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Associate Ambulance Practitioner > Recognition and management of diabetes > Flashcards

Recognition and management of diabetes Flashcards

1
Q

Diabetes

Prevalence

A
  • 2.9m of the UK population
  • 5% of the UK population
  • Estimated 4m UK & 300m worldwide by 2025
  • Deaths predicted to rise by 25%
  • 1,500 children in UK have Type II
  • 10% of NHS budget is spent on diabetes
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2
Q

Risk Factors

A

Non-modifiable

  • Familial
  • Age
  • Gender
  • Post menopausal

Modifiable

  • Smoking
  • Hypertension
  • Dyslipidaemia
  • Obesity
  • Physical inactivity
  • Excess alcohol

Stress

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3
Q

What happens to our food?

A
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4
Q

Pancreas

A
  • Grey gland 12-15 cm long
  • Lies in epigastric & left hypocondiac region
  • Broad head lies in curve of duodenum
  • Body lies behind the stomach
  • Narrow tail lies in front of left kidney
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5
Q

Pancreas

A

•Located in retroperitoneal space

•

•Is both an exocrine & endocrine gland

•

•Produces & releases

–Digestive enzymes into duodenum (Exocrine function)

–Insulin, glucagon into blood

(Endocrine function)

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6
Q

Pancreas

A

Contains specialised endocrine cells - islets of Langerhans, containing 4 types of hormone-secreting cells

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7
Q

Islets of Langerhans

A

Alpha Cells (unaffected in a diabetic) secrete the hormone glucagon which raises blood glucose level

Beta Cells Secrete the hormone insulin which lowers

blood glucose level

Delta Cells Secrete growth hormone inhibiting cells (GHIH) or somatostatin, inhibiting secretion of insulin & glucagon

F-Cells Secrete pancreatic polypeptide which regulates

digestive enzymes

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8
Q

Glucagon Release

A

Glucagon is released (by the Alpha cells) in response to low blood glucose levels and to events whereby the body needs additional glucose, such as in response to vigorous exercise.

  • Levels of blood glucose controlled by negative feedback
  • If blood glucose falls - alpha cells secrete more glucagon - blood glucose rises so stimulation slackens

•

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9
Q

Effects of Glucagon Release

A

When glucagon is released it can perform the following tasks:

•

  • Stimulate the liver to break down glycogen to be released into the blood as glucose
  • Activate gluconeogenesis, the conversion of amino acids into glucose
  • Break down stored fat (triglycerides) into fatty acids for use as fuel by cells
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10
Q

Effects of Insulin Release

A
  • Naturally produced hormone
  • Accelerates the conversion of glucose into glycogen for storage in the liver and muscles (Glycogenesis)
  • Accelerates the transport of glucose from blood into cells (Especially skeletal muscle)
  • Allows entry of amino acids into cells & synthesises proteins
  • Converts glucose into fatty acids (Lipogenesis)
  • Glucose entry to cells depends on the presence of insulin receptors on the target cells

*see tortora 11th ed pg 648, figure 18.19

•

•

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11
Q

Diabetes aetiology

A

Diabetes Mellitus

Disorder of the pancreas

Inadequate insulin for carbohydrate metabolism

Diabetes Insipidus (more rare)

Disorder of endocrine system

Inadequate anti-diuretic hormone (ADH)

Blood glucose levels are normal

Excessive thirst

Excessive production of dilute urine

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12
Q

Diabetes Mellitus

A

•Diabetes Mellitus is a disorder in which there is inadequate insulin for carbohydrate metabolism.

•

• Glucose absorbed from the gastro-intestinal tract cannot be metabolised or stored and so reaches higher than normal levels in the bloodstream

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13
Q

Types of Mellitus

A

Type I (IDDM)

  • More common in children & young adults
  • Sudden onset
  • Deficiency/absence of insulin
  • Treated with insulin

•

Type II (NIDDM)

  • More common in the elderly, late onset
  • Normally obese
  • Diet controlled with tablets (can be insulin)
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14
Q

Type I

A

•Absolute deficiency of insulin

•

•Regular injections required to prevent death

•

  • Auto immune disorder where pancreatic beta cells are destroyed in genetically susceptible people
  • Metabolism of untreated IDDM is similar to that of a starving person

–insulin not present to aid entry of glucose into body cells

–cells instead use fatty acids to produce adenosine triphosphate (ATP)

–by-products of fatty acid catabolism are organic acids called ketones

–ketone bodies form acidosis which lower the pH of the blood and result in DEATH

–By product of ketones is acetone smell on breath

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15
Q

Common Types of Insulin

A
  • Human Actrapid
  • Human Insulatard ge
  • Human Mixtard 30 ge
  • Human Monotard
  • Human Ultratard
  • Human Velosulin
  • Humulin 1
  • Humulin Lente
  • Humulin M1
  • Humulin S
  • Humulin Zn
  • Hypurin

•

  • Human Actrapid Penfill (pen)
  • Human Insulatard Penfill (pen)
  • Human Mixtard 10 Penfill (pen)
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16
Q

Type II

A
  • More common = 90% of all cases
  • Over 40 and overweight (occurring later in life)
  • Diabetes for these is because cells are less sensitive to insulin probably through down-regulation of insulin receptors
17
Q

Oral Hypoglycaemic Agents

A
18
Q

Sulphonylureas

A

Help the pancreas produce extra insulin

•

•Gliclazide

•

•Glibenclamide

•

•Tolbutamide

•

•Chlorpropamide

19
Q

Biguanides

A

•Increases the uptake of glucose by cells

•

•Must be some insulin production by the pancreas

•

•Only one currently available

20
Q

α-Glucosidase Enzyme Inhibitor

A

•Inhibits the enzymes in the gut that help to digest starches

•

•This can reduce the risk of hyperglycaemia after a meal

•

•Unfortunate side effects!

21
Q

Long Term Complications

A

•Cardiovascular Problems

–Atheroma leading to Peripheral Vascular Disease and MI

–Thickening of arteries leading to retinopathy, renal failure and peripheral neuropathy

•Infection

–Bacteria and fungi

•Renal failure

–Due to vascular changes

•Optical

–Retinopathy

Infection

Possibly because phagocyte activity is depressed by insufficient intracellular glucose.

Complications occur in areas affected by neuropathy. Feet when sensation and blood supply are impaired. Boils, carbuncles, vaginal candidiasis (thrush) and pyelonephritis (bacterial infection of kidney)

22
Q

Long Term Complications

A

Excessive glucose damages renal blood vessels because its not reabsorbed by the tubules. The remaining glucose raises osmotic pressure = reduced water reabsorbtion = increased urine volume = electrolyte imbalance = polyuria = hypovolaemia = extreme thirst = polydipsia

23
Q

Long Term Complications

A

Loss of vision due to cataracts as excessive glucose attaches to lens proteins causing cloudiness or damage to blood vessels on the retina

24
Q

Hypoglycaemia

A
  • Overdose of insulin
  • Not enough food or delay in taking foods
  • Overdose of medication
  • Too much exercise
  • Alcohol
  • Pregnancy
  • Gastrointestinal disturbances (D&V)
  • Recent illness
25
Q

Hyperglycaemia

A
  • Undiagnosed diabetes
  • Incorrect medication (rebellion or senility)
  • Inadequate adjustment to dose of insulin during illness

Symptoms

  • Polyuria – excessive urine
  • Polydipsia – excessive thirst
  • Polyphagia – excessive eating
26
Q

Hypo or Hyper glycaemia?

A
27
Q

Hypo or Hyper glycaemia?

A
28
Q

Management

Hypoglycaemia

A

Hypoglycaemia

  • ABC’s
  • Oxygen (If hypoxaemic)
  • Administer Hypostop

(if conscious)

  • Recovery position
  • Monitor Blood Glucose
  • IM Glucagon
  • Reassurance
  • Consider paramedic assistance for iv glucose
29
Q

Management

Hyperglycaemia

A

Hyperglycaemia

  • ABC’s
  • Oxygen (If hypoxaemic)
  • Recovery position
  • Monitor Blood Glucose
  • Reassurance
  • Consider Paramedic assistance for iv fluid if hypoperfused
30
Q

Blood sugar level

A
  • Obtain and record pre and post treatment
  • Ensure that level of >5mmol/L is achieved following administration of oral glucose
  • Patient may be left at home following full recovery with advice to take further food by mouth and left in the care of a responsible adult
  • Safety net and document
  • All other hypoglycaemic patients who have received treatment should be encouraged to attend hospital especially if they….
  • are elderly
  • are taking oral hypoglycaemic agents, as hypoglycaemia may occur
  • Have no history and 1st hypo episode
  • have blood glucose level < 5mmol/l after treatment
  • have not returned to normal mental status within 10mins of IV glucose (Paramedic intervention)
  • have been treated with glucagon
  • have any additional disorders or complicating factors eg. Chest pain, arrhythmias, alcohol, dyspnoea
  • Exhibit signs of infection (Urinary, upper resp.tract) and/or unwell
31
Q

Summary

A

•Coma is a serious complication of diabetes

•

•Ketoacidosis is a potentially fatal metabolic disorder

•

•Mortality rate is 2-4% for hypoglycaemia

•

•Mortality rate is 5-10% for hyperglycaemia

•

•Early diagnosis and treatment is the priority

Associate Ambulance Practitioner (63 decks)

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