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Endocrinology > 5 - Introduction to diabetes mellitus > Flashcards

5 - Introduction to diabetes mellitus Flashcards

1
Q

How does insulin affect HGO and muscle glucose uptake?

A

Decreases HGO (hepatic glucose output)

Increases muscle glucose uptake

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2
Q

How does insulin affect proteolysis?

A

Decreases proteolysis (stops the breakdown of proteins)

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3
Q

How does insulin affect lipids (lipolysis and ketogenesis)?

A 
Decreases both
(Ketogenesis is the breakdown of fatty acids and ketogenic amino acids to make ketone bodies)
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4
Q

What are 5 other things insulin is related to?

A
  • Lipoproteins
  • Smooth muscle hypertrophy
  • Ovarian function
  • Clotting
  • Energy expenditure
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5
Q

What transporter does glucose enter a cell through?

A

GLUT4 - insulin increases the amount of these transporters to increase glucose uptake.
Hydrophilic core and hydrophobic edge.

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6
Q

Where is GLUT4 found?

A

Muscle and adipose tissue

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7
Q

In a muscle cell, how does insulin affect proteins?

A

Stops proteolysis (stops the breakdown of proteins)

Increases protein synthesis (also increased by growth hormone)

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8
Q

What increases proteolysis in muscle cells and what are the amino acids used for?

A

Cortisol

Used to make O2 into CO2
Used to make gluconeogenic amino acids.

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9
Q

What is the difference between where glucose and glycogen are stored?

A

Glucose is always present in the blood

Glycogen is stored in the liver

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10
Q

What happens to gluconeogenic amino acids that enter the liver?

A
  • Used to make proteins

- Used to make new glucose (gluconeogenesis) to increase HGO

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11
Q

In the blood vessels and in adipose tissues, insulin has different effects on the formation and breakdown of triglycerides. Explain this.

A

In blood vessels, insulin encourages the breakdown of triglycerides.
Its broken down into non-esterified fatty acids and glycerol which can enter adipose tissue.

In adipose tissue, insulin encourages the formation of triglycerides. This can be from NEFAs and glycerol-3-p.

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12
Q

What 3 things encourage the breakdown of triglycerides in adipose cells into NEFAs?

A

Cats
Cort
GH

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13
Q

What is the omental or hepatic portal circulation?

A

Blood goes to the gut, picks up nutrients.
This blood goes to the liver so food can be processed BEFORE re-entering general circulation.
Adipocytes in central circulation are different to those in arms and legs. Omental adipocytes predict heart disease.

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14
Q

How is glycerol used to make glucose in the liver? Draw diagram

A

Triangle.
Glycerol enters and is made into Glycerol-3-p.
This can be made (reversibly) into triglycerides.
Glycerol-3-p makes glucose via gluconeogenesis. This is released from the liver.

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15
Q

What CANNOT be used to make glucose

A

Non-esterified fatty acids

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16
Q

What can the brain use as an energy source?

A

Glucose Ketone bodies

17
Q

What can the brain NOT use as an energy source?

A

Fatty acids (but muscle can)

18
Q

How are ketone bodies produced?

A
  1. Non esterified fatty acids enter the liver
  2. They are broken down into 2 carbon sections (acetyl CoA, acetoacetate, acetone + 3 OH-B)
  3. Make ketone bodies which are released from liver and go to brain during fasting.
19
Q

Why and how are ketone bodies measured?

A

Ketones measured in blood or urine.
If present = patient has low insulin

Ketones in presence of high glucose = Person is insulin deficient

20
Q

Draw a picture showing hepatic glycogenolysis in the liver.

A

Triangle.
Glucose enters liver
Made into glucose-6-p
With insulin - glucose-6-p made into glycogen.

With catacolanimes and glucagon - glycogen made back into glucose-6-p, which is made into glucose and released from liver.

21
Q

What happens once glucose enters muscle cells?

A

It can be stored as glycogen but this cannot then be released as glucose.
It MUST be used within the muscle cell itself - enters krebs cycle.

22
Q

What happens to the body in a FASTED state?

A
  • Low [Insulin]
  • High proteolysis and lipolysis
  • High HGO from glycogen and gluconeogenesis.
Low insulin:glucagon ratio
High NEFA
Muscles use lipids
Brain uses glucose then ketones
Ketogenesis increases.
23
Q

What happens to the body in the FED state?

A

Stored insulin is released.
High inulin:glucagon ratio

HGO stops
More glucose stored as glycogen
Gluconeogenesis stops
Protein synthesis increases
Lipogenesis increases
24
Q

What is type 1 diabetes?

A

Absolute insulin deficiency - no insulin produced by pancreas.

25
Q

Symptoms of T1DM?

A
  • Proteolysis (weight loss)
  • Hyperglycaemia
  • Glycosuria with osmotic symptoms (sugar in wee)
  • Ketonuria (ketones in wee)
  • Lipolysis
26
Q

What is insulin induced hypoglycaemia?

A
  • Giving too much insulin
  • Causes too much glucose to be stored as glycogen.
  • Glucose does not enter muscles
27
Q

What happens during insulin induced hypoglycaemia?

A

More GH released
More cortisol released

  • Counter regulatory response
    HGO will increase later with gluconeogenesis and glycogenolysis.
28
Q

Treatment for hypoglycaemia?

A

IM injection of glucagon to restore HGO.

29
Q

What is type 2 diabetes?

A

Insulin resistance.

Insulin surpasses ketogenesis and proteolysis.

30
Q

When insulin reaches the insulin receptor, is has 2 different actions, what are they?

A

Growth and proliferation

Metabolic actions

31
Q

What pathway leads to growth and proliferation?

A

MAPK pathway

32
Q

What pathway leads to metabolic actions?

A

P13K-Akt pathway

This is where insulin resistance occurs.

33
Q

What are the 2 actions of insulin resistance?

A
  1. Mitogenic on growth

2. Metabloc actions

34
Q

What does mitogenic on growth mean?

A

Hyperinsulinaemic effect

  • Lipoproteins
  • Smooth muscle hypertrophy (=high BP)
  • Ovarian function
  • Clotting
  • Energy expenditure
35
Q

What is the metabolic insulin resistance effect?

A

-Glucose
-Proteins
-Lipids
Are all normal

36
Q

What is associated with insulin resistance?

A 
High [TG]
Low [HDL]
Slightly higher glucose
High waist circumference
High BP
Insulin resistance
Adipocytokines
Inflammatory state
Energy expenditure
37
Q

Presentation of T2DM?

A
  • Insulin resistance
  • 60-80% obese
  • Dyslipidaemia (abnormal carriage of lipids in the circulation)
  • Later insulin deficiency
  • Hyperglycaemia
  • Less osmotic symptoms
  • With complications
38
Q

What diet changes should be made in T2DM?

A 
Calorie control
Reduce fats & refined carbs
Increase complex carbs
Increase soluble fibre
Decrease salt

Endocrinology (18 decks)

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