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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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1
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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
What is the presentation of type 1 diabetes?
Polyuria Polydipsia Fatigue Weight loss
26
What condition will the majority of T1DM patients present with?
Diabetes ketoacidosis
27
What happens in DKA in response to absence of insulin?
- 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
28
In terms of DKA maintenance treatment for adults, when is insulin stopped/reduced?
When ketone levels drop below 3 mmol/L
29
If ketone levels are above 3 mmol/L in DKA patients, what needs to be done?
Give more glucose or give more insulin
30
In DKA patients, what happens when patient is ready to eat and drink?
Let patient eat, then administer insulin SC (30 mins before stopping insulin infusion) then stop glucose IV then stop insulin infusion
31
What are the fluid restrictions for children and young people with DKA?
less than 10kg - 2ml/kg/hr 10-40kg 1ml/kg/hr >40kg - 40ml/hr
32
When can you consider moving adult DKA patient to maintenance fluid?
cBG < 15 mmol/L
33
What time period does replacement of fluid deficit take place over in children?
48 hours (unlike adults which is 24 hrs)
34
When is SC insulin started in management of DKA in children?
When cBG <14mmol/L, ketones <3mmol/L, resolved acidosis, oral fluids tolerated
35
What is the first line treatment for T1DM in adults and children?
Basal bolus insulin
36
Which type of insulin doesn't have a peak?
Long-acting as it mirrors basal insulin output in non-diabetics
37
Which type of insulin has a duration of 20-24 hours?
Long-acting
38
What is the duration of intermediate acting insulin?
12-18 hours
39
Which has a longer duration short-acting insulin or rapid acting?
short acting - duration 8-10 hrs, whereas rapid acting is 4-6 hrs
40
What does DAFNE stand for?
Dose adjustment for normal eating
41
Which type of insulin regime is accompanied by carb counting?
Basal bolus
42
Which type of insulin dose is calculated on potion size and carb content?
Short-acting
43
What is meant by biphasic insulin?
Contains a short or rapid acting insulin in a protamine suspension
44
What is the onset of biphasic insulin?
half an hour
45
Biphasic insulin is good for which groups of patients?
Those that are not able to carb count, those who struggle with multiple injections
46
Is the use of biphasic insulin regime more common for T1DM or T2DM?
T2DM
47
If someone in hospital is hypoglycaemic, what are they given?
If conscious, give dextrose tabs or glucogel. If unconscious, glucagon IM followed by 10% glucose 100ml/hr
48
What is the difference between type 1 and type 2 diabetes?
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
Who is at risk of T2DM?
``` Genetics Ethnicity Increased age Females Obesity Smokers ```
50
How do T2DM patients present?
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
A fasting plasma glucose of greater than _____ and a HbA1c is greater than or equal to ______ is indicative of diabetes
7 mmol/L | 48 mmol/mol
52
What is pre-diabetes defined as?
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
How do we treat T2DM?
Diet Exercise Drugs
54
What are some food recommendations for T2DM patients?
High-fibre Low fat dairy products Oily fish Avoid saturated and trans fatty acids, food aimed at diabetics
55
What advice on exercise can be given to T2DM patients?
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
How do the sulfonylureas work?
Directly stimulate insulin release from B-cells in pancreas
57
Name a sulfonylurea
Gliclazide
58
How do thiazolidinediones work?
Increase insulin sensitivity | Act on liver to decrease glucose production
59
Name a thiazolidinedione
Pioglitazone
60
How do biguanides work?
Inhibit gluconeogenesis in the liver resulting in lower hepatic glucose production
61
Name a biguanide
Metformin
62
How do alpha glucosidase inhibitors work?
Inhibit the enzymes that convert complex polysaccharide carbohydrates into monosaccharides
63
How do GLP1 agonists work?
Stimulate insulin release and suppress glucagon secretion
64
How do DPP4 inhibitors work?
Block the rapid degradation of GLP1
65
Name a GLP1 agonist
Dulaglutide
66
Name a DPP4 inhibitor
Sitagliptin
67
How do SGLT2 inhibitors work?
Block active transport of glucose from the glomerular filtrate
68
Name a SGLT2 inhibitor
Empagliflozin
69
Which class of antidiabetics require good renal function to work?
SGLT2 inhibitors
70
What is HbA1c?
The amount of glucose attached to Hb in RBCs
71
HbA1c is a good measure of average blood glucose for the last ___ to ___ months
3 to 6
72
What is the target HbA1c for a T2DM patient using lifestyle/diet to control diabetes in addition to one drug?
48 mmol/ml
73
What is the target HbA1c for a T2DM patient using lifestyle/diet to control diabetes and a drug associated with hypos or 2+ drugs?
53 mmol/ml
74
How often is HbA1c measured if HbA1c or therapy is changing?
3-6 monthly
75
What is the first line drug treatment for T2DM patients?
Metformin
76
Give a disadvantage for use of metformin in relation to tx regimen
Short half-life so TDS frequency
77
Give 3 advantages of using metformin as tx for T2DM
Cheap Weight neutral Low risk of hypos
78
What is the advantage of using SU rather than metformin?
Fewer GI side effects than metformin
79
What is the difference between proliferative and non-proliferative retinopathy?
In proliferative, new vessels form and leak blood into vitreous, blocking light entry. Whereas, non-proliferative no new vessels form
80
Is retinopathy reversible or irreversible?
Irreversible - leads to blindness
81
How is retinopathy caused?
High blood sugar leads to micro-thrombi in the retina which block the capillaries
82
How is neuropathy caused?
High blood sugars lead to reduced blood flow and death of nerves
83
Name a complication of neuropathy
Diabetic foot ulcers
84
What is Capsaicin used to treat?
Diabetic neuropathy
85
How is nephropathy caused in diabetes?
Nephrons become thickened and scarred so less effective
86
Name so macrovascular complications of T2DM
High insulin levels are associated with atherosclerosis which results in MI, stroke, vascular disease
87
What can be done to control cholesterol in order to prevent macrovascular complications of diabetes?
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
What is given to patients to control BP in order to prevent macrovascular complications?
CCB if African or Caribbean family origin | ACEI for all other patients
89
What are the signs and symptoms of cerebral oedema and what is it a complication of?
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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