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*Medicine: Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the epidemiology of diabetes?

A
  • One of the most common endocrine disease affecting all age groups
  • Prevalence 6% in UK
  • Around 10% of entire NHS budget spent on diabetes - 79% of this spent on complications of diabetes
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2
Q

Diabetes is caused by a deficiency or reduced effectiveness of endogenous insulin, resulting in elevated blood glucose.

What are features of T1DM?

A
  • Usually adolescent onset but may occur at any age
  • Autoimmune destruction of beta cells in pancreas, therefore insulin deficiency
  • Symptoms → weight loss, polyuria, polydipsia, DKA
  • Associated w/ other autoimmune disorders
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3
Q

What are features of T2DM?

A
  • Reduced insulin secretion +/- insulin resistance
  • Most are >40 yrs
  • Can be asymptomatic (often routinely picked up on bloods)
  • Symptoms → fatigue, polyuria, polydipsia
  • RFs → obesity, lack of exercise, calorie + alcohol XS
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4
Q

What are other causes of diabetes mellitus?

A
  • Medications → steroids / anti-HIV / new anti-psychotics
  • Pancreatic → pancreatitis / surgery / haemochromatosis / cancer
  • Endocrine → cushing’s / acromegaly / phaeochromocytoma / hyperthyroid
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5
Q

What are methods of checking glucose?

A
  • Finger-prick glucose (BM) → quick, easy, bedside
  • One-off blood glucose → fasting / non-fasting
  • HbA1c
  • Oral glucose tolerance test (OGTT)
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6
Q

What is HbA1c and when should it not be used?

A
  • Glycosylated haemoglobin
  • Represents avg blood glucose over last 2-3 months
  • NOT a method for checking glucose in following conditions:
    • suspected gestational diabetes
    • children
    • T1DM
    • haemolytic anaemia / haemoglobinopathies
    • HIV
    • CKD
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7
Q

The diagnostic criteria are determined by WHO.

What are the diagnostic results indicating diabetes?

A
  • Symptomatic:
    • fasting glucose _>_7mmol/L OR
    • random glucose _>_11.1 mmol/L (or after 75g OTT)
  • Asymptomatic:
    • above crtieria on TWO separate occasions
  • OR if HbA1c > 48 mmol/L (6.5%) (twice if asymptomatic)
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8
Q

What is impaired fasting glucose and impaired glucose tolerance?

A
  • Impaired fasting glucose (IFG) → fasting glucose 6.1-7.0 mmol/l
  • Impaired glucose tolerance (IGT) → fasting plasma glucose < 7.0 mmol/l and OGTT 2hr value 7.8-11.1 mmol/l

Diabetes UK: Ppl w/ IFG should then be offered OGTT to rule out diabetes diagnosis, a result below 11.1 mmol/l but above 7.8 mmol/l indicates that person doesn’t have diabetes but does have IGT

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9
Q

What are the principles of management for diabetes?

A
  • Drug therapy to normalise blood glucose levels
  • Monitor for and treat complications
  • Modify any other risk factors for other conditions eg. cardiovascular disease
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10
Q

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. 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.

What is the management of type 1 diabetes?

A
  • Always require insulin to control blood sugar due to absolute deficiency of insulin w/ no pancreatic tissue left to stimulate with drugs
  • Different types of insulin available according to duration of action
  • HbA1c → monitor every 3-6 months + target < 48 mmol (6.5%)
  • Self-monitor BM 4 times/day (before each meal + before bed)
  • More frequent monitoring under certain situations
  • BM targets → 5-7mmol walking + 4-7mmol before meals at other times
  • NICE recommend adding metformin if BMI > 25 kg/m2
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11
Q

In which situations is more frequent monitoring recommended for T1 diabetics?

A

If frequency of hypoglycaemic episodes increases, examples:

  • during periods of illness
  • before, during + after sport
  • when planning pregnancy
  • during pregnancy and while breastfeeding
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12
Q

Insulin therapy revolutionised the management of diabetes mellitus when it was developed in the 1920s. It is still the only available treatment for type 1 diabetes mellitus (T1DM) and is widely used in type 2 diabetes mellitus (T2DM) where oral hypoglycaemic agents fail to gain adequate control.

How can insulin be classified?

A
  • By manufacturing process:
    • porcine
    • human sequence insulin
    • analogues
  • By duration of action:
    • rapid-acting
    • short-acting
    • intermediate-acting
    • long-acting
    • premixed preparations
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13
Q

Patients often require a mixture of preparations (e.g. both short and long acting) to ensure stable glycaemic control throughout the day.

What are key features of rapid-acting insulin analogues?

A
  • Act faster + have shorter duration of action than soluble insulin
  • May be used as bolus in ‘basal-bolus’ regimes (rapid/short-acting ‘bolus’ insulin before meals w/ intermediate/long-acitng ‘basal’ insulin once or twice daily)
  • Examples: insulin aspart (NovoRapid) and insulin lispro (Humalog)
  • Can inject at start of meal, or just after
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14
Q

What are key features of short-acting insulins?

A
  • Soluble insulin examples → Actrapid (human) and Humulin S (human)
  • May be used as bolus dose in ‘basal-bolus’ regimes
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15
Q

What are intermediate-acting insulins?

A
  • Isophane insulin
  • Many pts use isophane insulin in a premixed formulation
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16
Q

What are long-acting insulins?

A
  • Insulin determir (Levemir) → given once or twice daily
  • Insulin glargine (Lantus) → given once daily
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17
Q

What are examples of premixed preparations of insulin?

A
  • Combine intermediate acting insulin w/ either a rapid-acting insulin analogue or soluble insulin
  • Novomix 30 → 30% insulin aspart (rapid), 70% insulin aspart protamine (intermediate)
  • Humalog Mix25 → 25% insulin lispro (rapid), 75% insulin lispro protamine (intermediate); Humalog Mix50 → 50% insulin lispro, 50% insulin lispro protamine
  • Humulin M3 → biphasic isophane insulin (human) - 30% soluble (short), 70% isophane (intermediate)
  • Insuman Comb 15 → biphasic isophane insulin (human) - 30% soluble (short), 70% isophane (intermediate)
18
Q

How is insulin administered?

A
  • Vast majority subcutaneously
  • Insulin gets broken down by digestive enzymes
  • Important to rotate injection sites to prevent lipodysrophy
  • Insulin pumps available (‘continues subcut insulin infusions) → deliver continuous basal infusion + prevent patient-activated bolus dose at meal times
  • IV insulin for acutely unwell pts (DKA)
  • Inhaled insulin available but unused
  • Oral insulin analogues in development
19
Q

What is the insulin regimen of choice for all adults?

A
  • Multiple daily injection basal-bolus insulin regimens (rather than twice-daily mixed)
  • BDS insulin determir (Levemir) is regime of choice; OD insulin glargine or insulin determir 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 w/ T1DM
20
Q

What constitutes dietary advice for diabetes?

A
  • Encourage high fibre, low glycaemic index sources of carbs
  • include low-fat dairy products + oily fish
  • Control intake of foods containing saturated fats + trans fatty acids
  • Limited substitution of sucrose-containing foods for other carbs is allowable, but care should be taken to avoid excess energy intake
  • Discourage use of foods marketed specifically at people w/ diabetes
  • Initial target weight loss in an overweight person is 5-10%
21
Q

What is the conservative management for diabetes mellitus?

A
  • Education about the condition
  • Support from specialist diabetic nurse → helps monitor any complications; foot check; blood pressure + urine dip
  • Smoking cessation
  • Exercise + weight loss
  • Diet changes
  • Foot-care advice
22
Q

What is the drug management of T2DM?

A
  • Majority controlled using oral medication
  • First-line → METFORMIN
  • Second-line → sulfonylureas, gliptins, pioglitazone
  • If oral medication not controlling sugars, then insulin used
23
Q

What are HbA1c targets for T2DM?

A
  • Individual targets should be agreed w/ pts to encourage motivation
  • Check HbA1c every 3-6 months until stable, then 6 monthly
  • NICE encourage relaxing targets for elderly or frail
  • Targets depend on treatment/drugs used

It’s worthwhile thinking of the average patient who is taking metformin for T2DM, you can 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%)

24
Q

Oral hypoglycaemic agents: Metformin

A
  • Biguanide
  • Increases insulin sensitivity; reduces hepatic gluconeogenesis
  • SEs → GI upset, lactic acidosis
  • First-line in T2DM
  • Cannot be used in pts w/ eGFR < 30
25
Q

Oral hypoglycaemic agents: Sulfonylureas

A
  • Examples: gliclazide, glimepiride
  • Stimulate pancreatic beta cells to secrete insulin
  • SEs → hypoglycaemia, weight gain, hyponatraemia, SIADH, liver dysfunction
26
Q

Oral hypoglycaemic agents: Glitazones / Thiazolidinediones

A
  • Example: pioglitazone
  • Activate PPAR-gamma receptor in adipocytes to promote adipogenesis + fatty acid uptake
  • SEs → weight gain, fluid retention, liver dysfunction, fractures
27
Q

Oral hypoglycaemic agents: DPP4 Inhibitors (-gliptins)

A
  • Gliptins
  • Increase incretin levels → inhibit glucagon secretion
  • Generally well tolerated
  • Increased risk of pancreatitis
  • Don’t cause weight gain
28
Q

Oral hypoglycaemic agents: SGLT-2 Inhibitors (-gliflozins)

A
  • Selective sodium-glucose co-transporter-2 inhibitor
  • Examples: canagliflozin, dapagliflozin, empagliflozin
  • Inhibits reabsorption of glucose in kidney
  • SEs → UTI, normoglycaemic ketoacidosis, increase risk of lower limb amputation
  • Typically result in weight loss
29
Q

Other hypoglycaemic agents: GLP-1 agonists (-tides)

A
  • Incretin mimetic → inhibits glucagon secretion
  • Subcutaneous
  • SEs → N+V, pancreatitis
  • Typically result in weight loss
30
Q

What do you use for risk factor modification in T2DM?

A
  • BP target < 140/80 (or 130/80 if end-organ damage) → ACE-I
  • Pts w/ 10yr CV risk >10% (QRISK) → ATORVASTATIN 20mg
  • T1DM BP Target = 135/85

ACE-i → renoprotective; black pts offered ACE-i + either thiazide or CCB

31
Q

What messages should be given to all patients with diabetes, if they become unwell?

A
  • Inc freq of BM monitoring to 4-hrly or more
  • Fluid intake → 3L / 24hrs
  • Sugary drinks if unable to eat
  • Ensure box of ‘sick day supplies’
  • Access to mobile phone reduces DKA likelihood
  • Continue oral hypoglycaemics if not eating much (exception = metformin if pt dehydrated)
  • If pt on insulin, don’t stop due to risk of DKA
32
Q

What is maturity-onset diabetes of the young (MODY)?

A
  • T2DM < 25 yrs
  • Inherited autosomal dominant condition
  • Diff types → MODY3 (60%), MODY2 (20%), MODY5 (rare)
  • Family hx of early onset diabetes is often present
  • Ketosis is not a feature at presentation
  • Pts w/ most common form are v sensitive to sulfonylureas
  • Insulin not usually necessary
33
Q

What is the mechanism of Diabetic Ketoacidosis (DKA)?

A
  • Normally body metabolises carbs → efficient energy production
  • Ketoacidosis is alternative pathway in starvation states
  • Far less efficient + produces acetone as by-product
  • In acute DKA → XS glucose, but lack of insulin means glucuose not taken up into cells for metabolism, so pushing body into starvation-like state
  • Uncontrolled lipolysis occurs
  • Combination of severe acidosis and hyperglycaemia can be deadly
34
Q

Who gets DKA?

A
  • May be complication or first presentation of T1DM
  • Rarely, under extreme stress, T2DMs may develop DKA
  • Common precipitating factors → infection, missed insulin, MI, surgery, pancreatitis, chemo
35
Q

What is the clinical presentation of DKA?

A
  • Gradual drowsiness + lethargy
  • Abdominal pain + vomiting
  • Polyuria, polydipsia, dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’)
36
Q

What is the diagnostic criteria for DKA?

A
  • Hyperglycaemic → BM > 11 mmol/L
  • Ketonaemia → > 3 mmol/L or significant ketonuria (++)
  • Acidaemia → pH <7.2
  • Bicarbonate < 15 mmol/l
37
Q

What is the management for DKA?

A
  • ABCDE
  • Fluids → 1L 0.9% NaCl / 1 hour (if SBP < 90, give 500ml bolus / 15mins)
  • Insulin → add 50U human soluble insulin to 50ml 0.9% saline; infuse continuously at 0.1U/kg/hr; ocnt pt’s regular long-acting insulin at usual doses + times
  • Monitoring → check BM + ketones hourly; check VBG at 2h-4h-8h-12h-24h
  • Catheter → if not passed urine by 1h, aimf or UO 0.5 ml/kg/h; consider NG tube if vomiting/drowsy
  • Avoid hypoglycaemia → if BM < 14, start 10% glucose at 125ml/h to run alongside saline + prevent hypo
  • K+ replacement
38
Q

DKA: For fluid therapy, what should you be careful about in children & young adults?

A
  • Slower infusion
  • Higher risk of cerebral oedema
  • Often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc.
  • Usually occurs 4-12hrs following commencement of treatment but can present anytime
  • If suspicion → CT head + snr review
39
Q

What are the guidelines for potassium replacement in DKA?

A
  • Plasma K+ falls w/ treatment as K+ enters cells
  • Do NOT add K+ to the 1st bag
  • Thereafter, add K+ according to most recent VBG result
40
Q

What are complications of DKA and its treatment?

A
  • Gastric stasis
  • Thromboembolism
  • Arrhythmias 2o to hyperkalaemia/iatrogenic hypokalaemia
  • Iatrogenic due to incorrect fluid therapy: cerebral oedema, hypokalaemia, hypoglycaemia
  • Acute resp distress syndrome
  • Acute kidney injury

*Medicine: Endocrinology (10 decks)

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