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The Patient (Y3-1) > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is the blood glucose reading of a hypoglycaemic patient?

A

<2.5 mmol/L

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2
Q

What is the blood glucose reading of a hyperglycaemic patient?

A

> 10 mmol/L sustained

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3
Q

What is healthy fasting normoglycaemia defined as?

A

3-5 mmol/L

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4
Q

What is healthy post-prandial normoglycaemia defined as?

A

7-8 mmol/L

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5
Q

Describe the homeostasis of hyperglycaemia

A

Rise in blood sugar due to food intake or endogenous glucose produced in liver.
Insulin released from B-cells in pancreas.
Acts on a number of different tissues including liver, muscle etc.
Blood glucose lowered - negative feedback loop

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6
Q

Describe the homeostasis of hypoglycaemia

A

Deliberate or overnight fasting leads to low blood glucose.
Glucagon released from the a-cells of the pancreas
Leads to endogenous glucose production by liver which will lead to rise in blood sugar

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7
Q

Insulin is metabolised by the kidney. True or false?

A

False - metabolised by the liver

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8
Q

What is the function of the the pancreas?

A

99% of the function is in production of enzymes to digest food. Other 1% lies with islets of langerhans which have 5 different cell types.

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9
Q

What are the 5 cell types in the islets of langerhans and what do they release?

A 
a - release glucagon
B - release insulin
delta - release somatostatin
epison - release ghrelin
PP - release pancreatic polypeptide
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10
Q

What happens in the B-cells when glucose enters the blood upon intake of food?

A

Glucose uptake by selective glucose transporter on B-cells
Cells undergo electrical change as a result:
K-channels close
Cell depolarises
Ca2+ enters the cell
Insulin is released

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11
Q

What happens as a consequence of digestion and presence of sugar in the upper intestine?

A

Detection of sugar by endocrine cells in the gut results in the release of GLP-1 which travels to B-cells and upon encounter of GLP-1 receptor, it activates them which results in cell signalling and insulin release

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12
Q

How does insulin lower blood sugar?

A

Insulin released from B-cells -? binds to insulin receptors in tissues -> configuration change -> endogenous kinase activity switched on -> phosphorylation of receptors downstream -> transport protein on -> more glucose transported across membrane
More transporters placed on membrane -> increased efficiency of glucose uptake

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13
Q

How does insulin promote hypoglycaemia?

A 
Increases the transport of glucose into cells
Converts glucose to glycogen
Decreases glycogen breakdown
Increases fat stores
Increases protein production
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14
Q

Describe the homeostasis of hyperglycaemia

A

Rise in blood sugar due to food intake or endogenous glucose produced in liver.
Insulin released from B-cells in pancreas.
Acts on a number of different tissues including liver, muscle etc.
Blood glucose lowered - negative feedback loop

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15
Q

Describe the homeostasis of hypoglycaemia

A

Deliberate or overnight fasting leads to low blood glucose.
Glucagon released from the a-cells of the pancreas
Leads to endogenous glucose production by liver which will lead to rise in blood sugar

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16
Q

Insulin is metabolised by the kidney. True or false?

A

False - metabolised by the liver

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17
Q

What is the function of the the pancreas?

A

99% of the function is in production of enzymes to digest food. Other 1% lies with islets of langerhans which have 5 different cell types.

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18
Q

What are the 5 cell types in the islets of langerhans and what do they release?

A 
a - release glucagon
B - release insulin
delta - release somatostatin
epison - release ghrelin
PP - release pancreatic polypeptide
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19
Q

What happens in the B-cells when glucose enters the blood upon intake of food?

A

Glucose uptake by selective glucose transporter on B-cells
Cells undergo electrical change as a result:
K-channels close
Cell depolarises
Ca2+ enters the cell
Insulin is released

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20
Q

What happens as a consequence of digestion and presence of sugar in the upper intestine?

A

Detection of sugar by endocrine cells in the gut results in the release of GLP-1 which travels to B-cells and upon encounter of GLP-1 receptor, it activates them which results in cell signalling and insulin release

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21
Q

How does insulin lower blood sugar?

A

Insulin released from B-cells -? binds to insulin receptors in tissues -> configuration change -> endogenous kinase activity switched on -> phosphorylation of receptors downstream -> transport protein on -> more glucose transported across membrane
More transporters placed on membrane -> increased efficiency of glucose uptake

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22
Q

How does insulin promote hypoglycaemia?

A 
Increases the transport of glucose into cells
Converts glucose to glycogen
Decreases glycogen breakdown
Increases fat stores
Increases protein production
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23
Q

What is used as first-aid treatment for severe hypoglycaemia?

A

Glucagon injection when oral glucose not possible or desired

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24
Q

What is diazoxide therapy used for?

A

Hypoglycaemia - it reverses the action of glucose on B-cells and therefore induces hyperglycaemia

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25
Q

What is the presentation of type 1 diabetes?

A

Polyuria
Polydipsia
Fatigue
Weight loss

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26
Q

What condition will the majority of T1DM patients present with?

A

Diabetes ketoacidosis

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27
Q

What happens in DKA in response to absence of insulin?

A
  • Increased glycogenolysis and gluconeogenesis plus reduced uptake of glucose by tissues
  • Increased urine output (to remove glucose)
  • Suppressed lipolysis -> accumulation of free fatty acids -> ketones
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28
Q

In terms of DKA maintenance treatment for adults, when is insulin stopped/reduced?

A

When ketone levels drop below 3 mmol/L

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29
Q

If ketone levels are above 3 mmol/L in DKA patients, what needs to be done?

A

Give more glucose or give more insulin

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30
Q

In DKA patients, what happens when patient is ready to eat and drink?

A

Let patient eat, then administer insulin SC (30 mins before stopping insulin infusion) then stop glucose IV then stop insulin infusion

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31
Q

What are the fluid restrictions for children and young people with DKA?

A

less than 10kg - 2ml/kg/hr
10-40kg 1ml/kg/hr
>40kg - 40ml/hr

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32
Q

When can you consider moving adult DKA patient to maintenance fluid?

A

cBG < 15 mmol/L

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33
Q

What time period does replacement of fluid deficit take place over in children?

A

48 hours (unlike adults which is 24 hrs)

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34
Q

When is SC insulin started in management of DKA in children?

A

When cBG <14mmol/L, ketones <3mmol/L, resolved acidosis, oral fluids tolerated

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35
Q

What is the first line treatment for T1DM in adults and children?

A

Basal bolus insulin

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36
Q

Which type of insulin doesn’t have a peak?

A

Long-acting as it mirrors basal insulin output in non-diabetics

37
Q

Which type of insulin has a duration of 20-24 hours?

A

Long-acting

38
Q

What is the duration of intermediate acting insulin?

A

12-18 hours

39
Q

Which has a longer duration short-acting insulin or rapid acting?

A

short acting - duration 8-10 hrs, whereas rapid acting is 4-6 hrs

40
Q

What does DAFNE stand for?

A

Dose adjustment for normal eating

41
Q

Which type of insulin regime is accompanied by carb counting?

A

Basal bolus

42
Q

Which type of insulin dose is calculated on potion size and carb content?

A

Short-acting

43
Q

What is meant by biphasic insulin?

A

Contains a short or rapid acting insulin in a protamine suspension

44
Q

What is the onset of biphasic insulin?

A

half an hour

45
Q

Biphasic insulin is good for which groups of patients?

A

Those that are not able to carb count, those who struggle with multiple injections

46
Q

Is the use of biphasic insulin regime more common for T1DM or T2DM?

A

T2DM

47
Q

If someone in hospital is hypoglycaemic, what are they given?

A

If conscious, give dextrose tabs or glucogel. If unconscious, glucagon IM followed by 10% glucose 100ml/hr

48
Q

What is the difference between type 1 and type 2 diabetes?

A

In type 1, patients don’t produce insulin. In type 2, patients are resistant to insulin or there is impairment of insulin secretion relative to requirements

49
Q

Who is at risk of T2DM?

A 
Genetics
Ethnicity
Increased age
Females
Obesity
Smokers
50
Q

How do T2DM patients present?

A

Usually asymptomatic - picked up by health monitoring at risk groups or if patients present with complications.
Some patients present with increased thirst, urination and blurred vision

51
Q

A fasting plasma glucose of greater than _____ and a HbA1c is greater than or equal to ______ is indicative of diabetes

A

7 mmol/L

48 mmol/mol

52
Q

What is pre-diabetes defined as?

A

Fasting plasma glucose of less than 7 mmol/L
2-hour venous plasma glucose (after ingestion of 75g oral glucose load) of 7.8 mmol/L or greater, and less than 11.1 mmol/L

53
Q

How do we treat T2DM?

A

Diet
Exercise
Drugs

54
Q

What are some food recommendations for T2DM patients?

A

High-fibre
Low fat dairy products
Oily fish
Avoid saturated and trans fatty acids, food aimed at diabetics

55
Q

What advice on exercise can be given to T2DM patients?

A

At least 150 mins a week of moderate activity or 75 mins a week of intense activity plus muscle strengthening activity twice a week

56
Q

How do the sulfonylureas work?

A

Directly stimulate insulin release from B-cells in pancreas

57
Q

Name a sulfonylurea

A

Gliclazide

58
Q

How do thiazolidinediones work?

A

Increase insulin sensitivity

Act on liver to decrease glucose production

59
Q

Name a thiazolidinedione

A

Pioglitazone

60
Q

How do biguanides work?

A

Inhibit gluconeogenesis in the liver resulting in lower hepatic glucose production

61
Q

Name a biguanide

A

Metformin

62
Q

How do alpha glucosidase inhibitors work?

A

Inhibit the enzymes that convert complex polysaccharide carbohydrates into monosaccharides

63
Q

How do GLP1 agonists work?

A

Stimulate insulin release and suppress glucagon secretion

64
Q

How do DPP4 inhibitors work?

A

Block the rapid degradation of GLP1

65
Q

Name a GLP1 agonist

A

Dulaglutide

66
Q

Name a DPP4 inhibitor

A

Sitagliptin

67
Q

How do SGLT2 inhibitors work?

A

Block active transport of glucose from the glomerular filtrate

68
Q

Name a SGLT2 inhibitor

A

Empagliflozin

69
Q

Which class of antidiabetics require good renal function to work?

A

SGLT2 inhibitors

70
Q

What is HbA1c?

A

The amount of glucose attached to Hb in RBCs

71
Q

HbA1c is a good measure of average blood glucose for the last ___ to ___ months

A

3 to 6

72
Q

What is the target HbA1c for a T2DM patient using lifestyle/diet to control diabetes in addition to one drug?

A

48 mmol/ml

73
Q

What is the target HbA1c for a T2DM patient using lifestyle/diet to control diabetes and a drug associated with hypos or 2+ drugs?

A

53 mmol/ml

74
Q

How often is HbA1c measured if HbA1c or therapy is changing?

A

3-6 monthly

75
Q

What is the first line drug treatment for T2DM patients?

A

Metformin

76
Q

Give a disadvantage for use of metformin in relation to tx regimen

A

Short half-life so TDS frequency

77
Q

Give 3 advantages of using metformin as tx for T2DM

A

Cheap
Weight neutral
Low risk of hypos

78
Q

What is the advantage of using SU rather than metformin?

A

Fewer GI side effects than metformin

79
Q

What is the difference between proliferative and non-proliferative retinopathy?

A

In proliferative, new vessels form and leak blood into vitreous, blocking light entry. Whereas, non-proliferative no new vessels form

80
Q

Is retinopathy reversible or irreversible?

A

Irreversible - leads to blindness

81
Q

How is retinopathy caused?

A

High blood sugar leads to micro-thrombi in the retina which block the capillaries

82
Q

How is neuropathy caused?

A

High blood sugars lead to reduced blood flow and death of nerves

83
Q

Name a complication of neuropathy

A

Diabetic foot ulcers

84
Q

What is Capsaicin used to treat?

A

Diabetic neuropathy

85
Q

How is nephropathy caused in diabetes?

A

Nephrons become thickened and scarred so less effective

86
Q

Name so macrovascular complications of T2DM

A

High insulin levels are associated with atherosclerosis which results in MI, stroke, vascular disease

87
Q

What can be done to control cholesterol in order to prevent macrovascular complications of diabetes?

A

Offer 20mg atorvastatin to T1DM patients who are older than 40 yrs or have had diabetes for more than 10 years or have established nephropathy or other CVDs.
Offer it to T2DM patients who have a 10% risk or more of developing CVD in 10 yrs using QRISK

88
Q

What is given to patients to control BP in order to prevent macrovascular complications?

A

CCB if African or Caribbean family origin

ACEI for all other patients

89
Q

What are the signs and symptoms of cerebral oedema and what is it a complication of?

A

Complication of DKA - caused by rapid movement of water into brain cells.
Signs and symptoms: bradycardia, altered mental state, dilated pupils

The Patient (Y3-1) (8 decks)

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