DM - Aetiology, presentation + diagnosis Flashcards Preview

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Flashcards in DM - Aetiology, presentation + diagnosis Deck (12)
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1
Q

What are the potential secondary causes of DM?

A
  1. Pancreatic disease (Pancreatitis, Trauma, Neoplasia etc)
  2. Endocrine disease (Acromegaly, Cushing’s, Glucogonoma etc)
  3. Drug-induced (Glucocorticoids, B-blockers, Thiazides)
  4. Genetic defects of B-cell function
  5. Infections (Congenital rubella, CMV etc)
  6. Gestational diabetes
2
Q

Compare T1DM and T2DM.

A

T1DM:

  • ketosis prone
  • insulin deficient
  • autoimmune (GAD + ICA antibodies)
  • acute onset
  • non-obese
  • juvenile onset (usually <35)
  • HLA DR3 + DR4
  • FHx +ve in 10%

T2DM:

  • non-ketosis prone
  • insulin resistance ± deficiency
  • non-autoimmune (metabolic syn)
  • insidious onset
  • obesity associated
  • onset usually >35
  • no HLA relation
  • FHx +ve in 30%
3
Q

What is the pathogenesis of T2DM?

A
  • complex interaction of environmental factors (obesity, lack of physical activity) and diabetogenic genes (contribute to insulin resistance)
  • both factors cause insulin resistance and B-cell failure, which are exacerbated by hyperglycaemia
    → ‘glucose toxicity’ = high levels of glucose lead to poorer B-cell function leading to reduced insulin secretion
  • ‘Thrifty gene hypothesis’ = favour fat storage + insulin resistance (protective mechanism in times of famine)
4
Q

Define metabolic syndrome.

A
  1. Central obesity
  2. Any 2 of the following:
    - low HDL concentration
    - high BP
    - high triglycerides
    - high fasting glucose
5
Q

What is the pathogenesis of T1DM?

A
  1. Characterised by pancreatic B-cell destruction, usually leading to absolute insulin deficiency
    - autoimmune destruction of pancreatic islets in predisposed individuals (usually islet cell and glutamic acid decarboxylase antibodies +ve
    - may be idiopathic (antibody -ve)
  2. Environmental factors:
    - peak age of 5-7
    - puberty
    - seasonal variations
    - coxsackie or parvovirus exposure
  3. Genetic:
    - HLA DR3/4
  4. Combination of genetic + environmental factors result in the development of insulitis (inflammation of pancreatic B-cells)
    - infiltration of activated T-lymphocytes
    - develop symptoms of DM when >90% of B-cells are destroyed
6
Q

What is a normal HbA1c? What HbA1c level indicates good glycaemic control in a diabetic patient?

A
  1. Normal HbA1c: <42 mmol/mol

2. Good glycaemic control in a diabetic: <53 mmol/mol

7
Q

What results would you expect in a diabetic patient in the following tests?

(a) Fasting plasma glucose (mmol/L)
(b) 2h plasma glucose after OGTT (mmol/L)
(c) Resting plasma glucose (mmol/L)
(d) HbA1c (mmol/mol) (%)

A

(a) ≥7.0
(b) ≥11.1
(c) ≥11.1
(d) ≥48 (6.5%)

8
Q

What results would you expect in impaired glucose tolerance in the following tests?

(a) Fasting plasma glucose (mmol/L)
(b) 2h plasma glucose after OGTT (mmol/L)
(c) HbA1c (mmol/mol) (%)

A

(a) <7.0
(b) 7.8-11.0
(c) 42-47 (6.0-6.4%)

9
Q

What results would you expect in impaired fasting glucose in the following tests?

(a) Fasting plasma glucose (mmol/L)
(b) 2h plasma glucose after OGTT (mmol/L)

A

(a) 6.1-6.9

(b) <7.8

10
Q

What results would you expect in a diabetic patient in the following tests?

(a) Fasting plasma glucose (mmol/L)
(b) 2h plasma glucose after OGTT (mmol/L)
(c) Resting plasma glucose (mmol/L)
(d) HbA1c (mmol/mol) (%)

A

(a) ≤6.0
(b) <7.8
(c) <7.8
(d) <42 (5.9%)

11
Q

How do people with diabetes often present (T1 + T2)?

A

T1DM (classic ‘osmotic’ symptoms):

  • polyuria
  • polydipsia
  • noturia
  • weight loss
  • fatigue
  • blurred vision
  • pruritis
  • recurrent urinary and genitourinary tract infections
  • may present acutely as DKA

T2DM:

  • symptoms tend to be more vague, subclinical and of longer duration
  • polyuria
  • poldipsia
  • may present acutely with HHS
  • may present with complications: skin infections, foot problems, retinopathy, acute MI/stroke
12
Q

Describe the relationship between obesity and insulin resistance.

A
  • Obesity causes excessive growth of adipose depots with adipocyte hypertrophy and hyperplasia
  • This fat overload results in the activation of stress/inflammatory pathways and subsequent paracrine/autocrine-mediated insulin resistance
  • This is turn increases adipocyte FFA release which stimulates resident macrophages and adipocytes causing increased expression of pro-inflammatory cytokines
  • Additionally, these hypertrophied unstable adipocytes eventually die and release their lipid contents causing additional migration of macrophages to clear dead or dying adipocytes
  • All of these events result in adipose tissue inflammation, impaired insulin signalling and insulin resistance