E3 - Diabetes 1 Flashcards
(75 cards)
1
Q
What is diabetes mellitus and what is it characterised?
A
- Chronic metabolic disorder
- Characterised by hyperglycaemia (high blood glucose)
2
Q
What are the two main types of DM and which is more common?
A
- Type 1; insulin deficiency (lack of in the body, 5 - 15% of DM)
- Type 2; impaired β-cell function (relative deficiency) and/or loss of insulin sensitivity; cells/tissues in body no longer recognising insulin as well (insulin resistance) 85 - 95% of DM.
3
Q
Why is the term NIDDM (non-insulin-dependent diabetes mellitus) for Type 2 no longer used?
A
Patients with advanced Type 2 DM will require insulin; classification on aetiology instead of treatment now.
4
Q
What are the typical signs and symptoms of DM common to both Type 1 & Type 2?
A
- Glycosuria; glucose in urine
- Polyuria; increased frequency/volume of urination
- Polydipsia (thirst)
- Fatigue & malaise (lack of energy/discomfort/unease; body unable to use glucose)
- Blurred vision (changes in the refractive index in the lens)
- Infections e.g. candidiasis (sugar in urine attractive environment for bacteria/fungus)
5
Q
How does DM cause glycosuria and subsequently polyuria?
A
- Glucose normally totally reabsorbed in renal tubule in normal glomerular filtrate
- If plasma glucose elevated, amount of glucose in glomerular filtrate exceeds capacity for reabsorption; some glucose is left in the urine (glycosuria)
- Glucose in urine increases urinary osmotic pressure = decreased renal water absorption
- Osmotic diuresis follows where more water stays in the urine with the glucose, resulting in polyuria (excessive urine production)
6
Q
How does DM lead to polydipsia (thirst)?
A
Polyuria (excessive urine production) from osmotic diuresis leads to dehydration (fall in blood volume) and increased plasma osmolality (due to hyperglycaemia/less water reabsorption) leads to polydipsia (thirst).
7
Q
What are the signs & symptoms unique to Type 1 DM?
A
- Weight loss; breakdown of protein/fats due to lack of insulin
- Ketoacidosis (symptoms include nausea & vomiting, acetone breath ‘pear drops’)
8
Q
What are the signs & symptoms unique to Type 2 DM?
A
- Secondary complications
- Altered mental status (lack of glucose availability/usage in the CNS)
9
Q
Why do Type 2 DM patients commonly present with secondary complications?
A
Type 2 is slow in onset and many patients are asymptomatic, remaining undiagnosed for prolonged periods of time.
10
Q
What are the normal fasting and random blood glucose levels?
A
- Fasting
11
Q
How is DM diagnosed?
A
If patient presents with signs & symptoms and one positive results from the following:
- Fasting ≥ 7.0 mmol/L
- Random ≥ 11.1 mmol/L
- OGTT ≥ 11.1 mmol/L
- HbA1c > 48 mmol/mol (or 6.5%)
12
Q
What does OGTT stand for and what does it entail?
A
- Oral glucose tolerance test
- When patient consumes 75g glucose and plasma glucose concentration is measured 2hrs after; positive for DM if ≥ 11.1 mmol/L
13
Q
What is HbA1c a measure of and what are the normal ranges?
A
- Glycated/glycosylated haemoglobin (attachment of glucose to haemoglobin)
- Normal range: 20 - 42 mmol/mol, 4.0 - 6.0%
14
Q
What are the advantages of the HbA1c test and why?
A
- Gives indicator of plasma glucose levels of the prior 2-3 months; long term control
- As RBDs have a lifespan of 120 days; Hb being found in RBDs
15
Q
If the patient is asymptomatic, can they still be diagnosed with DM?
A
If two glucose tests have values exceeding the norm then a positive diagnosis of DM can be made; not all patients with Type 2 present with signs & symptoms (can be at earlier stage of DM)
16
Q
What is ‘pre-diabetes’ and what is the treatment for it?
A
- Mildly impaired glucose tolerance/impaired fasting glycaemia
- Fasting ≥ 6.1 but
17
Q
What is Type 1 DM?
A
Autoimmune condition; body develops autoantibodies and attacks self, resulting in progressive destruction of β-cells where 80-85% destruction = Type 1 DM. Other islet cells not affected.
18
Q
How does Type 1 DM come about and when does onset occur?
A
- Susceptibility genes & environmental triggers e.g. viruses, toxins
- Onset usually
19
Q
What is the 4 Ts campaign for T1DM?
A
- Toilet (polyruia)
- Thirsty (polydipsia
- Tired (fatigue & malaise)
- Thinner (weight loss)
Simple way for parents/carers to look out for onset of T1DM.
20
Q
Is T1DM rapid or slow onset and what does it mean for secondary complications?
A
- Rapid onset (pathophysiological changes [destruction of β cells] occur much earlier)
- Resulting in no secondary complications at diagnosis; doesn’t go untreated/unseen for time
21
Q
How is T1DM treated?
A
- Exogenous insulin (replace insulin that would have been made by β-cells)
- Regular exercise
- Healthy diet
22
Q
What is T2DM?
A
Relative insulin deficiency (impaired β-cell function) and/or insulin resistance (decreased sensitivity to recognise insulin, fewer insulin receptors, impaired insulin signalling pathways)
23
Q
How much of the UK population has T1DM compared to T2DM?
A
- T1DM; 0.6%
- T2Dm; 5.4% (many undiagnosed)
24
Q
What is the onset of T2DM and how this changed?
A
- > 40 years
- Gradual onset
- Used to be associated with middle-age, but sedentary lifestyle/greater calorific intake = younger T2DM onset
25
Who is more at risk of developing T2DM?
> 25 years African/Caribbean/South Asian (India/Pakistan/Bangladesh) more prone for T2DM akin to CVD/obesity
26
What are the risk factors of T2DM?
- Susceptibility genes & environmental triggers
- Reduced physical activity
- Increased calorie consumption
27
What is the 'Measure Up' campaign?
Campaign to highlight the link between T2DM risk and a large waist circumference (M: 37", F: 31.5")
28
How often are secondary complications present in T2DM?
25% of patients at time of diagnosis, usually overweight.
29
Are ketones present in T1DM/T2DM?
- T1DM; yes, tendency to ketosis
| - T2DM; no
30
How is T2DM managed across the patient populace?
10 - 20%; Diet
| 80 - 90%; Drugs (20% of these requiring insulin w/advanced T2DM)
31
What are the secondary causes of DM in the endocrine system?
What links them?
- Cushing's syndrome; excess cortisol
- Acromegaly; excess growth hormone
- Phaeochromocytoma; tumour cells of the adrenal medulla lead to excess adrenaline
(Counter-regulatory hormones to insulin, resulting in hyperglycaemia)
32
What are the secondary causes of DM with relation to pancreatic disease? Why is this so?
- Chronic pancreatitis
- Surgery
- Cystic firbrosis
- Tumour
Contribute to loss of β-cell function.
33
What are the secondary causes of DM with relation to genetic disorders?
- Down's syndrome
| - Prader-Willi
34
What drugs can lead to DM and why?
- Steroids
- Beta-blockers
- Diuretics
Can lead to imbalances in glucose/lipid metabolism leading to drug-induced DM.
35
What are the aims of management for DM (1 & 2)?
- Alleviate symptoms (thirst, polyuria, tiredness)
- Normalise metabolic parameters (glucose, lipids etc. back to normal level)
- Improve quality of life
- Educate (establish concordance)
- Prevent long-term/secondary complications (micro/macrovascular)
36
What diet should DM patients follow?
- Regular meals (don't skip to avoid fluctuations in blood glucose)
- Low in fat/sugar/salt
- High in fibre/complex CHOs (low glycaemic index)
- 5 A Day fruit & veg
37
What lifestyle advice should DM patients follow?
- Alcohol awareness (
38
Why is alcohol awareness important for DM patients?
Warning signs of hypoglycaemia can be dampened w/alcohol
39
Why should diabetics exercise and stop smoking?
Exercise; improves insulin sensitivity/usage + weight loss and reduce CVD risk; smoking.
40
Which patients are treated with insulin?
- T1DM
| - T2DM with inadequate control with drugs/in pregnancy
41
What are the different sources of insulin?
- Animal (porcine/bovine)
| - Human (semi-synthetic; enzymatically modified porcine insulin, recombinant via e.coli/yeast)
42
How is insulin classified, what are the groups and how long do they take to act/last?
Via onset and duration of action:
- Short-acting (within 15-30 minutes, last for 2 hours)
- Intermediate-acting (peaks at 2 hours, lasts 6-8, -12 hours)
- Long-acting (no peak, lasts 12-24 hours)
- Biphasic/pre-mixed
43
What characterises short-acting insulin and what are some analogues?
- Soluble
| - (Rapid: Lispro, Aspart)
44
Give an example of intermediate-acting insulin.
Isophane (complexed with protamine, NPH)
45
What characterises long-acting insulin and what are some analogues?
- Insulin zinc suspension
| - Glargine, Detemir
46
What is biphasic/pre-mixed insulin composed of?
Mix of short and intermediate-acting insulins
47
When is SC insulin preferred and how is it administered? What other advice is given?
- Usual route, convenient
- Needles w/syringe, or pre-loaded cartridge pen
- Injection site: fatty areas e.g. top of arms, lower abdomen, tops of thighs, back/tops of buttocks
- Rotate location of injection
48
How do subcutaneous infusion pumps work?
Catheter goes S.C., insulin delivered via pump and can adjust levels with/before meals etc.
49
When is insulin given I.V.?
Fine control in serious illnesses/emergency situations:
- diabetic ketoacidosis
- surgery (peri-operative; pre, intra, post)
50
What is Afrezza and what are its benefits?
- Inhalable insulin device
- Phase III trials
- Needle not requied
- Respiratory complications?
51
What is islet transplantation and what does it entail?
- Cell transplantation therapy of islet cells from cadavers to patients
- Requirement for immunosuppressoin to prevent rejection
52
What is the issue with islet transplantation but what are the advantages?
- Patient often need more than one (95 transplants in 65 patients)
- But usually result in insulin independence in T1DM
53
What acute complications can arise from T1DM?
- Hypoglycamia
| - Diabetic ketoacidosis
54
When is a patient considered hypoglycaemic and when do symptoms start to present?
-
55
How can hypoglycaemia develop in T1DM?
- Insulin overdose
- Excessive exericse
- Insufficient CHO intake relative to insulin injected
56
How can hypoglycaemia develop in T2DM?
- Sulphonylureas (elderly)
- Hepatic/renal disease
- Some drugs
57
What are the symptoms of hypoglycaemia and why do these occur?
- Palpitations
- Tremors
- Sweating
- Anxiety
Due to counter-regulatory activity of SNS; adrenoceptors activated due to low blood glucose.
58
What are the symptoms of hypoglycaemia associated with glucose deficiency of the brain? (neuroglycopaenia)
- Loss of concentration
- Slurred speech
- Behaviour/mood changes
- Seizures
- Loss of conciouness
59
What is the treatment for hypoglycaemia (low blood glucose) in a conscious patient?
Sugary drink/food e.g:
- Sugary tea
- Lucozade (not Coke etc.; artificial sweeteners)
- Sugar tablets e.g. Dextrose
- Glucogel; 40% w/v detrose gel (can be swallowed or absorbed buccally)
10-15 minutes for recovery then give snack e.g. biscuits/toast for sustained CHOs (after rapid-glucose; actions of insulin are still ongoing need to compensate)
60
What is the treatment for hypoglycaemia in an unconscious patient?
EMERGENCY
- Glucose IV (20 or 10%)
- Glucagon (IM, IV or SC); can be given by rando
61
Why can glucagon not be given for hypoglycaemia (unconcious) if patient has consumed alcohol?
Glucagon's actions are on the liver; alcohol impairs liver function (metabolised there)
62
What is diabetic ketoacidosis?
Hyperglycaemia & metabolic acidosis (ketosis)
63
How does diabetic ketoacidosis occur?
- Omission/reduction in insulin dose
- Illness/infection
- Emotional upset (especially in adolescence)
- Menstruation/pregnancy ketosis
(additional stresses on the body; use up insulin more)
- Rare syndromes of insulin resistance more prevalent in T2DM
64
What is ketogenesis?
Synthesis of ketone bodies by the liver, from fatty acid breakdown products.
65
How does ketogenesis occur?
Excess acetyl CoA from fatty acid chains combine to form acetoacetate, which is transformed to β-hydroxybutyrate & acetone; ketone bodies.
66
How does ketosis (excess ketones) occur?
- Starvation/T1DM
- Lack of glucose; greater metabolism of fatty acids broken down for energy
- Means more Acetyl CoA and ketones (acetoacetate, β-hydroxybutyrate & acetone) in blood
67
What does ketosis lead to?
Accumulation of excess ketones leads to metabolic acidosis (decrease in blood pH); acetoacetate and β-hydroxybutyrate are acidic.
68
How does insulin relate to hepatic ketogenesis?
- Insulin inhibits this process
| - Glucagon stimulates it
69
What are the consequences of the loss of insulin action on muscle/adipose tissue/the liver?
Muscle; protein breakdown to AAs (instead of building)
Adipose; lipolysis (instead of genesis) to fatty acids + glycerol
Liver: gluconeogenesis, glycogen breakdown
70
How are AAs and fatty acids/glycerol utilised after protein breakdown/lipolysis?
They become substrates for gluconeogenesis in the liver, leading to hyperglycaemia (leading to osmotic diuresis).
71
What are the signs & symptoms of metabolic acidosis?
- Nausea & vomiting
| - Breathlessness (patient tries to correct acid/base imbalance; respiratory compensation)
72
What happens if osmotic diuresis is not treated?
```
Dehydration leads to:
- peripheral circulatory failure
- renal failure (decreased blood supply to kidneys)
- low cerebral blood flow
>>>Death
```
73
What happens if metabolic acidosis isn't treated?
- CNS depression
- Diabetic coma
>>> Death
74
How is diabetic ketoacidosis treated?
Urgent hospital admission (10-20% mortality rate):
- Insulin IV infusion (suppresses ketogenesis, reduces blood glucose, corrects electrolyte imbalance)
- Replacement of fluids, electrolytes (Sodium chloride 0.9%, saline, may need KCl, glucose 10%)
- Treat underlying cause
75
How is glycaemic control monitored?
- Urine testing; ketones, glucose (dipstick for diagnosis/referral - pink)
- Blood glucose testing; mainstay monitoring by patient
- HbA1c test indicator of glycaemic control of last 2-3 months (half life of RBCs which last 120 days)
