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Endocrinology > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

What is the boundary for hypoglycaemia

A

<4-5MM

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2
Q

What can hypoglycaemia cause

A

Impaired brain function

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3
Q

What can happen when glucose level is under 3mM

A

unconsciousness, coma , death

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4
Q

Which hormones control glucose regulation

A 
Insulin
Glucagon
Cortisol
Catecholamines
Somatrophin
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5
Q

What is type 1 DM

A

Elevated glucose levels where insulin is required to prevent ketoacidosis

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6
Q

What is type 2 DM

A

More common. Defined in terms of glucose but is also related to hypertension and dyslipidaemia

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7
Q

When does hypoglycaemia occur

A

Imbalance between diet, exercise and insulin

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8
Q

What does treatment aim to help

A

Symptoms, complications (morbidity) and mortality

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9
Q

What is common in DM treatment

A

Diet, insulin and capillary glucose monitoring

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10
Q

How much of the pancreas do langerhans take up and what does the rest of the pancreas do

A

2%

Involved in exocrine secretions via pump

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11
Q

What cell junctions can you find between langerhans cells

A

Gap junctions to allow small molecules to pass and tight junctions to form small intercellular spaces

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12
Q

What are the types of langerhans cell

A

alpha - glucagon
beta - insulin
delta - somatostatin

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13
Q

What are the principal actions of insulin

A

Increased glycogensis
Increased glycolysis
Increased glucose transport into cells via GLUT4
Decreased lipolysis
Increased lipogenesis
Increased amino acid transport and increased protein synthesis

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14
Q

What are the principal actions of glucagon

A 
Increased hepatic glycogenolysis
Increased blood glucose
Increased amino acid transport to the liver
Increased gluconeogenesis
Increased lipolysis
Increased gluconeogenesis
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15
Q

Which factors regulate the release of insulin

A

Increasing blood glucose
Certain amino acids
Certain gastro intestinal hormones (GLP)
Sympathetic control (-) and parasympathetic (+)

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16
Q

What factors regulate the release of glucagon

A

Decreasing blood glucose
Certain amino acids
Certain gastro intestinal hormones
Sympathetic (++) and parasympathetic (+) control

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17
Q

Describe the beta-cell sensing mechanism of glucose

A

Glucose -> G-6-P -> Metabolic pathways -> insulin synthesis and release.
Glucokinase/ hexokinase IV is the “glucose sensor” as it is in the rate limiting step

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18
Q

Describe the process of insulin secretion

A
  1. glucose enters via GLT 2
  2. conversion to G-6-P by glucokinase
  3. ATP blocks the ATP sensitive K+ channel
  4. Voltage dependent Ca+ channel opens
  5. Insulin secreted
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19
Q

Describe the insulin receptor

A

Mostly on muscle, can be on liver
not responsible for type II DM
Made of alpha and beta subunits

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20
Q

What does the alpha subunit of the insulin receptor do

A

Recognises the 3D insulin structure

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21
Q

What does the beta subunit of the insulin receptor do

A

Has tyrosine kinase domains where phosphorylation occurs

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22
Q

What is GLP-1

A

Glucagon-like peptide 1

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23
Q

What does the GLP-1 do

A

Gut hormone that is secreted in response to nutrients in the gut. Stimulates insulin secretion and glucagon suppression. Increases satiety.

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24
Q

What is the half life of GLP-1

A

Short half life due to rapid degeneration from enzyme dipeptidyl peptidase-4 (DPPG-4)

25
Q

How is GLP-1 produced

A

Transcription product of proglucagon gene, mostly from the langerhans cells

26
Q

What is the effect of insulin on glucose

A

Decreased hepatic glucose output and increased muscle intake

27
Q

What is the effect of insulin on protein

A

Decreased proteolysis

28
Q

What is the effect of insulin on lipids

A

Decreased lipolysis and decreased ketogenesis

29
Q

What is GLUT-4

A

A receptor that allows glucose uptake through the membrane. They lie in vesicles and become incorporated into the membrane by insulin resulting in a 7 fold increase in uptake

30
Q

What does cortisol stimulate

A

Proteolysis

31
Q

Which hormones stimulate protein synthesis

A

Insulin and IGF I

32
Q

What is the main short term energy store

A

Glycogen

33
Q

After short-term fasting what is used to maintain glucose levels

A

gluconeogenesis using proteins

34
Q

Describe the formation of glycerol and NEFA from TAG

A
  1. Triglyceride is broken down by lipoprotein lipase, promoted by insulin
  2. Glucose enters through GLUT-4, stimulated by insulin
  3. Glucose can be broken down and two components can be used to form triglyceride, these being glycerol-3-p and NEFA, again promoted by insulin
  4. This can be used to stop the break down of triglyceride into glycerol and NEFA
35
Q

Describe the circulation glycerol

A
  1. Glycerol reaches the liver
  2. It enters the cell and is phosphorylation
  3. Formation o triacyl glycerol
  4. This can be used to synthesise glucose (hepatic glucose output)
36
Q

What is the importance of the way glycerol circulates

A

Blood flows through the gut before the liver, allowing for food to be processed before entering the liver. Adipocytes in the central circulation of different those in the limbs

37
Q

What can eat brain utilise as an energy source

A

Glucose and ketone bodies (NOT fatty acids)

38
Q

What is fat used for in metabolism

A

Broken down and used in Krebs> Non-esterified fat cannot be used to synthesise glucose

39
Q

How are ketone bodies formed

A
  1. Fatty acids enter the liver
  2. Fatty acids are broken down into segments
  3. Formation of ketone bodies (acetoacetate and 3-hydroxybutarate)
40
Q

Which molecule can be used as an indication of insulin

A

Ketone bodies as insulin inhibits their formation

41
Q

What occurs during fasting

A 
Low insulin to glucose ratio
Increasing non-esterified fatty acids
Increase in proteolysis and lipolysis
Break down of glycogen
Gluconeogenesis
42
Q

What occurs during prolonged fasting

A

Decrease in amino acids
Increased ketogenesis
Brian uses ketone

43
Q

Which molecules do the muscle and brain use

A 
Muscle = lipids
Brain = glucose
44
Q

What occurs when one is fed

A

Stored insulin is released then a second phase insulin release
High insulin to glucagon ratio
Hepatic glucose output is stopped
Increase in glycogen formation
Decreases in gluconeogensis and proteolysis
Increase in protein synthesis and lipogenesis

45
Q

What are the signs and symptoms of type 1 DM

A 
Weight loss 
Hyperglycaemia
Glycosuria with osmotic symptoms
Ketonuria
Given an intramuscular injection of insulin
46
Q

What causes weight loss in T1 DM

A

Proteolysis and lipolysis

47
Q

What is the difference between T1 and T2 DM

A 
T1 = absolute insulin deficiency
T2 = insulin resistance
48
Q

Where does insulin resistance reside

A

Adipose, muscle and liver

49
Q

Why don’t T2 DM patients lose weight

A

There is enough insulin to suppress proteolysis and lipolysis

50
Q

What are the two pathways that occur when insulin meets its receptor

A

MPAK or PI3K-Akt

51
Q

How does insulin resistance affects the pathways

A

PI3-Akt is inhibited so the MAPK pathway is enhanced

52
Q

What are the two pathways responsible for

A 
MAPK = growth, proliferation, growth in utero, blood pressure and dyslipidaemia 
PI3-Akt = metabolic actions (glucose, fat and amino acids)
53
Q

What are the effects of hyperinsulinaemia via the MPAK pathway

A

Excess stimulation of the mitogenic pathway
Low LDL cholesterol and high HDL
Smooth muscle hypertrophy -> high blood pressure
Ovarian function (polycystic ovary syndrome)
Clotting
Energy expenditure

54
Q

What are the effects of the insulin resistance via IP3-Akt

A

Glucose, protein and lipid metabolism affected

55
Q

What happens to lipoproteins in humans with T2 DM

A

Predominantly abnormal lipoproteins that is lipid carriage in the circulation, contributing to damage to the artery

56
Q

What is insulin resistance associated with

A

Hyperglycaemia
Greater waist circumference
High blood pressure
High triglyceride and low LDL

57
Q

What can patients with T2 DM present with

A 
Obesity (60-80%)
Dyslipidaemia
Hyperglycaemia
Insulin resistance and later deficiency 
Complications due to central adiposity 
Less osmotic symptoms
58
Q

Describe the features of a diet for patients with DM

A 
Total calorie control
Reduce calories as fat and as refined carbohydrate
Increase calories as complex carb 
Increase soluble fibre
Decrease sodium intake

Endocrinology (9 decks)

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