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Year 1 Medicine Newcastle > Case 5 > Flashcards

Case 5 Flashcards

1
Q

What is Type-1 diabetes characterised by

A

Insulin deficiency
Auto-immune condition
Destruction of ß-cells in pancreas

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2
Q

What is Type-2 diabetes characterised by

A

Insulin resistance
Associated with obesity
Most common in certain racial groups
Interplay between genes and environemtn

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3
Q

What is the mode of action fo insulin

A

Binds to the insulin receptor on the CSM
Intracellular cascade to translocate GLUT4 to the CSM
Glucose is transported into the cell through these transporters

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4
Q

How do you distinguish between Type-1 and 2 diabetes

A

Measure the insuling levels (type 1 is low 2 is high)

Send a blood sample to the lab that will test for antibodies

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5
Q

What is considered an abnormal blood glucose level and should be investigated further

A

Fasting >7mmol/L

Random measurement > 11.1 mmol/L

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6
Q

What would show up for Type 1 diabetics in urinalysis

A

Ketones in the urine

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7
Q

Who should be screened for type 2 diabetes

A 
Overweight individuals 
Vascular disease sufferers
Hypertension 
Over 40 
Previous gestational diabetes 
Pre-diabetic states
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8
Q

What is HbAC1

A

This is an indicator of how much glucose is in the blood as the maount fo glucose on its surface can be measured

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9
Q

What reading on HbAC1 is diagnostic of chronic hyperglycaemia

A

48mmol/mol

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10
Q

How does the impaired glucose tolerance drink work

A

It’s a drink containing 75% glucose

Blood tests are at 120 minutes and diagnosed as having ‘impaired glucose tolerance’ if blood glucose levels 7.8mmol/l

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11
Q

What level constitutes impaired fasting glycaemia

A

6.1mmol/L

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12
Q

What are typical diabetic symptoms

A 
Thirst
increased urination 
Tiredness 
Weight loss 
Blurred vision
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13
Q

How does Type 1 diabetes present differently to type 2

A

Much more acute rapid symptom onset
Generally young patients
Clear marked symptoms as opposed to mild symptoms
Mostly no family history
Most present as an emergency instead of complications

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14
Q

What is secondary diabetes

A

This is after medication, particularly steroids

Can also affect after pancreas conditions or rare endocrine conditions

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15
Q

Is diabetes attributed to one or many genes

A

It is described as polygenic as it can be attributed to many genes

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16
Q

What may there be a history of in Type 1 diabetes

A

Other autoimmune diseases such as thyroid disease or inflammatory bowel disease

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17
Q

What are examples of monogenic diabetes and how do these affect patients

A

Neonatal diabetes and Maturity Onset Diabetes of the Young (MODY)
Strong family history and onset before 25
Often diagnosed with Type 1 diabetes but don’t need to be treated with insulin in general

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18
Q

What are the risk factors for pregnant women of gestational diabetes

A

Overweight or obese
History of gestational diabetes
Large baby in previous pregnancies

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19
Q

When does gestational diabetes resolve

A

After delivery of the baby

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20
Q

How does gestational diabetes occur

A

Some hormones released during pregnancy interfere and cause insulin resistance

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21
Q

What cardiovascular problems can diabetes lead to

A 
Increased risk of 
Stroke
CVD
Hypertension 
PVD
Absent foot pulses
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22
Q

What else can diabetes lead to beyond cardiovascular disease

A

Retinopathy
Nephropathy
Erectile dysfunction
Neuropathy

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23
Q

How do insulin and glucagon react after a meal

A

Insulin rises and glucagon drops in a response to blood glucose rising

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24
Q

What is ATP important for

A 
Muscle contraction 
Active transport 
Biosynthesis 
Cellular Processes 
Adaptive thermogenesis
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25
Q

What is metabolism

A

The chemical processes by which cells produce the substances needed to sustain life

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26
Q

What is catabolism

A

A degradative process when you produce energy from the breakdown of energy rich molecules

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27
Q

What is anabolism

A

A biosynthetic process where you combine small molecules to produce complex molecules

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28
Q

What is gluconeogensis

A

The production of glucose

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29
Q

What is glycogenesis

A

The production of glycogen from glucose

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30
Q

Where is glucagon secreted

A

å-cells of the pancreas

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31
Q

Where is GLUT1 found

A

RBCs

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32
Q

Where is GLUT2 found

A

The liver and kidney

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33
Q

Where is GLUT3 found

A

Glucose uptake in neurone

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34
Q

Where is GLUT4 found

A

Adipose tissues and skeletal muscles

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35
Q

What is the cotransporter for Na+/glucose known as

A

SLGT

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36
Q

Where does glycolysis occur

A

In the cytoplasm

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37
Q

What is the end product from one molecule of glucose in glycolysis in aerobic conditions

A

2 pyruvate
2 ATP
2 NADH

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38
Q

What is the product of glycolysis in anaerobic conditions

A

2 lactate

2 ATP

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39
Q

What are the two stages of aerobic glycolysis

A

Stage 1 is the consumption of 2 ATP

Stage 2 produces 2 NADH and 4 ATP

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40
Q

What are the key occurrences in the first stage of glycolysis

A

Start with a 7-carbon glucose molecule and produce two three-carbon molecules (glyceraldehyde or DHAP)
Requires 2 ATP
DHAP is always converted into glyceraldehyde before stage 2 begins

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41
Q

What is the ATP production in stage 2 of glycolysis known as

A

Substrate level phosphorylation

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42
Q

What happens to pyruvate after glycolysis

A

It is transferred to the mitochondria and converrted to Acetyl CoA

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43
Q

What enzyme converts pyruvate into Acetyl CoA

A

Pyruvate dehydrogenase through oxidative decarboxylation

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44
Q

Why is no NADH produced in anaerobic respiration

A

Because it is required to convert pyruvate into lactate

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45
Q

Where can lactate be converted back to glucose

A

In the liver

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46
Q

Why are the enzymes in glycolysis found at key points

A

Because each reaction they catalyse is irreversible

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47
Q

What are the three key enzymes involved in the regulation of glycolysis and at which points

A

Hexokinase catalyses reaction 1 (glucose to glucose-6-phosphate)
Phosphofructokinase catalyses the 3rd reaction (Fructose-6-phosphate to fructose-1, 6BP)
Pyruvate Kinase (only in the liver) catalyses the final reaction of phosphoenolpyruvate into pyruvate

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48
Q

What are the characteristics of hexokinase

A

Has a very high affinity for glucose

Low Vmax of glucose which means it converts it slowly

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49
Q

What inhibits hexokinase

A

G6P its product

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50
Q

What’s the difference between glucokinase in the liver and hexokinase in other tissues

A

Has a lower affinity for glucose and a higher Vmax to convert it quickly
Stimulated by glucose and not inhibited by G6P

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51
Q

Why does the lack of inhibition by G6P of glucokinase help with its function

A

This means it still works well when intracellular glucose levels are high after a meal

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52
Q

What is the characteristics of PFK1 phosphofructorkinase

A

Inhibited by ATP (high cellular energy levels)
Stimulated by AMP (cell energy low)
Activated by fructose 2,6-biphosphate even when cell energy levels are high

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53
Q

What enzyme is regulated in the liver for glycolysis and why

A

Pyruvate kinase

Activated by fructose-1,6-BP so linked with PFK1 as this is its product

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54
Q

How does fructose affect insulin levels

A

It doesnt

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55
Q

Where is fructose processed

A

In the liver

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56
Q

What is fructose initially converted to in the liver and what can this be used for

A

glyceraldehyde which is fed into glycolysis

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57
Q

What else can fructose be used to produce beyond glyceraldehyde

A

It can be used for glycerol production and this can be sued for gluconeogenesis or as a building block for lipids

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58
Q

What does fructokinase catalyse

A

The conversion of fructose into fructose 1-P

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59
Q

What reaction does Aldolase B catalyse

A

The conversion of Fructose 1-P into glyceraldehyde or DHAP

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60
Q

What is the lack of fructokinase known as and how does it present

A

Essential fructosuria with fructose in the urine

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61
Q

What does aldolase B deficiency result in

A

Hereditary fructose intolerance

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62
Q

What are the symptoms of hereditary fructose intolerance

A 
Nausea
Vomiting 
Abdominal distress 
Chronic growth restriction
Severe liver damage on function tests 
Hypoglycaemia on blood tests
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63
Q

When does hereditary fructose intolerance present

A

During weaning (moving onto solid food)

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64
Q

What does oxidative decarboxylation produce

A

Acetyl CoA from pyruvate

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65
Q

What is created beyond Acetyl CoA during oxidative decarboxylation

A

CO2 and NADH

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66
Q

What activates pyruvate dehydrogenase

A

pyruvate dehydrogenase kinase when Acetyl CoA, ATP or NADH levels are high

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67
Q

Where does the krebs cycle occur

A

In the mitochondrial matrix

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68
Q

What does the Krebs cycle rely on

A

O2 being present, must be aerobic conditions

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69
Q

What upregulates the Krebs cycle

A

Ca2+ and ADP

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70
Q

What down regulates the Krebs cycle

A

NADH and ATP

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71
Q

What does one molecule of Acetyl CoA produce in the Krebs cycle

A

3 NADH
1 FADH2
GTP + ADP

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72
Q

What transfers electrons from NADH and FADH2 to O2

A

The electron transport chain

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73
Q

What is the chemiosmotic model

A

How the transfer of electrons across the electron transport chain generates O2 from ATP

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74
Q

Where does oxidative phosphorylation occur

A

In the inner mitochondrial membrane

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75
Q

What does membrane protein complex I do

A

Contains NADH dehydrogenase and NADH transfers electrons to this complex

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76
Q

What does membrane protein complex II do

A

This is succinate dehydrogenase and FADH2 transfers electrons to this complex

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77
Q

How many membrane protein complexes are there in oxidative phosphorylation

A

4

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78
Q

What is the final electron acceptor

A

O2

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79
Q

What is the electrochemical gradient produced by O2 pulling the electrons along the electron transport chain known as

A

The proton motive force

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80
Q

How many protons does FADH2 move along the membrane and why

A

2 as it doesn’t come into contact with complex 1

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81
Q

How many protons does NADH move across the membrane

A

3

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82
Q

How do protons re enter the mitchondrial matrix

A

Through complex V (ATP synthase) and this phosphorylates ADP to ATP

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83
Q

How much ATP, in perfect conditions, is produced from one glucose molecule

A

36

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84
Q

How do carbon monoxide and cyanide interfere with oxidative phosphorylation

A

These inhibit the transfer of electrons from complex IV to O2 and thus the whole system becomes backlogged
Therefore ATP production cannot continue

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85
Q

How does oligomycin stop oxidative phosphorylation

A

It stops protons from moving through Complex V

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86
Q

How does dinitrophenol stop oxidative phosphorylation

A

It’s an uncoupling chemical that allows protons to bypass Complex V and move directly through the membrane so ATP isn’t synthesised

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87
Q

What do uncoupling proteins do

A

These create a proton leak in the mitochondrial membrane so protons can bypass COmplex V

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88
Q

What is an example of an uncoupling protein

A

UCP1/thermogenin and it generates heat in humans and does this by bypassing Complex V instead

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89
Q

When an amino acid is converted into a carbon skeleton in a cell what is the by product

A

A nitrogen waste

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90
Q

What happens to the nitrogen waste by product of amino acid break down in cells

A

It is converted into urea and taken out by the urine

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91
Q

What is the main source of nitrogen in the body

A

Dietary proteins

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92
Q

What are the three sources of amino acids

A

Hydrolysis of dietary proteins
De novo synthesis
Degradation of tissue proteins

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93
Q

Where are non essential amino acids sourced from

A

Metabolic intermediates or from the carbon skeleton of amino acids

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94
Q

Where are essential amino acids obtained

A

In our diet

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95
Q

What are examples of nitrogen compounds in the body- sourced from amino acids

A 
Cellular proteins
Hormones 
Neurotransmitters
Haemoglobin 
Cytochromes 
Melanin 
Nucleotides
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96
Q

What are the three sources for the amino acid pool

A

Protein biosynthesis
Biosynthesis of other nitrogen containing compounds
Oxidation for energy and excretion of nitrogen atoms

97
Q

What is your nitrogen balance

A

The difference between the intake and the excretion of. nitrogen

98
Q

What is a positive nitrogen balance

A

It is when nitrogen intake is greater than excretion and occurs in those growing or pregnant

99
Q

What is a negative nitrogen balance

A

When nitrogen intake is less than excretion and occurs during times of starvation

100
Q

What are the two steps in removal of the amine group to form a carbon skeleton

A

Transamination

Oxidative deamination

101
Q

What is the main site of amino acid catabolism

A

The liver

102
Q

Where does transamination occur

A

In the cytosol and mitochondria

103
Q

What occurs in transamination

A

The amino group is removed and transferred to form glutamate and an å-keto acid

104
Q

What catalyses transamination

A

Aminotransferases

105
Q

What organs does oxidative deamination occur in

A

The kidney and liver

106
Q

What reactions occur in oxidative deamination

A

The amino group of glutamate is released to form å-ketoglutarate and ammonia alongside NADH

107
Q

What enzyme catalyses oxidative deamination

A

Glutamate dehydrogenase

108
Q

What can glucogenic acids be converted to

A

Pyruvate or Krebs cycle intermediates

109
Q

What can ketogenic acids be converted to

A

Acetoacetate or Acetyl CoA or acetoacetate CoA

110
Q

What occurs to the free ammonia produced in oxidative deamination

A

It is immediately converted to non-toxic urea in the liver

111
Q

What reaction occurs in normal tissues when ammonia is produced

A

It combines with glutamate to form glutamine

112
Q

What enzyme catalyses the reaction between glutamate and glutamine

A

Glutamine synthase

113
Q

How is ammonia processed in a skeletal muscle

A

It combines with pyruvate to form alanine, a gluconeogenic precursor

114
Q

What can defects in liver function cause if the urea cycle cannot be processed as efficiently

A

Hyperammonia

115
Q

What are symptoms of hyperammonia

A 
CNS based as neurotoxin 
Slurring
Tremors 
Drowsiness 
Coma
116
Q

How does epinephrine affect insulin function

A

It inhibits the function as it is making sure there is energy readily available to be used in the fight or flight mechanism

117
Q

What is glycogensis

A

The production of glycogen when there is excess glucose

118
Q

What is glycogenolysis

A

The breakdown of glycogen from glucose in the liver and skeletal muscle

119
Q

How much energy is in the fat of a typical 70KG male

A

~15KG which equates to about 135,000Kcal

120
Q

How much energy is in proteins in the body of a 70KG male

A

6Kg for around 24,000Kcal

121
Q

How much glycogen is in the body fo a typical 70KG male

A

0.1KG at about 800Kcal

122
Q

How much glycogen can be found in the muscle

A

around 400g

123
Q

What is fat stored as as an energy source

A

Triacyl glycerides or TAGs

124
Q

What can TAGs be broken down into to generate energy

A

Glycerol and fatty acids

125
Q

What can glycerol be used to generate in the body

A

glucose

126
Q

What can fatty acids be converted to for energy

A

Ketone bodies in the liver

127
Q

Where is the main protein store

A

Skeletal muscles

128
Q

When there is not enough glucose through gluconeogensis or diet what must be used as an energy source

A

Ketone bodies and fatty acids

129
Q

What is an example of a key ketone body that the body generates and uses

A

3-hydroxybutyrate

130
Q

Where is 3-hydroxybutyrate generated and from what subatnce

A

In the liver from fatty acids

131
Q

How do fatty acids travel to adipocytes where they are stored

A

In VLDL packages that act as vesicles

132
Q

What organ can fatty acids not be used directly by and what do they need to be converted into before they can be used

A

The brain requires ketone bodies instead of fatty acids

133
Q

Why do Type 1 diabetics produce an excess of ketone bodies- even in a fed state

A

Because their insulin is completely inactive the body thinks they are in a state of starvation and thus produces the chemical compounds required during a state of starvation

134
Q

Why do Type 2 diabetics not normally show an uncontrolled breakdown of TAGs in adipocytes

A

They still give off a small amount of insulin normally and this is enough to suppress this

135
Q

How are ketone bodies formed

A

Excess Acetyl CoA produced by fatty acid oxidation is converted into ketone bodies

136
Q

What are the three main ketone bodies

A

3-hydroxybutyrate
Acetoacetate
Acetone

137
Q

What occurs to ketone bodies to produce energy

A

They are oxidised by the Krebs cycle to produce ATP

138
Q

What does the liver use as an energy source instead of ketone bodies

A

Fatty acids

139
Q

How can you tell a person is breaking down ketone bodies as an energy source

A

They will have acetone in their breath that smells like pear drops

140
Q

What is the main enzyme that is involved in converting glucose into glycogen

A

Glycogen synthase

141
Q

What is glycogen synthase promoted and activated by

A

It is activated when it is dephosphorylated and promoted by insulin

142
Q

What enzyme converts glycogen back into glucose

A

Glycogen phosphorylase

143
Q

What is glycogen phosphorylase promoted by

A

Glucagon

144
Q

What are fatty acids synthesised from

A

Excess Acetyl CoA from excess carbohydrate catabolism

145
Q

What happens to the excess Acetyl CoA transported to the cytoplasm from the mitochondria

A

It forms malonyl CoA by Acetyl CoA carboxylase

146
Q

How is Acetyl CoA carboxylase regulated

A

Activated by high insulin levels
Activated by citrate
Inhibited by fatty acids

147
Q

What enzyme catalyses malonyl CoA to fatty acids

A

fatty acid synthase

148
Q

how many carbons does the main product of fatty acid synthesis have

A

16

149
Q

How is fatty acid synthesis powered

A

The oxidation of NADPH to form NADP

150
Q

What pathway produces NADPH

A

Hexose monophosphate pathway

151
Q

What is the first step of fatty acid synthesis after malonyl CoA is formed

A

Malonyl CoA (3C) is combined with Acetyl CoA (2C) to form a 4C compound as one carbon is cleaved off

152
Q

What is the by-product of fatty acid synthesis and what is the reaction powered by

A

CO2 and H2O are by-products alongside two CoA molecules

This reaction is powered by NADPH which is oxidised to NADP+ to provide reducing power

153
Q

What does the product of each fatty acid reaction combine with to form the next product

A

Malonyl CoA under the same conditions

154
Q

What is the difference in products between the first fatty acid synthesis reaction and subsequent ones

A

The carbon chain increases in number each time

Only 1 CoA enzyme is subsequently produced as a by-product

155
Q

How are the fatty acids processed so they can be transported around the body as an energy store

A

They are combined with glycerol to form TAGs

156
Q

Why are TAGs the chosen energy storage unit instead of FA

A

They are insoluble which means they can be packed into the cell whereas FA are soluble

157
Q

What enzyme breaks down TAGs to extract energy from them

A

Hormone sensitive lipase

158
Q

What does hormone sensitive lipase break down fatty acids into

A

Fatty acids and glycerol

159
Q

What activates hormone sensitive lipase

A

Epinephrine, norepinephrine and glucagon

160
Q

What happens to the products in the break down of TAGs

A

Glycerol is transported to the liver
FAs bind to plasma albumin and are transported in the blood to enter cells
FAs have variable lengths

161
Q

What does ß-oxidation of fatty acids produce

A

Acetyl CoA

162
Q

How are long chain fatty acids transported into the mitochondrial matrix and how long are they

A

12-22Cs and transported via the carnitine shuttle

163
Q

How are medium and short chain fatty acids transported into the mitochondrial matrix and how long are they

A

<12Cs and diffuse through mitochondrial membranes

164
Q

What are fatty acids activated to in the mitochondrial matrix

A

Fatty Acidcyl CoAs

165
Q

What is different about VLCFAs in the mitochondrial matrix when they are initially transported

A

They need to be degraded in the peroxisome

166
Q

What is the first stage of ß-oxidation

A

The removal of two carbons to form a 14C substance and Acetly CoA

167
Q

What are by products of ß-oxidation

A

NADH and FADH2

168
Q

What is Acetyl CoA produced in ß-oxidation used for

A

In normal tissues the Krebs cycle however in the liver ketogenesis

169
Q

How much ATP do you get from one 16C fatty acid

A

131

170
Q

What enzyme varies based on the chain length of each fatty acid in ß-oxidation

A

Acyl CoA dehydrogenase

171
Q

In the fed state what are amino acids converted to in skeletal muscles

A

Proteins

172
Q

In the fed state what are amino acids converted to in the liver

A

Pyruvate, Acetyl CoA and then TAGs

173
Q

What happens to amino acids in the fasting state

A

They are moved from the skeletal muscles and converted into ketone bodies through Acetyl CoA or glucose via Pyruvate

174
Q

What does an absence of insulin mean for protein metabolism

A

This results in increased protein breakdown, gluconeogenesis and glyocogenolysis

175
Q

What does the complete absence of insulin mean for the breakdown of lipids

A

Lipolysis is increased so there are increased blood FAs and ketogensis which can lead to ketoacidosis

176
Q

What are the three main substrates for gluconeogenesis

A

Lactate
Glycerol
å-ketoacids

177
Q

What is glycerol converted to in the liver in order to undergo gluconeogenesis

A

DHAP

178
Q

Where is the energy for gluconeogenesis sourced from

A

FA oxidation

179
Q

What enzyme converts pyruvate to oxaloacetate to bypass pyruvate kinase

A

Pyruvate carboxylase

180
Q

What enzyme converts oxaloacetate into 2-phisphoenolpyruvate

A

PEP carboxykinase

181
Q

What enzyme converts fructose 1,6-bis phosphate into fructose 6-P by bypassing phosphofructokinase

A

Fructose 1,6-bis phosphatase

182
Q

What enzyme catalyses the conversion of glucose 6-phosphate into glucose to bypass hexokinase

A

Glucose 6-phosphatase

183
Q

To produce one glucose molecule from two oxaloacetate what energy sources are needed

A

4 ATP
2 GTP
2 NADH

184
Q

Which demographics does obesity affect more prominently

A

Women from deprived areas
Older age groups
Black and ethnic minority groups
People with disabilities

185
Q

What is a key question when discussing weight with a patient if they have acknowledged they are overweight

A

Do you want to take action?

186
Q

How much physical activity should a child be doing a day

A

60 minutes

187
Q

What is insulin resistance

A

The decreased ability of target tissues to respond normally to circulating insulin

188
Q

What consequences can insulin resistance result in for bodily functions

A

Uncontrolled hepatic glucose production and decreased glucose uptake by target tissues

189
Q

at what point does Type 2 diabetes officially develop

A

When insulin resistant individuals develop impaired ß-cell function so that insulin resistance cannot be compensated by increased insulin production

190
Q

What is the intial advice to those who have been diagnosed with Type 2 diabetes

A

Healthy diet
Increase exercise and physical activity
Decrease alcohol intake
Avoid smoking and substance misuse

191
Q

What is the name for the group of hormones that are key appetite suppressing hormones

A

Anorexigenics

192
Q

What is leptin and what is its role

A

This is secreted by adipocytes and is secreted when fat stores are high and, when it decreases it increases appetite levels

193
Q

How does insulin secretion affect appetite

A

It decreases it

194
Q

What is Choleystokinin and where is it released

A

Released from the duodenum and jejenum and has a local effect of reducing gastric emptying and reduces appetite

195
Q

What is GLP-1

A

Glucagon like peptide released from the small intestine and colonic L-cells in proportion to ingested calories local effect of reducing gastric emptying

196
Q

What is PYY

A

peptide YY released from the small intestine and colonic L-cells in proportion to ingested calories local effect of reducing gastric emptying

197
Q

What is ghrelin

A

Ghrelin is secreted from the gut and stomach in absence of food to stimulate appetite

198
Q

What is the role of Metformin as an anti-diabetic drug

A

It inhibits liver gluconeogensis and helps insulin to move glucose into cells

199
Q

What are advantages of Metformin (4)

A

It can promote weight loss
It is very cheap and has a long track record
It improves Type 2 diabetes mortality
It rarely causes hyperglycaemia

200
Q

What are disadvantages of Metformin (4)

A

GI upset
Advised to take with food
Lactic acidosis is rare but can be fatal
With caution when impaired renal function/ heart failure/ liver disease

201
Q

What is the first line of treatment for Type 2 diabetes

A

Biguanides such as Metformin

202
Q

What is the mode of action of sulphonylureas

A

Bind to sulphonylurea receptors on the beta cells of the pancreas and block the K+ channel
This results in insulin secretion

203
Q

What is the suffix of sulphonylureas

A

-ide

204
Q

What are side effects of sulphonylureas

A

May stimulate hypoglycaemia, hyperinsulinaemia and weight gain as insulin can be in excess

205
Q

What is the suffix of Thiazolidinediones

A

-zone

206
Q

What is the mode of action of Thiazolidinediones

A

Activate transcription factor PPARy which activates genes in the lipid and glucose metabolism pathways
Peripheral lipogenesis increases
Lipolysis decreases
Decreases plasma fatty acid levels

207
Q

What are the negative and side effects of Thiazolidinediones

A 
Slow onset of action 
Fluid retention 
Cardiac failure
Weight gain 
Liver dysfunction 
Long term effects if withdrawn and may lead to cardiovascular events
208
Q

What are the two main groups of incretins

A

Glucagon like Peptide 1 and Gastric inhibitory polypeptide

209
Q

What role do incretins have in the body

A

Secreted by intestinal endocrinal cells
Help to produce more insulin when it is needed and reduce the amount of glucose produced by the liver when it is not needed

210
Q

What is the role of GLP1 in the body (6)

A

Secreted from L cells upon food ingestion
Reduces appetite in the brain
Suppresses glucagon secretion
Enhances insulin production and secretion
reduces hepatic gluconeogenesis
Slows the rate of stomach gastric emptying

211
Q

What is DPP-IV

A

An enzyme that rapidly degrades GLP-1

212
Q

Why should GLP-1 be given with enzyme inhibitors of DPP-IV

A

Because it rapidly degenerates GLP-1 so should be inhibited to counteract this

213
Q

What is the suffix of GLP-1 inhibitors

A

-liptin

214
Q

How are DPP-IV inhibitors taken

A

Orally

215
Q

What is the suffix of GLP-1 mimetics

A

-tide

216
Q

What is the function of rapid acting secretagogues

A

Non sulphonylurea beta cell stimulators

Rapid onset of action and short duration of activity so taken shortly before a main meal

217
Q

What are the disadvantages of secretagogues

A

Associated with weight gain and hypoglycaemia

Require multiple doses

218
Q

What is the mode of action of SGLT2 inhibitors

A

Inhibit SGLT2 in the proximal tubule to prevent reabsorption of glucose and present glucosuria

219
Q

What side effects can SGLT2 inhibitors present

A

Weight loss
low risk of hypoglycaemia
Can cause UTIs

220
Q

What is the NICE guidance for patient management for those with Type 1 DM

A

Multiple daily injection basal-bolus insulin regimens and guidance on how to use them

221
Q

What are the 4 types of insulin

A

Rapid acting
Short acting
Intermediate acting
Long lasting

222
Q

What is basal insulin

A

this provides a constant supply of insulin to bring down resting blood glucose levels
Intermediate or long lasting insulin

223
Q

What is bolus insulin

A

Has a short lived effect on blood sugar and is taken at meal times
Has characteristics of short or rapid acting insulin

224
Q

When in the day should you take a basal-bolus insulin regimen

A

Two times a day at breakfast and before dinner

225
Q

What are the characteristics of rapid acting insulin

A

5-15 minute onset

work for 4-5 hours

226
Q

What are examples of rapid acting insulin

A

NovoRapid

Humalog

227
Q

What are the characteristics of short acting insulins

A

30-60 minute onset
peak at 2-4 hours
duration of 8-10 hours

228
Q

When should you inject short acting insulin

A

20-30 mins before a meal

229
Q

What are some examples of short acting insulin

A

Actrapid and HumulinS

230
Q

What are the characteristics of intermediate acting insulin

A

1-2 hour onset
5-7 hour peak
13-18 hour action

231
Q

How frequently should you take intermediate acting insulins

A

twice daily

232
Q

What is an example of intermediate acting insulin

A

HumulinI

233
Q

What are exmaples of long acting insulin

A

Lantus
Levemir
Tresiba

234
Q

What are the characteristics of long lasting insulin

A 
Onset:
Lantus 1-2 hours 
Levemir 2-4 hours
Peak:
Lantus flat
Levemir ~8-12 hours 
Last around 24 hours
235
Q

How many days a week should adults be improving their muscle strength

A

2

236
Q

What constitutes moderate exercise

A

Fast breathing and increased heart rate

237
Q

What constitutes vigorous exercise

A

This should lead a person to be unable to maintain conversation at the time

238
Q

How long in a day should those 5 and under be active for

A

180 minutes

239
Q

What are the main benefits of physical activity

A

Decreased blood pressure
Cancer prevention
Large impact with diabetes

Year 1 Medicine Newcastle (8 decks)

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