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Diabetes Mellitus

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Republic Of Yemen 3ed level

J. U. For Medical & Health sci.


Faculty Of Nursing First term
Definition:
 Diabetes mellitus is a clinical syndrome characterised by
an increase in plasma blood glucose (hyperglycaemia).

 Diabetes has many causes but is most commonly due to


type 1 or type 2 diabetes.

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 Anatomy of pancreas:
 The pancreas is composed of an endocrine and exocrine part each
fulfilling diverse functions.
 While the exocrine acinar cells secrete digestive enzymes via the
pancreatic duct system into the small intestine ,the endocrine islet
cluster cells secrete specific hormones into the bloodstream.
 The image is adapted and modified from an Opens tax College
resource

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 Anatomy of pancreas

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 Insulin
• Polypeptide hormone produced by B- cells of islets of Langerhans of
pancreas
• Insulin is a protein made of 2 chains- alpha and beta
• Anabolic hormone
• Structure Of Insulin

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 A etiology and pathogenesis of diabetes
 A etiology and pathogenesis of diabetes In both of the common
types of diabetes, environmental factors interact with genetic
susceptibility to determine which people develop the clinical
syndrome, and the timing of its onset.
 However, the underlying genes, precipitating environmental factors
and pathophysiology differ substantially between type 1 and type 2
diabetes. Type 1 diabetes was previously termed insulin-dependent
diabetes mellitus' (IDDM) and is invariably associated with insulin
deficiency requiring replacement therapy.

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 Type 2 diabetes was previously termed 'non-insulin-dependent
diabetes mellitus' (NIDDM) because patients retain the capacity
secrete insulin, and measured insulin levels are often higher than
those seen in people without diabetes.
 In type 2 diabetes, though, there is an impaired sensitivity to insulin
(insulin resistance) and, initially, affected individuals can usually be
treated without insulin replacement therapy. However, 20% or more
of patients with type 2 diabetes will ultimately develop insulin
deficiency requiring replacement therapy, so IDDM and NIDDM
were misnomers.

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• 20.9 Aetiological classification of diabetes mellitus

 Type 1 diabetes
• Immune-mediated
• Idiopathic
 Type 2 diabetes
• Other specific types
• Genetic defects of β-cell function (see Box 20.10)
• Genetic defects of insulin action (e.g. leprechaunism, lipodystrophies)
• Pancreatic disease (e.g. pancreatitis, pancreatectomy, neoplastic disease, cystic fibrosis, haemochromatosis,
fibrocalculous pancreatopathy)
• Excess endogenous production of hormonal antagonists to insulin, e.g.:
1. Growth hormone – acromegaly
2. Glucocorticoids – Cushing’s syndrome
3. Glucagon – glucagonoma
4. Catecholamines – phaeochromocytoma
5. Thyroid hormones – thyrotoxicosis
• Drug-induced (e.g. glucocorticoids, thiazide diuretics, phenytoin)
• Uncommon forms of immune-mediated diabetes (e.g. IPEX syndrome)
• Associated with genetic syndromes (e.g. Down’s syndrome, Klinefelter’s syndrome, Turner’s syndrome,
DIDMOAD (Wolfram’s syndrome), Friedreich’s ataxia, myotonic dystrophy)
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Gestational diabetes Osama foud Alshoapi
 Type 1 diabetes:
 Pathology:
 Type 1 diabetes is a T cell-mediated autoimmune disease involving destruction of
the insulin-secreting β cells in the pancreatic islets
 80–90% of the functional capacity
 Type 1 diabetes is associated with other autoimmune disorders

 Risk factors:
• Genetic predisposition
• Genetic factors account for about one-third of the susceptibility to type 1
diabetes, the inheritance of which is polygenic

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 Type 1 diabetes:
 Environmental predisposition
 The concordance rate between monozygotic twins is less than 40% , and wide
geographic and seasonal variations in incidence.
 Direct toxicity to B cells or by stimulating an autoimmune reaction directed
against B cells. Potential candidates fall into three main categories:
 viruses, specific drugs or chemicals, and dietary constituents.

 Type 1 diabetes in adults


• While type 1 diabetes is classically thought of as a disease of children and young
adults (most commonly presenting between 5 and 7 years of age and at or near
puberty), it can manifest at any age, with as much as half of cases thought to
develop in adults.

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• It is also possible for patients who have a more insidious onset of diabetes to have
an autoimmune a etiology: these people are sometimes described as having slow-
onset type 1 diabetes or latent autoimnmune diabetes of adulthood (LADA).
• LADA is defined as the presenoe of islet autoantibodies in high titre (usually GAD
antibodies), without rapid progression to insulin therapy (whioh would usually
signify type 1 diabetes). Patients with LADA can often present and be managed
similarly to those with type 2 diabetes, but they do progress more rapidly to
requiring insulin treatment for glucose control.
• Not all expert ommnittees recognise LADA as a diagnostic category, hovwever,
and consider LADA to be just a subset of autoimmune type 1 diabetes developing
in adulthood.

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• Clinical features of Type 1 diabetes

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 Type 2 diabetes
 Pathology:
• Initially ,insulin resistance leads to elevated insulin secretion in
order to maintain normal blood glucose levels. However ,in
susceptible individuals ,the pancreatic β cells are unable to sustain
the increased demand for insulin and a slowly progressive insulin
deficiency develops.

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• Risk factors of Type 2 Diabetes
• Genetic predisposition

• 20.7 Risk of developing type 2 diabetes for siblings of individuals with type 2 diabetes

Age at onset of type 2 Age-corrected risk of type 2


diabetes in proband (years) diabetes for siblings (%)
25-44 53
45-54 37
55-64 38
65-80 31

Type 2 diabetes
• Environmental and other risk factors
• Diet and obesity
 Tenfold in people with a body mass index (BMI) of more than 30 kg/m2
• Age

14 Type 2 diabetes is more common
Osamain the
foud middleaged and elderly .
Alshoapi
Symptoms of hyperglycaemia
1. Thirst, dry mouth
2. Polyuria
3. Nocturia
4. Tiredness, fatigue, lethargy
5. Change in weight (usually weight loss)
6. Blurring of vision
7. Pruritus vulvae, balanitis (genital candidiasis)
8. .Nausea
9. Headache
10.Hyperphagia; predilection for sweet foods
11.Mood change, irritability, dificulty in concentrating, apathy

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 Investigations
• 20.2 Diagnosis of diabetes and pre-diabetes
 Diabetes is confirmed by:
• either plasma glucose in random sample or 2 hrs after a 75 glucose load ≥ 11.1
mmol/L (200 mg/dL) or
• fasting plasma glucose ≥ 7.0 mmol/L (126 mg/dL) or
• HbA1c ≥ 48 mmol/mol
 In asymptomatic patients, two diagnostic tests are required to confirm diabetes; the
second test should be the same as the first test to avoid Confusion
 ‘Pre-diabetes’ is classified as:
• impaired fasting glucose = fasting plasma glucose ≥ 6.1 mmol/L (110 mg/dL) and <
7.0 mmol/L (126 mg/dL)
• impaired glucose tolerance = fasting plasma glucose < 7.0 mmol/L (126 mg/dL) and
2-hr glucose after 75 g oral glucose drink 7.8–11.1 mmol/L (140–200 mg/dL)
 HbA1c criteria for pre-diabetes vary. The National Institute for Health and Care
Excellence (NICE) guidelines (UK) recommend considering an HbA1c range of 42–47
mmol/mol to be indicative of pre-diabetes; the American Diabetes Association
(ADA) guidelines suggest a range of 39–47 mmol/mol. The ADA also suggests a
lower fasting plasma glucose limit of ≥ 5.6 mmol/L (100 mg/dL) for impaired fasting
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glucose.
 Glycated haemoglobin
 In diabetes, the slow non-enzymatic covalent attachment of glucose
to haemoglobin (glycation) increases the amount in the HbA1
(HbA1c) fraction relative to nonglycated adult
 haemoglobin (HbA0).
 Although HbA1c concentration reflects the integrated blood glucose
control over the lifespan of erythrocytes (120 days), HbA1c is most
sensitive to changes in glycaemic control occurring in the month
before measurement.

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• 20.3 How to perform an oral glucose tolerance test (OGTT)
 Preparation before the test
 Unrestricted carbohydrate diet for 3 days
 Fasted overnight for at least 8 hrs
 Rest for 30 mins
 Remain seated for the duration of the test, with no smoking
 Sampling
 Measure plasma glucose before and 2 hrs after a 75 g oral glucose drink

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