Module 2 - Diabetes Flashcards

1
Q

What is the target BGL reading

A

Between 4-8mmol/L (4-6 when fasting)

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2
Q

Describe the function of the pancreas

A

Produces hormones involved in glycaemic control
Houses the Islets of Langerhans:
Secretions of glucagon (alpha cells), insulin (beta cells), somatostatin, pancreatic polypeptide

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3
Q

Describe insulin

A

Secreted by Beta cells
Secretion promoted by increased blood glucose levels
Facilitates uptake of glucose by cells and the synthesis of proteins, lipids and nucleic acids

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4
Q

What is diabetes mellitus

A

A metabolic disease resulting in chronically raised blood glucose levels as a result of the body’s inability to produce or use insulin
Insufficient release of insulin by pancreatic beta islet cells or resistance to insulin resulting in hyperglycaemia (high blood sugar)

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5
Q

What is gestational diabetes

A

Glucose intolerance in pregnancy
Risk factors: high-risk ethnic group, polycystic ovary disease, overweight, advanced maternal age
Child can develop diabetes as result
Placenta releases hormones which affect the work of insulin
Body in pregnancy needs 3x as much insulin as normal Pancreas can’t make enough therefore glucose remains in blood stream = high BGL

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6
Q

What is latent autoimmune diabetes of adulthood

A

Type 1 developed later in lifetime

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7
Q

What is diabetes insipidus

A

Occurs when body can’t regulate how it handles fluids. It is caused by hormonal abnormalities (lack of ADH released from pituitary or ADH not working properly) and isn’t related to diabetes. Patients suffer extreme thirst and heavy urination

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8
Q

What is type 3 diabetes

A

Has links with alzheimer’s disease - insulin resistance in the brain

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9
Q

Compare hormone levels of type 1 and 2 diabetes

A

Type 1- insulin low or absent, glucose increased and insulin sensitivity is normal or increased

Type 2- normal to high insulin, can progress to low, increased glucose and reduced insulin sensitivity

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10
Q

Describe type 1 diabetes

A

Acute onset insulin deficiency
Autoimmune disease where beta cells destroyed
Manifestations: hyperglycaemia, polydipsia (thirst), polyuria, polyphagia (eating), weight loss and fatigue
No cure, can be managed by maintaining healthy lifestyle, regular blood glucose testing and insulin injections
Accounts for 10-15% diabetes cases

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11
Q

Describe pathophysiology of type 1 diabetes

A

Insulin deficient
Pancreas stops making insulin (beta cells destroyed)
Body cannot turn glucose into energy to be used by cells so will start to burn own fat as a substitute (ketones)
Need daily insulin injections to prevent accumulation of ketones in the blood from burning of fat –> diabetic ketoacidosis
Depend on up to 4 injections/day & BSL testing several times
Onset usually occurs in people under 30 years old but can occur at any age

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12
Q

Common symptoms of type 1 diabetes

A
Polydipsia (increased thirst) 
Polyuria (increased urine) 
Feeling tired and lethargic - no glucose to use for energy 
Polyphagia (increased hunger) 
Having cuts that heal slowly (impaired blood supply)
Itching, skin infections (microorganisms stimulated by increased blood sugar level) 
Blurred vision
Unexplained weight loss
Mood swings
Headaches
Feeling dizzy
Leg cramps
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13
Q

Describe type 2 diabetes

A

Accounts for 85-90% of people who have diabetes
Progressive onset - usually affects older adults, however, more and more younger people are getting it
Overtime most will need tablets and many will also need insulin (natural progression of the disease)
Taking tablets or insulin as soon as they are required can result in fewer complications in the long-term

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14
Q

Describe pathophysiology of type 2 diabetes

A

Insulin resistance
Various implications:
Beta cell destruction - Pancreas makes some insulin but not the required amount (works ineffectively)
Decreased number of insulin receptors on target cells and decreased intracellular response to insulin by target cells
Insufficient levels glucose carried to cells which means hyperglycaemia persists stimulating further insulin release

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15
Q

Risk factors for type 2 diabetes

A
Obesity and increased BMI
Metabolic syndrome 
Physical inactivity 
Unhealthy diet
High blood pressure
Tobacco smoking
Family history of Type II diabetes, genetic factors (has strong genetic predisposition) 
Extra weight carried around the waist
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16
Q

Symptoms of type 2 diabetes

A

Same as type 1 but instead, slowly gaining weight and the presence of peripheral neuropathy

17
Q

How is type 2 diabetes treated through pharmacological agents

A

Oral hypoglycaemic agents (anti-diabetic agents):
Biguanides (e.g. metformin) and glitazones (e.g. rosiglitazone) to increase insulin sensitivity and glucose uptake
Sulfonylureas (e.g. glibenclamide) and meglinitides (e.g. repaglinide) increase the secretion of insulin
Acarbose slows the absorption of carbohydrates

Insulin therapy when oral medications fail to maintain euglycemia (normal levels of glucose in blood)

18
Q

Why can you not give type 1 diabetics hypoglycaemics

A

Hypoglycaemics are for insulin resistance (help cells become more receptive to insulin) whereas, type 1 sufferers are insulin deficient so therefore, wouldn’t have an effect

19
Q

How can type 2 diabetes be managed through non-pharmacological methods

A
Can be delayed or prevented through: 
Maintaining healthy weight
Exercise
Healthy food choices
Managing blood pressure
Managing cholesterol levels
Cease smoking
Medications and lifestyle modifications
20
Q

Testing time differences between type 1 and 2 diabetes

A

Type 2- Should be before breakfast (fasting normal 4-6mmol/L) and 2 hours after meals (post prandial) (normal 4-8mmol/L) –> always depends on when they eat

Type 1 - Before each meal and 2100hrs

21
Q

What is diabetic ketoacidosis

A

a part of hyperglycemia
Slow to rapid onset
Malaise, dry mouth, headache, polyuria, polydipsia, weight loss, nausea, vomiting, pruritus, abdominal pain, lethargy, shortness of breath, Kussmaul breathing, fruity or acetone odour to breath
14-40mmol/L, pH <7.3

22
Q

What is hyperglycaemic hyperosmolar state

A

Complication of Type 2 diabetes
Slow onset
Leads to severe dehydration (affects osmolarity)
Polyuria, polydipsia, hypovolaemia, dehydration, hypotension, tachycardia, hypoperfusion (reduced blood flow), weight loss, weakness, nausea, vomiting, abdominal pain, hypothermia, stupor, coma, seizures
35-110mmol/L

23
Q

What is hypoglycaemia

A

<4mmol/L
Caused by: Mismatch of food and insulin i.e. delaying or missing a meal, Insulin excess, Hypoglycaemic unawareness, Alcohol, Insulin regimens, States of extra demands: infection, stress/anxiety, more strenuous activity than usual

24
Q

signs and symptoms of hypoglycaemia

A
Sweating
Weakness, trembling, shaking 
Dizziness
Headache 
Lack concentration/behaviour change 
Tearful/crying
Hunger
Irritability
Numbness around lips and fingers
Double vision 
Palpitations
If untreated: confusion, drowsiness, loss of consciousness, fitting, coma
25
Q

What is hyperglycaemia

A
Caused by: 
Sickness
Infection
Management errors i.e. lack insulin/oral hypoglycaemias
Stress
Other medications – cortisol, diuretics
Excessive glucose/carb ingestion 

Treated through insulin

26
Q

What are some chronic complications of diabetes

A

Hyperglycaemia can cause macrovascular issues such as chronic heart disease, arrhythmia, heart attack and microvascular issues such as peripheral vascular disease, retinopathy (eyes), nephropathy (kidneys) and neuropathy (infertility and incontinence)

can also cause infection, glucose changes structure and function of proteins and lipids, stroke or numbness

27
Q

Outpatient resources for people with diabetes

A

Education at hospitals such as ‘Living with Diabetes’ course
NDSS - national diabetes services scheme - reduces cost of testing strips

28
Q

Describe Metformin

A

Is a Biguanide- prevents production of glucose in the liver
Is a hypoglycemic
Increase insulin sensitivity and glucose uptake
For adults and children over 10 with type 2 diabetes
Acidosis can occur when metformin accumulates