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CEP > WEEK 4 > Flashcards

WEEK 4 Flashcards

1
Q

What is the glucose profile of a non-diabetic person?

A

around 6mmol/L, with peaks due to dawn phenomenon (increased cortisol levels) and evening meal (range 4-10mmol/L)

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2
Q

What is the glucose profile of a (type 1) diabetic person?

A

Much larger range with higher average levels (6-15mmol/L)

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3
Q

What is hyperglycaemia?

A

High blood glucose levels

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4
Q

What is hypoglycaemia?

A

Low blood glucose levels

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5
Q

What is the BG threshold for hypoglycaemia?

A

<4mmol/L (four is the floor)

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6
Q

What is the BG threshold to drive?

A

> 5mmol/L (five to drive)

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7
Q

What are the NICE targets for BG?

A

4-7 pre-meal
5-7 on waking
5-9 90 mins after meal

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8
Q

What is the BG threshold for ketone testing?

A

at or >15mmol/L

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9
Q

Define diabetes

A

A lifelong condition that causes a person’s blood sugar levels to become too high

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10
Q

What are the symptoms of diabetes?

A 
none
weight loss
tiredness
candidiasis (thrush)
abscess
polyuria (excessive urination)
blurred vision
coma
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11
Q

What is the HbA1c test?

A

Test for glycosylated haemoglobin that reflects previous 10 weeks of ambient circulating glucose (doesn’t require fasting)

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12
Q

What does low HbA1c mean?

A

Low BG levels

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13
Q

What does high HbA1c mean?

A

High BG levels

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14
Q

What is the threshold HbA1c level for diagnosing Diabetes Mellitus?

A

6.5% or 48mmol/L

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15
Q

What are two standard ways of measuring blood glucose levels and what are their thresholds for diagnosing DM?

A

Random glucose -> ≥11.1 mmol/L
Fasting glucose -> ≥7.0 mmol/L
(repeat if they exceed threshold with no diabetic symptoms)

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16
Q

What is the oral glucose tolerance test?

A

Gold standard test for DM

done in fasting state, measure glucose t=0, 75g glucose drink over 5 min period, wait 2 hours, measure glucose t=2 hrs

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17
Q

What are the threshold levels of the oral glucose tolerance test?

A

Impaired fasting glycaemia (t=0)=6.1-6.9mmol/L
Impaired glucose tolerance (t=2h)=7.8-11.1mmol/L
Diabetic fasting value (t=0)= ≥7.0mmol/L
Diabetic 2 hour value (t=2h)= ≥11.1mmol/L

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18
Q

What are three ways to remove glucose from the bloodstream?

A

Liver
Muscle
Fat

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19
Q

What is the process of glucose absorption from the bloodstream?

A

Insulin binds to insulin receptors on cell-surface, glucose channels open (GLUT), glucose enters cells

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20
Q

What is the role of insulin?

A

To move glucose out of the bloodstream into liver/muscle/fat for storage/building (decreases BG)

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21
Q

What are the major metabolic functions of insulin?

A

Maintains supply of glucose to tissues
Regulates metabolism in muscle
Promotes protein synthesis
Inhibits fat breakdown

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22
Q

Where is insulin produced and secreted?

A

Beta cells in the pancreas

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23
Q

What is Type 1 diabetes?

A

Where the body’s immune system attacks and destroys the cells producing insulin (Insulin deficiency)

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24
Q

What is Type 2 diabetes?

A

Where the body doesn’t produce enough insulin, or the body’s cells don’t react to it (Insulin resistance and partial deficiency)

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25
Q

What is gestational diabetes?

A

Occurs during pregnancy, where women cannot produce enough insulin to absorb such high levels of BG

26
Q

Characteristics of Type 1 diabetes

A 
absolute insulin deficiency
onset typically <40 yrs but can be any age
onset usually dramatic
family history less common
presence of ketones
requires insulin therapy
27
Q

What is the cause of Type 1 diabetes?

A

Insulitis-autoimmune condition where lymphocytes think insulin-producing beta cells are foreign, so destroy them

28
Q

What is the triglyceride process caused by a lack of insulin?

A

triglycerides->fatty acids(->TCA cycle)->acetoacetate(urine ketones)->beta-hydroxybutyrate(blood ketones)/acetone(smell of pear drops on breath)

29
Q

Characteristics of Type 2 diabetes

A

Insulin resistance and relative insulin deficiency
onset typically >40 yrs (now getting younger)
genetic predisposition
associated with obesity
insidious onset of symptoms
no ketones
doesn’t require insulin therapy but is used by 1/3rd of Pts

30
Q

What are the ‘3 steed of a diabetics chariot’?

A

Diet
Exercise
Insulin (medication)
=glucose control

31
Q

What are the two forms of giving insulin throughout the day?

A

Slow-acting 1/2 injections/day

Fast-acting injections for every meal

32
Q

How many capillary glucose testing (finger-prick) throughout the day?

A

4/6 times a day (before each meal, bed and driving)

33
Q

What other medications are used to lower glucose?

A

Tablets:
Insulin sensitisers=causes body to be less resistant
Insulin secretogogues=makes more insulin
Gut absorption=glucose moves out of blood into gut
Glucose excretion=causes glucose to be removed
Incretin breakdown inhibitors=incretin which is released after eating and augments insulin secretion via pancreatic beta cells, has inhibitors to it’s breakdown
Injection:
Incretin mimetic=substitute for incretin

34
Q

What are the three amigos of monitoring in diabetes?

A

High BG, BP and lipids

35
Q

Medication for BP

A

ACE inhibitors
Beta blockers
Calcium channel blockers
Diuretics

36
Q

Medication for lipids

A

Statins

Fibrates

37
Q

What are the two types of complications of diabetes?

A

Microvascular (retinopathy, nephropathy, neuropathy)
Macrovascular (heart disease, renal artery disease, peripheral vascular disease, stroke)
gangrene=both micro- and macrovascular

38
Q

How do you reduce complications?

A

control of glucose for prevention of small vessel disease, control of lifestyle/smoking/BP/cholesterol for prevention of large vessel disease

39
Q

Is insulin a hyper- or hypoglycaemic agent and what is its release process?

A

Hypoglycaemic
Glucose enters beta cells, metabolism causes increased intracellular ATP, decreased ATP-sensitive K+ channel activity, decreased K+ efflux (depolarisation), opens V-gated Ca2+ channels which causes secretion of vesicles containing insulin/insulin release can also be from enzyme regulation or incretins

40
Q

What is the profile of insulin release in normal people?

A

Biphasic

41
Q

What are the two phases of insulin release?

A 
1st phase (largest release) due to Ca2+ mechanism
2nd phase (smaller release) due to enzymatic release
42
Q

What phase of insulin release do people with Type 2 diabetes not have?

A

1st phase

43
Q

What phases of insulin release do people with Type 1 diabetes not have?

A

Both phases

44
Q

Where are insulin receptors found?

A

Liver, Muscle and Fat

45
Q

What is the process of insulin binding to the insulin receptor?

A

Phosphorylation of IRS (insulin receptor substrate) as a response of insulin binding
Enzyme activation and gene transcription causes increased glucose uptake (expression of GLUT-4) and glycogen synthesis

46
Q

What are the routes of administration of insulin and why?

A

has to be given parenterally: s.c.; i.m.; i.v. due to insulin half life being short (t1/2=5 mins)

47
Q

What are the complications of insulin therapy?

A

Hypoglycaemia
Allergy
Lipodystrophy

48
Q

What are the oral hypoglycaemic agents?

A 
Biguanides (Metformin)
Sulphonylureas
Thiazolidinediones
Drugs based on incretin actions
Acarbose
SGLT2 inhibitors
49
Q

What is an example of Biguanides and what is it’s mechanism?

A

Metformin
Decreased gluconeogenesis in the liver via activation of AMP-activated protein kinase, increased glucose uptake in muscles

50
Q

What are the side effects of Biguanides?

A

No hypoglycaemic propensity, no increased appetite, lactic acidosis (not as bad with Metformin)

51
Q

When is Metformin often used?

A

Obese diabetics->combination therapy

52
Q

What are examples of Sulponylureas (SU) and what is it’s mechanism?

A

Tolbutamide (short-acting)/Glibenclamide (long-acting)/Gliclazide
SU binds to SURs in beta cells (part of Katp channel), causes channel to close (similar effect to increased intracellular ATP), depolarisation, V-gated Ca2+ channels open, causes increased insulin secretion
2ndary effect of increased tissue sensitivity to insulin

53
Q

What are the side effects of SU drugs?

A

Hypoglycaemia, appetite stimulation (don’t use for obese), contraindicated in pregnancy/breastfeeding

54
Q

What is an example of Thiazolidinediones and what is it’s mechanism?

A

Pioglitazone
Binds to TF, affecting gene expression:
Primary action at adipose tissue=increased fatty acid uptake and lipogenesis (weight gain)
Secondary action of decrease plasma fatty acids=increased glucose uptake and decreased gluconeogenesis

55
Q

What are the side effects of Thiazolidinediones?

A

Liver toxicity and heart failure (due to fluid retention due to Na+ retention in the Kidney)

56
Q

What are incretins?

A

GI hormones (eg. GLP-1) which act on the pancreas to increase insulin and decrease glucagon

57
Q

What are two types of drugs based on incretin actions and what are their mechanisms?

A

1) Inhibitors of dipeptidyl peptidase-4 (DDP-4) which metabolises incretins
2) Glucagon-like peptide-1 (GLP-1) agonists

58
Q

What is the mechanism of Acarbose?

A

alpha-glucosidase inhibitor which decreases carbohydrate absorption due to decreased carbohydrate metabolism (used for obese diabetics)

59
Q

What are SGLT2 inhibitors, what is their mechanism (and give an example)?

A

Sodium-glucose transporter-2 inhibitors which act on the PCT of the kidney to increase glucose and Na+ loss (Canagliflozin)

60
Q

What are the side effects of SGLT2 inhibitors?

A

Peripheral vascular disease, ketoacidosis (increased acidity of the blood)

CEP (9 decks)

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