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Year 3 > Diabetes mellitus type 1 & 2 (E&M) > Flashcards

Diabetes mellitus type 1 & 2 (E&M) Flashcards

1
Q

Define T1DM.

A

Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency (–> lipolysis and ketogenesis) - develops due to destruction of pancreatic beta cells, mostly by immune-mediated mechanisms

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2
Q

When does T1DM manifest commonly?

A

Childhood

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3
Q

What gene is T1DM associated with?

A

HLA DR3/4

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4
Q

What may we see in Fx of someone with T1DM?

A

Autoimmune disease

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5
Q

Why are T1DM patients prone to ketoacidosis?

A

Do not have sufficient insulin to suppress ketone body production, whereas T2DM patients have enough for this

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6
Q

What autoantigens are associated with T1DM? (4)

A
  • glutamic acid decarboxylase (GAD)
  • insulin
  • insulinoma-associated protein 2
  • cation efflux zinc transporter
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7
Q

Define T2DM.

A

Progressive disorder defined by deficits in insulin secretion and increased insulin resistance that lead to abnormal glucose metabolism and related metabolic derangements

Insulin resistance (decreased insulin sensitivity) and relative insulin deficiency (insulin production reduces over time)

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8
Q

What causes T2DM?

A

Strong genetic component and association with obesity and a sedentary lifestyle

  • genetic and environmental
  • obesity
  • pancreatic disease e.g. chronic pancreatitis
  • endocrine disease e.g. Cushing’s, acromegaly, phaeochromocytoma, glucagonoma
  • drugs e.g. corticosteroids, atypical antipsychotics, protease inhibitors
  • circulating autoantibodies to the extracellular domain of the insulin receptor
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9
Q

What is mature onset diabetes of the young (MODY)?

A
  • onset of T2DM <25 years old
  • autosomal dominant inheritance
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10
Q

What do we often see in Fx of MODY?

A

Early onset diabetes

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11
Q

What are the general clinical features of diabetes mellitus? (7)

A
  • hyperglycaemia
  • polyuria
  • polydipsia
  • nocturia
  • unexplained weight loss
  • fatigue
  • increased susceptibility to infection
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12
Q

How does T1DM present in 1/3 of cases?

A

Diabetic ketoacidosis is the 1st manifestation in 1/3 of cases

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13
Q

How does T1DM present specifically? (5)

A
  • DKA
  • nausea and vomiting
  • abdominal pain
  • Kussmaul breathing –> deep, rapid breathing
  • sweet smelling breath
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14
Q

How does T2DM present specifically? (5)

A
  • asymptomatic
  • some may present with hyperosmolar hyperglycaemic state (HHS) - BGC very high >40mmol and severe dehydration and confusion
  • acanthosis nigricans (hyperpigmentation)
  • infections - candidal, skin, UTIs
  • blurred vision
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15
Q

What might you see on examination of a patient with T2DM?

A
  • necrobiosis lipoidica diabeticorum (well-demarcated plaques on shins or arms with shiny atrophic surface and red-brown edges)
  • granuloma annulare (flesh-coloured papules coalescing in rings on back of hands and fingers)
  • diabetic dermopathy (depressed pigmented scars on shins)
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16
Q

Why might gastroparesis happen in diabetes mellitus patients?

A

Neuropathy of vagus nerve

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17
Q

How might gastroparesis present in DM? (3)

A
  • bloating
  • vomiting
  • erratic blood glucose control
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18
Q

What is the main risk factor for T1DM?

A
  • genetic predisposition (HLA-DR3/4 variation)
  • (geographical region, infectious agents, dietary factors = weak)
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19
Q

What are some risk factors for T2DM? (11)

A
  • obesity
  • hypertension
  • South Asian/Afro-Caribbean ethnicity
  • older age
  • gestational diabetes
  • Fx T2DM
  • PCOS
  • non-diabetic hyperglycaemia
  • dyslipidaemia
  • CVD
  • stress
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20
Q

What are the 1st line investigations ordered for diabetes mellitus?

A
  • fasting plasma glucose >/=7mmol/L
  • HbA1c >/=48mmol/mol (not in children, pregnant, blood transfusions/abnormalities - may be falsely normal)
  • oral glucose tolerance test (OGTT): 2-hour post-load glucose after 75g oral glucose >/=11/1mmol/L
  • random plasma glucose >/=11.1mmol/L
  • (T1DM in adults = clinical diagnosis)
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21
Q

What other investigations are considered for T1DM? (3)

A
  • plasma or urine ketones
  • C-peptide (should be low)
  • autoimmune markers (autoantibodies to GAD, insulin, islet cells, islet antigens IA2 and IA2-beta, and zinc transporter Zn8)
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22
Q

What other investigations are considered for T2DM? (9)

A
  • fasting lipid profile
  • urine ketones
  • ACR
  • serum creatinine and eGFR
  • ECG
  • ankle-brachial pressure index (ABPI)
  • random C-peptide
  • autoantibody testing
  • LFTs
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23
Q

What is HbA1c a measure of?

A

Average blood glucose over last 3 months

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24
Q

What HbA1c level is diagnostic of diabetes?

A

> =48 mmol/mol

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25
Q

What HbA1c level is pre-diabetes?

A

42-47 mmol/mol

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26
Q

What factors affect HbA1c reading?

A
  • Lower than expected (due to reduced RBC lifespan):
    • sickle cell
    • G6PD deficiency
    • hereditary spherocytosis
  • Higher than expected (due to increased RBC lifespan):
    • vitamin B12/folate deficiency
    • iron deficiency anaemia
    • splenectomy
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27
Q

What is the diagnostic criteria for diabetes mellitus?

A
  • symptoms + random plasma glucose >=11.1mmol/L OR
  • fasting plasma glucose >=7mmol/L OR
  • plasma glucose >=11.1mmol/L 2h after 75g oral glucose OR
  • HbA1c>=48mmol/mol
  • if asymptomatic with abnormal HbA1c or fasting glucose: must be confirmed with a repeat abnormal reading on a different day before diagnosis
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28
Q

What is impaired fasting glucose (IFG) defined as?

A

6.1-6.9 mmol/L

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29
Q

What is impaired glucose tolerance (IGT) defined as?

A
  • fasting plasma glucose <7.0mmol/L (IFG) AND
  • OGTT 7.8-11.1mmol/L
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30
Q

How can we distinguish between T1DM and T2DM?

A

C-peptide:

  • decreases in T1DM
  • increases in T2DM
31
Q

What bedside test can be done to investigate diabetes mellitus and what would we look for?

A

Urine dip:

  • glycosuria
  • ketonuria
  • microalbuminuria (early signs of nephropathy)
32
Q

What can we look for specifically in T1DM? (2)

A
  • anti-GAD antibodies
  • islet cell antibodies
33
Q

What are some differential diagnoses for diabetes mellitus?

A
  • non-diabetic hyperglycaemia (e.g. raised HbA1c, IFG, IGT)
  • LADA (positive for at least 1/4 antibodies commonly found in T1DM patients, low to normal initial C-peptide)
  • monogenic diabetes
  • ketosis-prone diabetes
  • gestational diabetes
  • neonatal diabetes
34
Q

What is the 1st line (and 2nd line) management for T1DM?

A
  • 1st line: basal-bolus insulin
    • combination of long acting (e.g. insulin glargine/detemir, subcutaneous injection OD) and short acting (e.g. insulin lispro/aspart/glulisine, before meals)
  • consider pre-meal insulin correction dose
  • consider metformin (add if BMI>25kg/m2)
  • 2nd line: fixed-dose insulin (adults only)
  • DKA: IV fluids (isotonic 0.9% NaCl)
35
Q

What do you add to management if a patient with T1DM is pregnant?

A

Low-dose aspirin PLUS basal-bolus insulin regimen

36
Q

When is metformin considered for T1DM?

A

When BMI>25

37
Q

What are DAFNE courses for T1DM?

A

Dose Adjustment for Normal Eating

38
Q

When should self-monitoring of BG

A

4 times a day, before each meal and before bed, with targets of 5-7mmol/L on waking and 4-6mmol/L before meals

39
Q

What is the target HbA1c for T1DM?

A

48mmol/mol (monitored every 3-6 months)

40
Q

What is an example prescription for newly diagnosed T1DM?

A

Basal-bolus using twice-daily insulin detemir

41
Q

What does metformin do?

A

Increases insulin sensitivity and reduces hepatic gluconeogenesis

42
Q

What are some side effects of metformin? (3)

A
  • lactic acidosis (therefore suspended during intercurrent illness like D&V or dehydration, sepsis, CT with contrast, renal failure, heart failure, frail/elderly)
  • GI side effects
  • weight neutral
43
Q

When is metformin contraindicated?

A

If eGFR<30 –> may accumulate in renal impairment = increased risk of lactic acidosis

44
Q

What do sulphonylureas (gliclazides) do?

A
  • (-azide)
  • stimulate release of insulin from beta cells in pancreas (act on ATP-sensitive K+ channels)
  • best choice for 2nd intensification in non-obese patients
45
Q

What are some side effects of sulphonylureas? (2)

A
  • hypoglycaemia
  • weight gain
46
Q

When are sulphonylureas contraindicated?

A

Severe renal impairment e.g. CKD

47
Q

What does sulphonylurea overdose result in? (2)

A
  • hyperinsulinaemia
  • high C-peptide
48
Q

Why are sulphonylureas withheld on the morning of surgery?

A

Risk of hypoglycaemia

49
Q

What do SGLT-2 inhibitors do?

A
  • (-flozin) / (-gliflozin)
  • reversibly inhibit sodium-glucose transporter 2 (SGLT-2) in the renal PCT to reduce glucose reabsorption and increase urinary glucose excretion
  • best choice for 2nd intensification in obese patients / CVD patients
50
Q

What are some side effects of SGLT-2 inhibitors? (4)

A
  • weight loss
  • UTIs (necrotising fasciitis)
  • Fournier’s gangrene
  • DKA when used with insulin (stop immediately)
51
Q

When are SGLT-2 inhibitors contraindicated?

A

Active foot disease e.g. skin ulceration

52
Q

What diseases mean we should add an SGLT-2 inhibitor to T2DM patients? (2)

A
  • CVD / high-risk of CVD
  • chronic heart failure
53
Q

What do DPP-4 inhibitors do?

A
  • (-gliptin)
  • reduce peripheral breakdown of incretins such as GLP-1
54
Q

What are some side effects of DPP-4 inhibitors? (3)

A
  • URTIs
  • flu-like symptoms
  • weight neutral (may increase satiety) - useful in obese patients
55
Q

When are DPP-4 inhibitors avoided?

A

Pancreatitis

56
Q

What are some side effects of pioglitazones? (5)

A
  • weight gain
  • fluid retention (= contraindicated in heart failure)
  • liver dysfunction
  • bladder cancer
  • fractures
57
Q

When are pioglitazones contraindicated?

A

Heart failure, bladder cancer

58
Q

What do GLP-1 agonists do?

A
  • e.g. exenatide
  • increase insulin secretion and inhibit glucagon secretion
  • only if triple therapy is not effective and BMI>35, or insulin contraindicated
59
Q

What are some side effects of GLP-1 agonists?

A
  • weight loss
  • should not give with pancreatitis
60
Q

What T2DM drugs can be continued on day of surgery?

A
  • DPP-4 inhibitors
  • GLP-1 agonists
61
Q

How do we manage T2DM at initial diagnosis?

A
  • lifestyle changes: diet, exercise, education, smoking cessation, glucose monitoring
  • PLUS agree HbA1c target
  • consider BP / lipid management
  • consider add-on pharmacotherapy for patients with CKD
62
Q

What are the steps for glycaemic control in T2DM?

A
  1. if HbA1c>=48mmol/mol despite lifestyle advice: metformin (contraindicated if eGFR<30 –> renal impairment + lactic acidosis)
    • if not tolerated due to GI side effects, try modified release metformin before using 2nd-line agent
  2. if HbA1c is above >=58mmol/mol add:
    • DPP-4 inhibitors e.g. -gliptins (in obese)
    • sulphonylureas e.g. -gliclazide (in obese)
    • SGLT-2 inhibitors e.g. -gliflozins (non-obese, or CVD)
    • pioglitazone
  3. add further drug from above (triple therapy) or try insulin-based treatment (basal insulin)
    • all patients on insulin need glucagon kit for treating hypoglycaemia
  4. if triple therapy ineffective/tolerated AND BMI>35: switch one drug to GLP-1 agonist (exenatide)
63
Q

What is first-line if T2DM has long standing CVD?

A

Metformin, once established add SGLT-2 inhibitor

64
Q

What is first, second and third-line for T2DM if metformin is contraindicated or not tolerated?

A
  1. DPP-4 inhibitor (gliptin) / sulphonylurea (-gliclazide) / pioglitazone
  2. if HbA1c >58: add another drug
  3. if HbA1c still >58: insulin
65
Q

What HbA1c targets should T2DM patients aim for?

A
  • 48mmol/mol if managed by lifestyle modifications alone or single antidiabetic drug
  • 53mmol/mol if 2+ drugs or single drug that may cause hypoglycaemia e.g. sulphonylurea
66
Q

What are the steps for BP management in T2DM?

A
  1. ACEi or ARB (if black)
  2. add CCB e.g. amlodipine or thiazide-like diuretic (TLD) e.g. indapamide
  3. ACEi + CCB + TLD
  4. check K+ and if <4.5 add spironolactone, if >4.5 add beta blocker
67
Q

How do we manage lipids in T2DM if Q-risk >10% (hyperlipidaemia)?

A
  • Atorvastatin 20mg OD
  • if patient has IHD/CVD/PAD: Atorvastatin 80mg OD
68
Q

Who do we give antiplatelet therapy to in T2DM and how much?

A
  • aspirin 75mg for patients with IHD/CVD/PAD
  • aspirin 75-100mg 1st line if pregnant
69
Q

How do we manage initial T2DM with symptomatic hyperglycaemia?

A

Insulin and sulfonylurea

70
Q

What do we do with T2DM medications if admitted to hospital after ACS?

A

Stop medications and start IV dose-adjusted insulin infusion and monitoring of glucose

71
Q

How do we manage end of life T2DM?

A
  • stop hypoglycaemic agents (insulin and sulphonylureas) due to reduced oral intake
  • individuals on insulin should have their regimen converted to OD long-acting insulin at 25% dose reduction
  • metformin is safe to continue unless there is renal impairment with eGFR<30ml/L
  • minimise blood glucose monitoring and the relax of blood glucose targets
72
Q

What are some overall complications of diabetes? (3 subtypes)

A
  • microvascular
    • retinopathy - background, pre-proliferative, proliferative, maculopathy
    • neuropathy - foot ulcers, carpal tunnel syndrome, autonomic neuropathy, gastroparesis (abdominal pain, N&V), urinary retention/impotence
    • nephropathy - microalbuminuria, proteinuria, renal failure, UTIs
  • macrovascular: MI, IHD, stroke, PVD
  • metabolic
    • diabetic ketoacidosis (T1DM)
    • hyperosmolar hyperglycaemic state (T2DM)
    • hypoglycaemia
  • (T2DM –> amputation, OSA, infection)
73
Q

What is a complication of fluid resuscitation in DKA?

A

Cerebral oedema (especially in younger patients)

In DKA, the blood sugar levels are high, leading to hyperosmolarity. When fluids are administered too rapidly, the sudden drop in blood osmolarity can lead water to move into cerebral tissue causing oedema. The features in keeping with cerebral oedema in our patient include deteriorating mental status/ level of consciousness, incontinence unexpected for age, abnormal neurogenic respiratory pattern (e.g. grunting, abnormal tachypnoea, apnoea) and vomiting.

74
Q

How do we manage DKA?

A

IV fluids (isotonic 0.9% NaCl)
(Following this, insulin therapy to correct hyperglycaemia and reduce ketone production)

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