T2DM Flashcards

1
Q

Definition?

A

Disorder defined by deficits in insulin secretion and action, leading to abnormal glucose metabolism and so metabolic pathologies.
90% of diabetes cases are T2

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2
Q

Risk factors?

A
  • Older age
  • Obesity
  • Gestational diabetes
  • Pre-diabetes
  • Family history
  • Non-white
  • Physical inactivity
  • POCS
  • Hypertension
  • Dyslipidaemia
  • CVD
  • Stress
  • Low birth weight for gestational age
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3
Q

Differentials?

A
  • Pre-diabetes-asymptomatic
  • DM T1
  • Latent autoimmune diabetes in adults-over 30’s, responsive to treatment, non-obese
  • Monogenic diabetes-non-obese, young-family history
  • Ketosis-prone diabetes-same as T1D-no evidence of autoimmunity
  • Diabetes-gestational-after 24 wks?
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4
Q

Epidemiology?

A

• Age: Older
• Sex: Women
• Ethnicity: BAME
Prevalence: 3.5 million in UK

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5
Q

Aetiology?

A

Insulin resistance and insensitivity caused by exposure to risk factors

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6
Q

Clinical presentation?

A
  • Risk factors
  • Asymptomatic-screening
  • Candidal infections
  • Skin infections
  • UTIs
  • Fatigue
  • Blurred vision
  • Polydipsia->16.6 mmol/L (>300 mg/dL), HbA1c >95 mmol/mol (>11%).
  • Polyphagia
  • Polyuria
  • Paraesthesias
  • Nocturia
  • Unintentional weight loss
  • Acanthosis nigricans
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7
Q

Pathophysiology?

A
  • Normal amount of insulin needed but insulin receptors not inserted into cell membrane
  • Mechanisms not fully understood
  • Adipokines -inflammation-linked to insulin resistance
  • Genetics-twin studies
  • More insulin produced via beta cell hyperplasia and hypertrophy
  • Works in the short term
  • Amylin aggregates in islets and so they become dysfunctional and die off-insulin levels die and pts develop hyperglycaemia
  • But some circulating insulin available
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8
Q

Investigations-first line and findings?

A
  • HbA1c-48 mmol/mol (6.5%) or greater
  • Fasting plasma glucose->6.9 mmol/L (>125 mg/dL)
  • Random plasma glucose-≥11.1 mmol/L (≥200 mg/dL)
  • 2 hr post-load glucose after 75g oral glucose-≥11.1 mmol/L (≥200 mg/dL)
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9
Q

Investigations?-second line and findings?

A
  • Fasting lipid profile
  • Urine ketones
  • Random C peptide
  • Urinary albumin excretion
  • Serum creatinine and eGFR
  • ECG
  • ABI
  • Dilated retinal exam
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10
Q

Management-first line?

A
  • Lifestyle changes
  • Glycaemic management
  • BP management
  • Lipid management
  • Antiplatelet therapy
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11
Q

Management-HG or symptomatic?

A

Basal-bolus insulin and CVD risk management

Metformin

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12
Q

Management-NHG-first line?

A

1-metformin and CVD risk reduction

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13
Q

Management-NHG-second line?

A
  • SGLT2 inhibitor
    • GLP-1 agonist
    • DPP4 inhibitor
    • Sulphonylurea or meglitinide
    • Basal insulin
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14
Q

Management-NHG-third line?

A
  • Alpha glucosidase inhibitor

* Thiazolidinedione

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15
Q

Management-NHG-fourth line?

A
  • Individual regimen
    • Switch to basal-bolus insulin
    • Metformin
    • Bariatric
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16
Q

Pregnant management?

A

Diet and basal-bolus insulin?

17
Q

Prognosis?

A
  • Increased chance of CVD event
  • 15% higher excess mortality
  • Insulin deficiency worsens overtime
  • Can participate in activities of daily living if well-managed
18
Q

Complications?

A
• Diabetic kidney disease
• Impaired vision
• Lower extremity amputation
• CVD
• CHF
• Stroke
• Infection
• Periodontal disease
• Treatment-related hypoglycaemia
• Depression
• Obstructive sleep apnoea
• DKA
Non-ketoic hyperosmolar state
Autonomic/peripheral neuropathy
19
Q

Non-ketoic hyperosmolar state?

A
  • higher plasma osmolarity from dehydration and increased conc
    • Water leaves cells into blood vessels down an osmotic gradient, leading to dehydration and polyuria-sometimes ketonemia and acidosis
20
Q

macrovascular?

A

• Can be in the form of CHD, cerebrovascular disease, or PAD
• Due to metabolic risk factors like obesity, dyslipidaemia and hypertension
Managing these/anti hypertensives, statins will prevent these-anticoagulants will be secondary

21
Q

microvascular?

A
  • Diabetic nephropathy, retinopathy and neuropathy
    • Due to chronic hyperglycaemia (primary factor) resulting in glycation of proteins and lipids causing impaired protein and cell membrane function and so tissue damage
22
Q

nephropathy?

A

Increased permeability and thickening of basement membrane and stiffening of teh efferent arteriole causing glomerulosclerosis and increased filtration
Signs-foamy urine, renal failure and uraemia/proteinuria
M-glycaemic control, anti-hypertensives, diuretics, CCBs and salt/protein dietary restrictions

23
Q

neuropathy?

A

Glycation of axonal proteins
Signs-symmetric loss of sensation in distal parts-stocking glove presentation, dysesthesia, pain at night , areflexia, motor control
M-glycaemic control, pain management (anti-convulsant and TCA’s and SNRIs) and opioids

24
Q

retinopathy?

A

Glycation of axonal proteins and retinal vessels
Signs-visual impairment, oedema, microaneurysms
M-laser, VEGF injection

25
Q

Diabetic foot?

A
  • Can be due to ischaemia or neuropathy-impaired wound healing or sensation
  • Signs-painless, charcot joints, swelling warmth erythema or cool pale with no pulse
  • Prevention-control, regular foot exams and self care
  • M-debridement, wound dressing, footwear, antibiotics, revascularisation, amputation