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Endocrinology > Insulin & Diabetes > Flashcards

Insulin & Diabetes Flashcards

1
Q

Hormones that increase blood glucose levels

A
  • Glucagon
  • chatecholamines
  • somatotrophin
  • cortisol
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2
Q

Hormone that decreases blood glucose

A

Insulin

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3
Q

What is type 1 diabetes defined as

A

Elevated glucose levels where insulin is required to prevent ketoacidosis

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4
Q

What is type 2 diabetes

A

Elevated glucose levels, related to hypertension and dyslipidaemia

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5
Q

Does T1DM require insulin?

A

YES

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6
Q

Does T2DM require insulin?

A

No, mature onset diabetes

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7
Q

Does MODY require insulin

A

(Monogenic) maturity onset diabetes of the Young, usually not insulin dependant

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8
Q

Types of MODY

A

HNF1alpha, mutation stops transcription factor which aids insulin production - sulfonylureas used

Glucokinase, activates at higher glucose level than normal (4mmmol) doesn’t require medication usually

Permanent neonatal diabetes, kcnj11 mutation which keeps K+ ion channels open all the time

Maternally inherited diabetes and deafness

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9
Q

Most common type of diabetes

A

Type 2

Then type 1

Then monogenic

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10
Q

How can glucose me measured

A

Capillary glucose monitoring

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11
Q

How does hypoglycaemia occur?

A

Lack of balance between diet, exercise and insulin

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12
Q

Why is glucose so important

A

Major energy substrate for CNS, brain function impaired if less than 4-5mM

Unconscious and Coma occurs at less than 2mM

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13
Q

Most of the pancreas produces what kind of secretions?

A

Exocrine from accini via ducts to small intestine

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14
Q

Islets of langerhans are endocrine areas of the pancreas, what type of cells do they consist of?

A

Alpha cells produce glucagon
Beta cells produce insulin
Delta cells produce somatostatin

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15
Q

What cellular structures allow for paracrine signalling?

A

GAP junctions allow signalling molecules to pass between cells

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16
Q

What is the function of somatostatin

A

Calms the insulin or glucagon secretion, inhibiting release of both of too much is produced.

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17
Q

Glucagon has a metabolic effect of increasing blood glucose, insulin’s metabolic effect is to decrease blood glucose sand what else?

A

Stimulates growth and development, the mitogenic effect of insulin.

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18
Q

Beta cells can be stimulated to produce insulin by what?

A
  • Increased blood glucose
  • certain amino acids
  • gastrointestinal hormones
  • parasympathetic activity
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19
Q

Beta cells are inhibited to produce insulin by?

A
  • Glucagon
  • somatostatin
  • sympathetic activity
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20
Q

What does insulin do?

A

Decreases lipolysis and promotes lipogeneis

Increased amino acid transport and increased protein synthesis

Inhibits ketogenesis

Increased glycogenesis, increased glycolysis, increased glucose transport into cell via GLUT4

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21
Q

What stimulates glucagon production from alpha cells?

A
  • decreases blood glucose
  • certain amino acids
  • sympathetic activity
  • certain gastrointestinal hormones
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22
Q

What inhibits glucagon release by alpha cells?

A

Insulin, somatostatin and parasympathetic activity

23
Q

What does glucagon do?

A

Increased amino acid transport to liver for GLUCONEOGENESIS

Increased lipolysis, increased gluconeogenesis

Increased hepatic glycogenolysis

24
Q

What is the glucose sensor in the beta cell?

A

Glucokinase, it is the enzyme involved in the rate limiting step hence increase in glucose influx via GLUT2 means rate of ATP production increases and closure of more ATP sensitive K+ ion channels leading to influx of Calcium and exocytosis of insulin.

25
Q

What makes up proinsulin and it’s clinical relevance?

A

ProInsulin has C-peptide attaches to it which is cleaved to produce insulin. Hence c peptide in blood can show endogenous production of insulin by pancreas hence indicate pancreatic function.

26
Q

What is the incretin effect?

A

Glucose absorbed via the intestines leads to higher insulin levels than when glucose directly infused into blood.
Eg Glucagon like Peptide 1 (GLP1), secreted in response to nutrients in blood from L cells.

STIMULATES INSULIN PRODUCTION AND INHIBITS GLUCAGON

27
Q

Why do incretins have short half life?

A

Rapidly degenerated by dipeptidyl pepridase-4 enzymes (DPPG4)

28
Q

What is the insulin receptor?

A

Tyrosine kinase receptor, two alpha units where the insulin binds and two beta cytoplasmic domains which are crossphosphorylated allowing phosphorylation of cell protein substrates hence triggering a cellular signal.

29
Q

What does the metabolic arm of the insulin pathway do?

A

Decreases hepatic glucose output
Increases uptake of glucose in muscles
Decreases proteolysis, lipolysis and ketogenesis

30
Q

What is involved in the mitogenic arm of the insulin pathway?

A

Regulates:

Lipoproteins 
Smooth muscle hypertrophy
Ovarian function 
Clotting
Energy expenditure 
Growth and proliferation
31
Q

Where is GLUT4 mostly expressed?

A

Muscle and adipose tissue

Inserted into the membrane via vesicles in response to insulin, leads to massive increase in glucose uptake

32
Q

In regards to proteins, what stimulates protein synthesis?

A

Insulin
Growth hormone
IGF1

33
Q

In regards to proteins, what inhibits protein synthesis?

A

Insufficient insulin

Cortisol

34
Q

What inhibits amino acids from entering the krebs cycle?

A

Insulin

35
Q

What promotes hepatic glucose output?

A

Glucagon stimulates uptake of gluconeogenic amino acids into the liver

Glucagon promotes proteolysis

Glucagon, catecholamines and cortisol increase HGO

36
Q

Which store of energy is used up first?

A

Glycogen in muscle and liver
Then protein
Then fat

37
Q

What are omental adipocytes?

A

Adipocytes around the waste, have endocrine capacity. Higher central adiposity more likely to develop diabetes and heart disease.

38
Q

How does insulin promote lipogenesis?

A

Insulin promotes lipoprotein lipase to produce glycerol and non esterified fatty acids (NEFAs). Insulin then promotes the recombining of these to form TAGs. Also promoting conversion of glucose into NEFAs by producing acetyl coA.

39
Q

What promotes lipolysis To glycerol and NEFAs?

A 
Low insulin
Glucagon 
Growth hormone 
Catecholamines 
Cortisol
40
Q

Why can’t our brain use fatty acids?

A

Our brain made of farts hence enzymes would degrade brain fats too.

41
Q

Insulin usually inhibits ketone body formation, why do t1 diabetics have ketones in blood?

A

As they are insulin deficient

42
Q

Where is the main store of glycogen?

A

Liver, for hepatic glucose output

43
Q

Can muscle release glucose from glycogen?

A

No, there is no glucose output from muscles.

44
Q

In fasted state, there is low insulin to glucagon ratio what does this mean?

A

Glucose levels should be roughly normal
Increased Lipolysis therefore increased NEFAs
Increased proteolysis but amino acid conc low as used for gluconeogenesis
Muscles use lipids
Increased ketogenesis if prolonged

45
Q

What happens in fed state?

A 
High insulin to glucagon ratio
HGO stops 
Glycogenesis increases 
Increased protein synthesis 
Increased lipogenesis 
Decreases gluconeogenesis
46
Q

Presentation of T1DM

A 
Insulin deficiency
Weight loss 
Hyperglycaemia 
Glycosuria
Polyuria + polydipsia 
Ketonuria

Ketoacidosis leads to kaussmals respiration, deep laboured breathing to try and increase blood pH.

47
Q

Subcutaneous Insulin induced hypoglycaemia is usually fine, why?

A

Glucagon detects low blood sugar and has its effects, HGO increases.

intramuscular injection of glucagon needed if severe hypoglycaemia.

48
Q

In T2DM why is there no ketoacidosis or weight loss?

A

Insulin resistance, enough insulin still produced to prevent lipolysis and ketogenesis. But not enough insulin to reduce glucose levels in blood.

49
Q

Describe the mitogenic and the metabolic pathway of insulin

A

The mitogenic pathway is triggered by binding of insulin: it triggered the ras MAPK pathway which causes growth and proliferation. This pathway is also responsible for controlling High BP and abnormal dyslipidemia.

Metabolic pathway is the PI3K-Akt Pathway giving rise to metabolic actions.

50
Q

Insulin resistance in T2DM occurs in which pathway?

A

Metabolic, glucose not absorbed and remains high in blood.
This causes compensatory hyperinsulinaemia which overstimulates mitogenic arm. This cause proatherogenic, high bp and prothrombotic effects.

Polycystic ovary syndrome may occur.

51
Q

What is insulin resistance associated with?

A
  • High triglyceride and low HD/high LDL
  • fasting glucose above 6mM
  • High waist circumference
  • hypertension

This leads to adipocytokines being released which cause beta cell dysfunction and inflammatory mediators being released.

52
Q

Presentation of T2DM

A 
Insulin resistance 
Obesity 
Dyslipidemia 
Later insulin deficiency 
Hyperglycaemia
53
Q

Who does type 2 diabetes have more complications?

A

As there are cardiovascular effects too due to dyslipidemia

54
Q

Controlling diet for diabetes

A 
Reduce calorie intake
Reduce fat
Reduce simple carbs 
Increase slow release complex carbs 
Increase fibre 
Decrease sodium

Endocrinology (8 decks)

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