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RED - Endocrine Pharmacology & Therapeutics > E3 - Diabetes 1 > Flashcards

E3 - Diabetes 1 Flashcards

1
Q

What is diabetes mellitus and what is it characterised?

A
  • Chronic metabolic disorder

- Characterised by hyperglycaemia (high blood glucose)

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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.
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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.

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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)
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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)
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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).

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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’)
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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)

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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.

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10
Q

What are the normal fasting and random blood glucose levels?

A
  • Fasting
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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%)
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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
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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%
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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
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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)

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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
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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.

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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
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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.

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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
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21
Q

How is T1DM treated?

A
  • Exogenous insulin (replace insulin that would have been made by β-cells)
  • Regular exercise
  • Healthy diet
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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)

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23
Q

How much of the UK population has T1DM compared to T2DM?

A
  • T1DM; 0.6%

- T2Dm; 5.4% (many undiagnosed)

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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
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25
Q

Who is more at risk of developing T2DM?

A

> 25 years African/Caribbean/South Asian (India/Pakistan/Bangladesh) more prone for T2DM akin to CVD/obesity

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26
Q

What are the risk factors of T2DM?

A
  • Susceptibility genes & environmental triggers
  • Reduced physical activity
  • Increased calorie consumption
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27
Q

What is the ‘Measure Up’ campaign?

A

Campaign to highlight the link between T2DM risk and a large waist circumference (M: 37”, F: 31.5”)

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28
Q

How often are secondary complications present in T2DM?

A

25% of patients at time of diagnosis, usually overweight.

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29
Q

Are ketones present in T1DM/T2DM?

A
  • T1DM; yes, tendency to ketosis

- T2DM; no

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30
Q

How is T2DM managed across the patient populace?

A

10 - 20%; Diet

80 - 90%; Drugs (20% of these requiring insulin w/advanced T2DM)

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31
Q

What are the secondary causes of DM in the endocrine system?

What links them?

A
  • 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
Q

What are the secondary causes of DM with relation to pancreatic disease? Why is this so?

A
  • Chronic pancreatitis
  • Surgery
  • Cystic firbrosis
  • Tumour

Contribute to loss of β-cell function.

33
Q

What are the secondary causes of DM with relation to genetic disorders?

A
  • Down’s syndrome

- Prader-Willi

34
Q

What drugs can lead to DM and why?

A
  • Steroids
  • Beta-blockers
  • Diuretics

Can lead to imbalances in glucose/lipid metabolism leading to drug-induced DM.

35
Q

What are the aims of management for DM (1 & 2)?

A
  • 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
Q

What diet should DM patients follow?

A
  • 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
Q

What lifestyle advice should DM patients follow?

A
  • Alcohol awareness (
38
Q

Why is alcohol awareness important for DM patients?

A

Warning signs of hypoglycaemia can be dampened w/alcohol

39
Q

Why should diabetics exercise and stop smoking?

A

Exercise; improves insulin sensitivity/usage + weight loss and reduce CVD risk; smoking.

40
Q

Which patients are treated with insulin?

A
  • T1DM

- T2DM with inadequate control with drugs/in pregnancy

41
Q

What are the different sources of insulin?

A
  • Animal (porcine/bovine)

- Human (semi-synthetic; enzymatically modified porcine insulin, recombinant via e.coli/yeast)

42
Q

How is insulin classified, what are the groups and how long do they take to act/last?

A

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
Q

What characterises short-acting insulin and what are some analogues?

A
  • Soluble

- (Rapid: Lispro, Aspart)

44
Q

Give an example of intermediate-acting insulin.

A

Isophane (complexed with protamine, NPH)

45
Q

What characterises long-acting insulin and what are some analogues?

A
  • Insulin zinc suspension

- Glargine, Detemir

46
Q

What is biphasic/pre-mixed insulin composed of?

A

Mix of short and intermediate-acting insulins

47
Q

When is SC insulin preferred and how is it administered? What other advice is given?

A
  • 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
Q

How do subcutaneous infusion pumps work?

A

Catheter goes S.C., insulin delivered via pump and can adjust levels with/before meals etc.

49
Q

When is insulin given I.V.?

A

Fine control in serious illnesses/emergency situations:

  • diabetic ketoacidosis
  • surgery (peri-operative; pre, intra, post)
50
Q

What is Afrezza and what are its benefits?

A
  • Inhalable insulin device
  • Phase III trials
  • Needle not requied
  • Respiratory complications?
51
Q

What is islet transplantation and what does it entail?

A
  • Cell transplantation therapy of islet cells from cadavers to patients
  • Requirement for immunosuppressoin to prevent rejection
52
Q

What is the issue with islet transplantation but what are the advantages?

A
  • Patient often need more than one (95 transplants in 65 patients)
  • But usually result in insulin independence in T1DM
53
Q

What acute complications can arise from T1DM?

A
  • Hypoglycamia

- Diabetic ketoacidosis

54
Q

When is a patient considered hypoglycaemic and when do symptoms start to present?

A

-

55
Q

How can hypoglycaemia develop in T1DM?

A
  • Insulin overdose
  • Excessive exericse
  • Insufficient CHO intake relative to insulin injected
56
Q

How can hypoglycaemia develop in T2DM?

A
  • Sulphonylureas (elderly)
  • Hepatic/renal disease
  • Some drugs
57
Q

What are the symptoms of hypoglycaemia and why do these occur?

A
  • Palpitations
  • Tremors
  • Sweating
  • Anxiety

Due to counter-regulatory activity of SNS; adrenoceptors activated due to low blood glucose.

58
Q

What are the symptoms of hypoglycaemia associated with glucose deficiency of the brain? (neuroglycopaenia)

A
  • Loss of concentration
  • Slurred speech
  • Behaviour/mood changes
  • Seizures
  • Loss of conciouness
59
Q

What is the treatment for hypoglycaemia (low blood glucose) in a conscious patient?

A

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
Q

What is the treatment for hypoglycaemia in an unconscious patient?

A

EMERGENCY

  • Glucose IV (20 or 10%)
  • Glucagon (IM, IV or SC); can be given by rando
61
Q

Why can glucagon not be given for hypoglycaemia (unconcious) if patient has consumed alcohol?

A

Glucagon’s actions are on the liver; alcohol impairs liver function (metabolised there)

62
Q

What is diabetic ketoacidosis?

A

Hyperglycaemia & metabolic acidosis (ketosis)

63
Q

How does diabetic ketoacidosis occur?

A
  • 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
Q

What is ketogenesis?

A

Synthesis of ketone bodies by the liver, from fatty acid breakdown products.

65
Q

How does ketogenesis occur?

A

Excess acetyl CoA from fatty acid chains combine to form acetoacetate, which is transformed to β-hydroxybutyrate & acetone; ketone bodies.

66
Q

How does ketosis (excess ketones) occur?

A
  • 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
Q

What does ketosis lead to?

A

Accumulation of excess ketones leads to metabolic acidosis (decrease in blood pH); acetoacetate and β-hydroxybutyrate are acidic.

68
Q

How does insulin relate to hepatic ketogenesis?

A
  • Insulin inhibits this process

- Glucagon stimulates it

69
Q

What are the consequences of the loss of insulin action on muscle/adipose tissue/the liver?

A

Muscle; protein breakdown to AAs (instead of building)
Adipose; lipolysis (instead of genesis) to fatty acids + glycerol
Liver: gluconeogenesis, glycogen breakdown

70
Q

How are AAs and fatty acids/glycerol utilised after protein breakdown/lipolysis?

A

They become substrates for gluconeogenesis in the liver, leading to hyperglycaemia (leading to osmotic diuresis).

71
Q

What are the signs & symptoms of metabolic acidosis?

A
  • Nausea & vomiting

- Breathlessness (patient tries to correct acid/base imbalance; respiratory compensation)

72
Q

What happens if osmotic diuresis is not treated?

A 
Dehydration leads to:
- peripheral circulatory failure
- renal failure (decreased blood supply to kidneys)
- low cerebral blood flow
>>>Death
73
Q

What happens if metabolic acidosis isn’t treated?

A
  • CNS depression
  • Diabetic coma
    »> Death
74
Q

How is diabetic ketoacidosis treated?

A

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
Q

How is glycaemic control monitored?

A
  • 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)

RED - Endocrine Pharmacology & Therapeutics (7 decks)

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