Diabetes mellitus is a group of metabolic disorders in which persistent hyperglycaemia (random plasma glucose more than 11.1 mmol/L) is caused by deficient insulin secretion, resistance to the action of insulin, or both: Insulin deficiency and insulin resistance lead to the abnormalities of carbohydrate, fat, and protein metabolism that are characteristic of diabetes mellitus
causes prevelance
Genetic: heriidatroy, when a sibling has it increase risk of 6-7%, and 30-70% if they are tiwns and 1-9% if it’s a parent
Environments: diet, vit D exposure, obesity. Early exposure to viruses associated with islet inflammation (such as enterovirus) and decreased gut- microbiome diveraty
Socuioeconomic factors
Incidence and prevelance: 4.7 millions people have diabetes. 36,000 childer under 19, most childer diagnosed between 10 and 14 years
Microvascular complications (due to damage to small blood vessels)
nephropathy : diabetic kindney disease
retinopathy: small blood vessel damage to the retina- leads to progressive loss of vision and blindness
neuropathy: nerve damage [icliudoing direct damange by the hyperglycemic and decrease of blood flow to nerves through damanaged small blood bvessels
*diabetic foot/ and
• Autonomic neuropathy is a late-stage complication of diabetes where the neurons of the autonomic nervous system become damaged owing to chronic hyperglycaemia. It presents in different ways and affects a variety of organs, including the skin (sweating), blood vessels (postural hypotension), gastrointestinal tract (gastroparesis and diarrhoea), heart, bladder function, and sexual function. It may also blunt the symptoms of hypoglycaemia [NICE, 2015a].
Men with diabetes are 3 times more likely to have imputance
Macrovascular complications damage to large blood vessels
Artohorscrelosisi: increseases CVD. Such as
MI, HF, stroked, peripheral arterial disease,[intermittent cludication] **risk increases >40 years of age.
Metabolic complaication
DKA, diabetic ketonacidosis: Insulin deficiency results in an increase in counter-regulatory hormone production (glucagon, cortisol, growth hormone, and catecholamines). This type of hormonal imbalance enhances hepatic glycogenolysis (glucose production through the breakdown of glycogen stores) and gluconeogenesis (formation of glucose from other substrates), resulting in severe hyperglycaemia
Enhanced lipolysis due to the lack and uptake of glucose, [increases serum free fatty acids]
• NB: DKA is a medical emergency because it leads to dehydration and electrolyte imbalances [Karslioglu French, 2019]. The mechanisms responsible for fluid depletion in DKA include osmotic diuresis due to hyperglycaemia, vomiting, and inability to take in fluid owing to a diminished level of consciousness. Electrolyte shifts and depletion are in part related to the osmotic diuresis.
Hyperglycaemia: blood glucose fall lower that 3.5 mmols.
Sever hypoglycaemia results in ci=onvulsions, sweating, inability to swallow, loss of conciouness and coma
Other autoimmune conditions
• People with type 1 diabetes are at increased risk of developing other autoimmune diseases, most commonly thyroid disease (Graves' disease or Hashimoto's thyroiditis, 15–30%), autoimmune gastritis and/or pernicious anaemia (5–10%), coeliac disease (4–9%), vitiligo (2–10%), and Addison’s disease (0.5%)
diagnosisng in adults
• Ketosis.
• Rapid weight loss.
• Age of onset younger than 50 years.
• Body mass index (BMI) below 25 kg/m2.
• Personal and/or family history of autoimmune disease.
in children
• Polyuria.
• Polydipsia.
• Weight loss.
• Excessive tiredness.
Suspect diabetic ketoacidosis (DKA) in a person with known diabetes or significant hyperglycaemia (finger-prick blood glucose level greater than 11 mmol/L) and the following clinical features:
Increased thirst and urinary frequency.
Weight loss.
Inability to tolerate fluids.
Persistent vomiting and/or diarrhoea.
Abdominal pain.
Visual disturbance.
Lethargy and/or confusion.
Fruity smell of acetone on the breath.
Acidotic breathing — deep sighing (Kussmaul) respiration.
Dehydration, which can be classified as:
Mild — only just clinically detectable.
Moderate — dry skin and mucus membranes, and reduced skin turgor.
Severe — sunken eyes and prolonged capillary refill time.
Shock (resulting from severe dehydration). The person is severely ill with:
Tachycardia, poor peripheral perfusion, and (as a late sign) hypotension (indicating decreased cardiac output).
Lethargy, drowsiness, or decreased level of consciousness (indicating decreased cerebral perfusion).
Reduced urine output (indicating decreased renal perfusion).
If DKA is suspected
Assess for precipitating factors of DKA, such as:
Infection (for example pneumonia or a urinary tract infection).
Physiological stress (such as trauma or surgery).
Non-adherence to insulin treatment regimen or intentional insulin omission in order to lose weight (diabulimia).
Other medical conditions (such as hypothyroidism or pancreatitis).
Drug treatment (such as corticosteroids, diuretics, and sympathomimetic drugs [for example salbutamol]).
Test for ketones (produced by the liver when there is a lack of glucose [starvation ketones] and as an alternative energy source when there is a relative insulin deficiency).
In an adult with suspected DKA, test for urine or blood ketones even if plasma glucose levels are near normal.
In a child or young person with suspected DKA, test for blood ketones. If this is not possible, arrange immediate admission to a hospital with acute paediatric facilities.
Ketones are high if above 2+ in the urine or above 3 mmol/L in the blood.
Consider the possibility of DKA in all people with type 1 diabetes who are unwell, bearing in mind that:
Hyperglycaemia may not always be present — children and young people on insulin therapy may develop DKA with normal blood glucose levels.
Low blood ketone levels (less than 3 mmol/L) do not always exclude DKA.
Hypoglycaemia
Hypoglycaemia presents with a wide variety of symptoms (autonomic and neuroglycopenic).
Suspect mild hypoglycaemia in a person with type 1 diabetes who presents with the following:
Hunger.
Anxiety or irritability.
Sweating.
Tingling lips.
Irritability.
Palpitations.
Tremor.
As blood glucose levels fall lower, the person may experience:
Weakness and lethargy.
Impaired vision.
Incoordination.
Reduced orientation.
Confusion.
Irrational behaviour.
Emotional lability.
Deterioration of cognitive function (when blood glucose levels fall lower than 3.0 mmol/L).
Severe hypoglycaemia may result in:
Convulsions.
Inability to swallow.
Loss of consciousness.
Coma.
after assessment, management
lifestyle: advice: diet, exerscie, alcohol, Information on managing other lifestyle and cultural issues, such as driving, fasting, holiday and travel, and shift work
DAFNE: dose adjustment for normal earing: Offer this programme 6–12 months after diagnosis or at any time that is clinically appropriate and suitable for the person, regardless of duration of type 1 diabetes
support: phsycological
individual care plan: After the initial plan is agreed, put arrangements in place to implement it without inappropriate delay. Arrange a review to reassess the person in the following weeks.
The initial diabetes assessment will include a general examination and a review of the following
Acute medical history.
Social, cultural, and educational history/lifestyle review.
Complications history/symptoms.
Long-term/recent diabetes history.
Other medical history/systems.
Family history of diabetes/cardiovascular disease.
Medication history/current medicines.
Vascular risk factors.
Smoking status, general examination, weight/body mass index.
Foot/eye/vision examination.
Urine albumin excretion/urine protein/serum creatinine.
Psychological wellbeing.
Attitudes to medicine and self-care.
Immediate family and social relationships and availability of informal support.
**Rapid- and short-acting insulins have a quick onset of action and a short duration of action. They are used to replicate the insulin normally produced by the body in response to glucose absorbed from a meal or sugary drink**
o Rapid-acting insulins have an onset of action of about 15 minutes and a duration of action is 2–5 hours. Examples include Humalog® (insulin lispro) and Novorapid® (insulin aspart).
o Short-acting (regular or neutral) insulins have an onset of action of 30–60 minutes and a duration of action of up to 8 hours. Examples include Actrapid® and Humulin S®.
text**Intermediate- and long-acting insulins have a slow onset of action and a long duration of action. They mimic the effect of endogenous basal insulin (insulin that is secreted continuously throughout the day**).
• Insulin in fixed combination with liraglutide is a combination of a long-acting basal insulin and liraglutide (a glucagon-like peptide-1 [GLP-1] receptor agonist licensed for the treatment of type 2 diabetes). Xultophy® is a combination of insulin degludec 100 units/mL with liraglutide 3.6 mg/mL in a prefilled pen.
• Intermediate-acting (isophane) insulins have an onset of action of approximately 1–2 hours, maximal effects between 3–12 hours, and a duration of action of 11–24 hours. Examples include Humulin I®, Insuman Basal®, and Insulatard®.
• Long-acting insulins have a duration of action of up to 24 hours; steady-state level achieved after 2–4 days to produce a constant level of insulin. Examples include Lantus® (insulin glargine), Levemir® (insulin detemir), and Tresiba® (insulin degludec).
• Biosimilar insulin is a biological copy of an original insulin. Abasaglar® is a biosimilar insulin product based on insulin glargine 100 units/mL (Lantus®) and is licensed for the treatment of diabetes in adults, adolescents, and children aged 2 years and older.
definitions of diabetes's
OGTT, gold standard test: oral glucoses tolerance test
fast night before.
take fast glucose BM [Without diabetes fasting glucose <6mmol, and under 7.8 after 2 hours of taking glucose
People with impaired glucose fasting 6-7mmols and between 7,9-11.0 mmols]
give 75grams of glucos and recheck after 2 hours BM=11.1
IGETSMASHED OTHER
Idiopathic- gallstones - ethanol(alcohol) - trauma - steroids - malignancy or mumps - autoimmune - scorpion stings - hypercalcaemia, hypertreamia, glycaemia - ERCP - drugs such as antifungals, statins. benzofurosamide
LADA: Latent autoimmune diabetes in adults: begins in adulthood and normally does not require insulin for glycaemic control in the 1st 6 month of diagnosis
DKA: diabetic ketoacidosis: polyurea, polydipsia, polyphagia. weight loss, abdominal pain. vomiting diarrhoea, ketone breath. lethargy. confusion/ vision disturbance. > RR
MODY: Maturity onset diabetis of the young
develope in the adolecent, hireditry
S+S: thirst, dehydration, blurry vision, polyuria, recurrent skin and yeast infections.
type 1: beta cell destruction
autoimmune disorder such as
: sciliac disease, graves, Addison's, vitiligo, pernicious anaemia
** check C peptide as this will be low or negligent
type 2: insulin resistant, decrease insulin production, caused by lifestyle obesity,
sick day rules: stopping medication that can be nephrotoxic such as, metformin, ace inhibitors, diuretics, flozins
endocrine: secretes hormone/chemicals *straight into the blood, this lets hormones travels to cells in other areas of the body*
Delta cells, found in the stomach, somatostatin producing cells: decrease glucagon and increased insulin secretion
Pancreatic peptides modulates digestion breaks down fats, inhibits gastric empting as well as biliary secretion
Beta cells, makes insulin reduces sugar levels. Detect sugar after eating sugary foods ** /amylin, inhibits food uptake delays gastric empting decreases glucose levels
Alpha cells, releases glucagon. Elevate sugar levels
Epsilon: produce a hormone Ghrelin which induces hunger, satiety
Secretion glands are: thyroid. Adrenal and l testes
EXOCRINE; secretes hormones /chemicals** into the ducts** which carry substances to the target tissues
Sweat, tears milk and digestive juices