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BRS Y1 > Week 4- Introduction to Diabetes Mellitus > Flashcards

Week 4- Introduction to Diabetes Mellitus Flashcards

1
Q

What effects does insulin have on glucose, protein and fat?

A

Glucose- increases muscle uptake and HGO

Protein- decrease proteolysis

Fat- decreases lypolysis and ketogensis

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2
Q

Where is GLUT 4 mainly found?

A

Myocytes (muscle) and adipocytes (fat)

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3
Q

What is GLUT 4?

A

A glucose transporter that is recruited and enhanced by insulin

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4
Q

What is the short term energy store?

A

Carbohydrates

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5
Q

Where are carbohydrate stores found?

A

Liver and muscle

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6
Q

What is used as an energy store after carbs run out?

A

Fat

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7
Q

What enzyme breaks down triglycerides?

A

Lipoprotein lipase

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8
Q

What hormone is needed to breakdown triglycerides?

A

Insulin

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9
Q

What is hepatic portal circulation?

A

Blood goes to gut then liver (smaller circulation route)- insulin can be released into this system

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10
Q

What effect does insulin have on ketone body synthesis?

A

Inhibits conversion of fatty acids to ketone bodies

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11
Q

What can low ketone body levels suggest about blood glucose?

A

Blood glucose is high as insulin is inhibiting ketone body synthesis

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12
Q

What is hepatic glycogenolysis?

A

Generation of glucose from stored glycogen in the liver

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13
Q

What is special about glucose in muscles?

A

It cannot be released only used internally

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14
Q

What are the 4 tests for diagnosing diabetes mellitus and what are their positive results?

A

Fasting glucose- >7.0 mmol/L
Random glucose- >11.1 mmol/L
Oral glucose tolerance test
HbA1c- >48 mmol/mol

Diagnosis requires 2 positive tests or 1 positive test and osmotic symptoms (polydipsia, polyuria, nocturia)

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15
Q

How does type 1 diabetes mellitus present?

A

Weight loss
Hyperglycaemia
Glycosuria with osmotic symptoms (polyuria, nocturia, polydipsia)
Ketones in blood and urine

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16
Q

What are useful diagnostic tests for type 1 DM?

A

Antibodies (GAD and IA2)
C-peptide
Presence of ketones

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17
Q

What happens if too much insulin is taken?

A

Reduced glucose output as hepatic gluconeogenesis is switched off and too much glucose uptake by muscles causing hypoglycaemia

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18
Q

What is impaired awareness of hypoglycaemia?

A

When theres reduced ability to recognize symptoms of hypoglycaemia due to loss of counterregulatory response, causes hypoglycaemia to be recurrent

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19
Q

What are autonomic symptoms of hypoglycaemia?

A

Sweating, pallor, palpitations, shaking

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20
Q

What are neuroglycopenic symptoms of hypoglycaemia?

A

Slurred speech, poor vision, confusion, seizures, loss of conciousness

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21
Q

What does a CBG test stand for?

A

Capillary blood glucose

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22
Q

For type 2 diabetes, where is insulin resistance mainly located?

A

Liver, muscle and adipose tissue

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23
Q

How does type 2 DM present?

A 
Hyperglycaemia
Overweight
Dyslipidaemia
Less osmotic symptoms 
Insulin resistance
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24
Q

What are risk factors for type 2 DM?

A 
Age
High BMI
Ethnicity
PCOS
Family history
Inactivity
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25
Whats the medical term for feeling thirsty?
Polydipsia
26
Whats the medical term for frequent urination?
Polyuria
27
What does Hba1c show?
Glucose levels over the past few months
28
What distinguishes a diagnosis of T1DM from T2DM?
If they have ketone bodies in their blood this shows it is T1DM as this shows they have no insulin
29
What is the renal threshold for glucose reabsorbtion? What happens once this threshold is surpassed?
10 mmol/L- after this point the glucose is excreted leading to large volumes of urine
30
What can C peptide indicate and why?
Indicates insulin levels as one mol of c peptide gives rise to one molecule of insulin
31
What are the main differences between T1DM vs T2DM?
Cant produce insulin vs produce to little/dont respond to it Sudden onset of symptoms vs gradual onset of symptoms Must take insulin daily vs can be managed by exercise/diet/oral medication (can be treated by insulin if progresses)
32
What is the basal bolus regimen?
A long term insulin dose (taken by those with T1DM) to maintain long term background insulin during the day (as insulin levels in normal people are never 0)
33
How do patients who take insulin measure their blood glucose?
Via capillary blood glucose monitoring (NOTE: not used for diagnosis only monitoring, usually venous blood glucose is used in diagnosis)
34
What are capillary blood glucose readings for fasting, before meals and hypoglycaemia?
Fasting: 5-7 Before meals: 4-7 Hypoglycaemia: <4 All have units of mmol/L
35
What is neuroglucopenia?
When blood sugar is so low there isnt enough glucose for the brain
36
Why do symptoms of hypoglycaemia arise?
Due to activation of the sympathetic system
37
What are the effects of insulin on cell metabolism?
Promotes the breakdown of protein into gluconeogenic amino acids Reduces the usage of oxygen
38
Aside from insulin, what molecules promote protein breakdown into gluconeogenic amino acids in myocytes?
Growth hormone IGF 1 Cortisol
39
What effect does glucagon have on gluconeogenic amino acids?
It promotes their uptake into cells via transporters and the synthesis of proteins from them
40
What 2 hormones promote gluconeogensis?
Cortisol and glucagon
41
What hormone inhibits gluconeogenesis?
Insulin
42
What happens to triglyceride levels after eating?
They rise
43
What is the enzyme that breaks down triglycerides?
Lipoprotein lipase
44
What effect does insulin have on lipoprotein lipase?
It promotes its action, resulting in more non esterified fatty acids which can be carried to the liver for storage
45
What effect does insulin have on triglyceride synthesis? How are triglycerides synthesised?
They are synthesised from glycerol and non esterfied fatty acids, insulin promotes triglyceride synthesis
46
What hormones encourage breakdown of triglycerides?
Growth hormone and cortisol
47
What does hepatic glucose output indicate?
Levels of production of new glucose
48
Describe overall what happens in gluconeogensis
Glycerol is converted to glucose- it is taken into the liver via transporter and converted to gly-3P before being converted to glucose
49
What effect does insulin have on ketone body synthesis?
It inhibits synthesis of ketone bodies
50
How are ketone bodies synthesised in the liver?
Fatty acids and acyl coA are converted to acetoacetane/acetyl coA/ acetone which give rise to ketone bodies
51
What is hepatic glycogenolysis?
The generation of glucose from glycogen stores in the liver (NOT the synthesis of new glucose)
52
What is special about muscle cells glucose release?
Muscle cells cant release glucose only use it internally (so when blood glucose is low muscles stop this uptake)
53
What happens to glucose levels, NEFA and amino acid levels during fasting?
Glucose levels fall (3-5.5 mmol/L) NEFA levels rise Amino acid levels fall when fasting is prolonged
54
What happens to proteinolysis, lipolysis and HGO in the fasting state?
All 3 increase, HGO increases from glycogen and gluconeogensis
55
What happens to proteinolysis, lipolysis and HGO in the fed state?
Proteinolysis and lipolysis falls,HGO stops
56
What device is used to measure capillary blood glucose?
Glucose meter
57
What 5 hormones are released during hypoglycaemia?
``` Glucagon Epinephrine (adrenaline) Norepinephrine Cortisol Growth hormone ```
58
What effect does the parasympathetic nervous system have on insulin secretion?
Promotes it
59
What effect does the sympathetic nervous system have on insulin secretion?
Inhibits it (to increase glucose availability for fight or flight)
60
What is ketoacidosis?
Metabolic acidosis due to too many ketone acids in the bloodstream

BRS Y1 (52 decks)

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