T5-L2: Diabetes Flashcards

1
Q

What hormone do Islets of Langerhans produce in the greatest quantity?

A

Insulin - via the Beta cells (75%)

  • Alpha cells produce glucagon (25%0
  • delta Cells Produce Somatosatin (5%)
  • F cells produce pancreatic polypeptide
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2
Q

What is C-peptide?

A

It is a byproduct of the production of Insulin. It is produced in equal quantities to Insulin and so can be used as a diagnostic measure when looking at the levels of Insulin in the blood.

Insulin is synthesised from pro-insulin from the endoplasmic reticulum. It is cleaved at multiple sights leading to equal producing of insulin and C-peptide.

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3
Q

What are the affects of insulin?

A

Metabolic effects - Increase glucose uptake. It also inhibits gluconeogenesis and glycogenolysis.

Pancreatic effects - High insulin levels reduce the glucagon secretions from alpha cells.

Vascular, Growth and cancer affects - Has vasodilatory properties.

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4
Q

How do we diagnose diabetes?

A
  • Fasting glucose of greater than 7 mmol/L
  • Random glucose of greater than 11mmol/L
  • Two separate reading posts OGTTT of greater than 11.1 mmol/L
  • HbA1c - greater than 48mmol/L
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5
Q

How do we diagnose prediabetes with HbA1c?

A

≥41 and <48 mmol/mol = pre-diabetes - these patients can be advice of lifestyle changes to delay the onset of diabetes

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6
Q

What the epidemiology of Type 1 diabetes?

A
  • Autoimmune destruction of insulin producing beta cells in the islets of Langerhans
    • Occurs at any age (but peaks around puberty)
    • Equal sex incidence but after 15% years of age, there is a two fold increase in the prevalence in men
      Common in the developing world
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7
Q

What is the pathogenesis and risk factors for Type 1 diabetes?

A

Pathogenesis

  • Due to autoantibodies as a result of humeral immunity
  • Exposure/trigger to environmental factors
  • AutoimmunityRisk factors
    - Family History - Genetics - HLA Class II - DR4-DQ8 and DR3-DQ2 (genetic susceptibility)
    - Perinatal factors - Low birth weight
    - Viral infections e.g. respiratory and enteroviruses
    Diet - cows milk
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8
Q

What is the presentation of Type 1 diabetes?

A

• Rapid onset (often few weeks)
• Weight loss + osmotic symptoms + low energy - e.g. thirst, polyuria, polydipsia and nocturia
• Abdominal pain - usually when you already have diabetic ketoacidosis
• Often slim
Present as diabetes ketoacidosis (DKA)

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9
Q

What autoantibodies can we detect in Type 1 diabetes?

A
  • Insulin autoantibodies

* Glutamic acid decarboxylase autoantibodies ( GAD) - GAD65 is the one we measure more common in T1DMN

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10
Q

What is the presentation of Type II Diabetes?

A

• Often overweight
• Symptoms present over few months
• Minimal weight loss ( unless left for long period)
• Can present with complications such as vision loss or foot ulcers or fungal infection
Can also present in state of Hyperosmolar Hyperglycemia State (HHS) or HONK - high blood glucose without the acidosis

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11
Q

What are the management options for Type II Diabetes?

A
  • Lifestyle - exercise, change in diet and weight loss
  • Oral therapy - Metformin is the first line
  • Insulin
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12
Q

What is the criteria for gestational diabetes?

A
  • Diabetes diagnosed in pregnancy
    - New diabetes not present prior to pregnancy
    - Hyperglycaemic first detected in pregnancy
    Fasting glucose above > 5.6 mmol/litre OR 2 hours plasma glucose level of 7.8mmol/litre. This is DIFFERENT from normal diabetes diagnosis.
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13
Q

What are the risk factors for gestational diabetes?

A

Risk factors:

	- BMI of over 30 
	- Previous macrosomic baby - baby over 4.5 kg 
	- Previous gestational diabetes 
	- Family history of diabetes 
	- Ethnic minority
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14
Q

What are the consequences of gestational diabetes?

A

Short term consequences:

- Macrosomia 
- Pre-eclampsia 
- Stillbirth 
- Neonatal morbidity 

Long term consequences

- Obesity in the child 
- Development of T2DM in the mother
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15
Q

What is MODY?

A

Mature onset diabetes of the young (MODY) - has further subsets. It is a AD condition and the most common cause of monogenetic diabetes and accounts for 2 in 5 cases of diabetes.

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16
Q

Give secondary causes of diabetes.

A

Diabetes causes by damage to the pancreas e.g.

- Pancreatitis (gallstones, alcohol)
- Pancreatomy 
- Cystic fibrosis 
- Hemochromatosis (build up of iron in the blood)

Drug induced Diabetes 

- Steroid - normally high dose and prolonger 
- Atypical anti-psychotics - can also lead to obesity 
- Immunotherapy e.g. Nivolumab used in melanoma treatment 
- Protease inhibitor used in HIV treatment
17
Q

Give example of endocrine disorders that can cause diabetes.

A
  • Cushing’s syndrome
  • Acromegaly
  • Somatostatin secreting tumours (somatostatin)
  • Glucagon secreting tumours (Glucagonoma)
18
Q

What hormones counter act Insulin/

A
  • GH
  • Glucagon
  • Epinephrine/Norepinephrine
  • Glucocorticoid
19
Q

What are stimuli for insulin release?

A
  • Glucose
  • Fatty acids and ketones
  • Vagal gut stimulation
  • Gut hormones
  • Drugs
  • Prostaglandins
20
Q

Give stimuli for the inhibition of insulin release.

A
  • Sympathetic stimulation
  • Adrenaline
  • Beta blockers
  • Dopamine
  • Seratonin
  • Somatosatin
21
Q

Give stimulation for glucagon release.

A
  • Amino acids
  • Beta adrenergic stimulation
  • Fasting, hypoglycaemia
  • Exercise
  • Cortisol
22
Q

Give stimulation of inhibition of glucagon release.

A
  • Ketones
  • Insulin
  • Glucose
  • Somatostatin
  • Free fatty acids
23
Q

What is the action of glucagon?

A
- Increase glucose levels
	• Glycogenolysis
	• Gluconeogenesis
	• Lipolysis
- Reduces intestinal motility and gastric acid secretion