetes Assessment and Management Flashcards

1
Q

Define T1DM

A

AI
Idiopathic
Absolute insulin deficiency
2° beta cell destruction

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2
Q

Define T2DM

A

Spectrum with insulin resistance and varying degrees of insulin secretion
Usually overweight +/- metabolic syndrome

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3
Q

What BGL is considered diabetic (fasting and non-fasting)?

A

FPG ≥7.0 mmol/L (normal less than 6.1 mmol/L)
Symptoms + RPG (usually 2 hours post-meal) ≥11.1 mmol/L
HbA1C ≥48mmol/mol (6.5%)
2 hour value ≥11.1 mmol/L in OGTT

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4
Q

LADA

A

Latent AI Diabetes in Adults

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5
Q

MODY

A

Maturity Onset Diabetes in the Young

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6
Q

What tests are used to diagnose diabetes?

A

FPG
HbA1C
OGTT (will provide fasting and 2 hour value)

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7
Q

What further tests should be ordered in someone with suspected diabetes to assess possible complications/co-morbidities and why?

A

FBE (for Hb; may have implications for assessment of HbA1C e.g. if anaemic)
Lipid profile
LFTs (potential fatty liver, also want to know baseline LFTs to see if management causes any derangement)
ABGs or VBGs (HCO3- for indirect assessment of pH, probably VBG because less painful but may not be able to do in GP setting; can also test ketones)
U&E
Urinalysis

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8
Q

When is an OGTT not indicated?

A

In severe hyperglycaemia (may even be dangerous; can cause hyperemesis)

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9
Q

What FPG range is considered normal?

A

Less than 6.1mmol/L

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10
Q

What FPG range constitutes impaired fasting glucose (IFG)?

A

6.1-6.9 mmol/L

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11
Q

What does HbA1C reflect and what is its clinical relevance?

A

Non-enzymatic glycation of Hb

Reflects 1-3 month glycaemic control (3 months = life of RBC)

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12
Q

Describe the usual first presentation of T1DM

A

Rapid presentation following onset of symptoms
Generally more acute, severe symptoms
May present with ketoacidosis

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13
Q

What aspect of a history might distinguish a patient with T1DM from a patient with T2DM?

A

Unintentional weight loss more likely with T1DM (glycosuria causes loss of energy, leads to liberation of fats)

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14
Q

What tests can assist in distinguishing T1DM from T2DM?

A

Antibodies (anti-GAD, anti-islet cell type 2)
Insulin
C-peptide (good 1:1 surrogate measure for insulin; not artificially elevated by medications that increase insulin)

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15
Q

What is the pathological process underlying T1DM?

A

AI destruction of pancreatic B cells (triggered by an environmental event in susceptible people)

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16
Q

What characterises the pre-diabetic stage in T1DM, and when does this progress to fulminant T1DM?

A

Pre-diabetic: multiple Abs in blood
Diabetic: when insufficient insulin is produced to maintain normal blood glucose (most B cells are destroyed at this point)

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17
Q

Is genetics more important as a risk factor in T1DM or T2DM?

A

T2DM (MZ concordance up to 80%; 50% in T1DM)

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18
Q

List possible complications of DM. What questions should be examined and what examinations should be performed to assess these?

A

Retinopathy: opthamology referral
PVD: ask cardiac risk factors, assess 6 P’s (pain, pallor, pulseless, parasthesia, paralysis, petrifyling cold)
Peripheral neuropathy: perform sensory neuro exam on lower limbs in particular

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19
Q

When might a diabetic experience blurring of vision?

A

During a hyperglycaemic episode (may also occur in hypoglycaemic episode)
If retinopathy has developed

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20
Q

What are the top priorities for treating a newly diagnosed type 2 diabetic?

A

Relieve symptoms
Prevent or delay long term complications (e.g. assess for signs of any complications, referral to dietitian and diabetic educator, assess need for medications)
Assist psychological adjustment and improve QOL

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21
Q

List 5 factors which influence the likelihood long term diabetic complications developing

A

Duration of diabetes
Degree of glucose control (as reflected by HbA1C)
Degree of BP control
Control of other CV risk factors (e.g. lipids, smoking)
Individual genetic susceptibility

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22
Q

What kind of agents can be used to treat T2DM?

A

Drugs to increase insulin sensitivity

Insulin secretagogues

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23
Q

Contraindications for metformin

A
Renal dysfunction (EGFR less than 35)
SEVERE liver dysfunction
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24
Q

Contraindications for sulphonylureas

A

Renal dysfunction (EGFR less than 35)
SEVERE liver dysfunction
T1DM
Severe obesity

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25
Mechanism of action of acarbose
Colonic transmembrane prevention of sugar absorption via inhibition of a-glucosidase (breaks down starches and disaccharides)
26
Adverse effects of acarbose
Osmotic diarrhoea | Flatulence
27
When is acarbose particularly indicated?
Post-prandial hyperglycaemia
28
TZDs
Thiazoidinediones (3rd line oral hypoglycaemic agents)
29
Mechanism of action of TZDs
Stimulates PPAR-y
30
SMBG
Self-monitoring blood glucose
31
How often should diabetic patients have their urine tested, and what is tested for?
Yearly or 6-monthly testing for creatinine, albumin, glucose
32
What 3 referrals are important to make when presented with a newly diagnosed diabetic?
``` Opthamologist (for assessment of retinopathy) Dietitian (for lifestyle changes) Diabetes educator (for NDSS registration, information about disease progression, medication choices, insulin monitoring, etc) ```
33
Where is SMBG particularly indicated?
In patients treated with insulin or sulphonylureas, where hypoglycaemia may occur
34
What lifestyle changes are emphasised by a dietitian treating diabetes?
Recommend weight loss Low GI CHOs Reduction of saturated fats
35
What is the effect of exercise on BGL?
Increases glucose uptake into muscle (improved sensitisation lasts 2-3 days) Stimulates release of stress hormones which increase glucose in the short term Decreased BGLs in long term
36
What is the risk for the exercising diabetic patient treated with insulin or SU?
Hypoglycaemia following exercise (can occur up to 24 hours later)
37
What kind of co-morbidities may render HbA1C an unreliable test of long term glycaemic control?
Conditions of increased RBC turnover (e.g. anaemia)
38
What is the approximate correlation between a HbA1C of 6-7% and plasma glucose levels?
HbA1C of 6-7% is equivalent to 7.5-9.5mmol/L plasma glucose
39
For each 1% fall in HbA1C what is the corresponding % reduction in microvascular complications?
25%
40
What is the current recommended HbA1C target?
7% (53 mmol/mol)
41
What is the current recommendations for management of T2DM, from first-line to later-line therapies?
Diet and exercise, addressing CV risk factors Oral monotherapy (metformin) Oral dual combination (add SU, DPP4 inhibitor) Oral triple combination (add acarbose, TZD, GLP-1 agonist) Oral + insulin Insulin
42
What is the relationship between mortality and morbidity, and macro-/micro-vascular complications of diabetes?
Mortality mostly due to macrovascular complications | Morbidity mostly due to microvascular complications
43
List 8 hypoglycaemic agents. Which of these are injectible agents?
``` Metformin SUs DPP4 inhibitors a-glucosidase inhibitors Thiazolidinediones SGLT2 inhibitors GLP-1 analogues (injectible) Insulin (injectible) ```
44
What is the usual 1st line therapy for T2DM?
Metformin
45
Mechanism of action of metformin
Inhibits hepatic glucose production
46
Adverse effects of metformin
Nausea | Diarrhoea
47
How can nausea as a side effect of metformin be minimised?
By using the slow release form (XR)
48
What is metformin contraindicated in renal failure?
Risk of lactic acidosis
49
Examples of SUs
Gliclazide (shorter-acting) Glipizide (shorter-acting) Glibenclamide (longer-acting) Glimepiride (longer-acting, once daily)
50
What is the maximum dose of metformin that can be given in an otherwise well person?
3g/day (but generally not tolerated)
51
Mechanism of action of SUs
Stimulate B cell insulin release
52
Adverse effects of SUs
Weight gain | Hypoglycaemia
53
Which SU has a lesser tendency to cause hypoglycaemia than the others?
Gliclazide
54
When must acarbose be taken in order to be effective?
At start of meal
55
Why is rosiglitazone black labelled in the US?
Mild statistical association with CV events
56
Adverse effects of TZDs
Weight gain Fluid retention and CCF Fractures
57
TZDs
Glitazones
58
Examples of TZDs
Pioglitazone | Rosiglitazone (rarely used)
59
Examples of GLP-1 analogues
Exenatide | Liraglutide
60
Mechanism of action of GLP-1 analogues
Improve pancreatic islet glucose sensing and insulin release (also decrease glucagon release) Slow gastric emptying and improve satiety (leads to weight loss in most pts)
61
In what diabetic pts are GLP-1 analogues particularly indicated?
Pts with obesity
62
Adverse effects of GLP-1 analogues
N+V Pancreatitis Hypoglycaemia (rare if used alone)
63
How are GLP-1 analogues administered?
SC injection pre-prandial | Liraglutide daily, exenatide BD
64
Examples of DPP-4 inhibitors
``` Sitagliptin Vildagliptin Saxagliptin Linagliptin Allogliptin ```
65
Mechanism of action of DPP-4 inhibitors
Prolong GLP-1 and GIP action, leading to improved B-cell sensing (increases insulin, decreases glucagon) and decreased appetite
66
What drugs are available in combination with metformin?
Some DPP-4 inhibitors
67
Adverse effects of DPP-4 inhibitors
Nausea | Hypersensitivity (very rare)
68
Mechanism of action of SGLT2 inhibitors
Inhibits SGLT2, the main glucose transporter in the renal tubule, to promote glycosuria and lower blood glucose
69
What are the benefits of SGLT2 inhibitors?
``` Weight loss (3kg on average) Mild reduction in BP due to reduced plasma volume ```
70
Examples of SGLT2 inhibitors available in Australia
Dapagliflozin | Cangliflozin
71
Adverse effects of SGLT2 inhibitors
Increased candidal genital infections | Long term effects unknown (relatively new drugs - limited post-marketing information)
72
How might GLP-1 analogues cause pancreatitis?
Via lipase elevation
73
How should metformin be introduced to a pt's drug regime?
Begin with lower dose (usually 500mg BD) and then increase if well tolerated (e.g. to 1g BD)
74
Describe the "basal bolus" insulin regimen, preferred for most type 1 diabetics
Short-acting insulin with meals | Long-acting 1-2 times/day to provide background insulin level
75
What alternative is available to the "basal bolus" insulin regimen?
Continuous insulin infusion via a portable pump
76
What are the major drawbacks of an insulin pump?
Only uses short-acting insulin; if pump breaks, DKA may occur Need to do a course (DAFNE) in order to be able to calculate amount of insulin required e.g. with pre-prandial bolus, exercise, overnight, etc
77
Examples of short-acting insulins
Aspart Glulisine Lispro
78
Examples of long-acting insulins
Determir | Glargine
79
Novorapid
Insulin aspart
80
Lantus
Glargine insulin
81
DAFNE
Dose Adjustment For Normal Eating
82
What BGLs are associated with greater fatigue and increased susceptibility to infection?
>13-14 mmol/l
83
What is the NDSS and what is its role?
National Diabetes Services Scheme | Subsidises diabetes-related products, provides information and support
84
How can a more accurate picture of BP be gained in a pt with suspected "white-coat" HTN?
24 hr ambulant BP monitor
85
How often do pts present with long term diabetic complications at the time of diagnosis?
50% (diagnosis is often very late)
86
5 main principals of T2DM management
Healthy eating and exercise (weight loss if overweight) Oral anti-diabetic agents SMBG for some pts Regular surveillance for microvascular complications CV risk reduction for macrovascular complications
87
What is SMBG particularly indicated?
For pts on medications where there is a risk of hypoglycaemia
88
What % of diabetics are overweight?
70%+
89
What are the Australian NHMRC guidelines for diabetes control?
6-8 mmol/L FPG or before meals | 6-10 mmol/L 2 hours post-prandial
90
Equation to convert HbA1C % to mmol/mol
~11 x (HbA1C%) - 24
91
Do TZDs act immediately or is there a delay before an effect is observed?
Takes 3-4 weeks to have an effect
92
What medication is additive when used with metformin, SUs and/or insulin?
TZDs
93
When are incretins released?
In response to the presence of glucose in the GIT
94
What is the role of GLP-1?
Increases insulin release Reduces glucagon release Slows gastric emptying and suppresses appetite
95
What is the role of GIP?
Increases insulin release
96
What is the role of DPP4?
Inactivates gut incretins
97
What is the role of PPAR-y?
Receptor for TZDs (endogenous ligands are FFAs and eicosanoids) Binding of TZDs decreases insulin resistance, increases synthetic of metabolic proteins and reduces the production of pro-inflammatory factors
98
When is post-meal glucose testing indicated?
Only in gestational diabetes
99
How often should blood glucose be measured?
~4 times/day
100
Describe the basal bolus regimen of insulin administration
Dose of short-acting before each meal | Long-acting taken usually at night
101
Mr WY, 34 year old real estate agent, presents to his GP with penile itching and rash, diagnosed as candida ballanitis Previously well FHx: mother has T2DM O/E: 88kg, height 173cm, BMI 29.4, waist circumference 105cm, BP 144/82, no other abnormal findings, finger-prick glucose measured (non-fasting) at 8.9 mmol/L What BGL is considered diabetes?
>= 7mmol/L | Non-fasting (random) >= 11.1 (usually after eating)