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NEURO-ENDO > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Under normal condition glucose concentrations are tightly controlled through the release of?

A

Insulin & glucagon

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2
Q

Define Diabetes

A

In the absence of insulin or under conditions of insulin insufficiency, Glucose continues to be broken down by the liver and there is impaired uptake by the tissues leading to prolonged periods of high blood glucose, dehydration, peripheral damage and diabetic coma.

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3
Q

Normal glucose level and diabetic glucose levels

A

Less 11.1

Diabetes: more and equal to 11.1

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4
Q

What is the HBAC1 test?

A

The Hb A1C test measures the level of glycation, giving an indication of glucose levels over the preceding 3 months.

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5
Q

Types of Diabetes?

A

Type 1= Diabetes mellitus

Type 2= Diabetes mellitus

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6
Q

Explain type 1 Diabetes mellitus

A

Insulin dependent

No or very little insulin

Autoimmune: destruction of insulin or B-cells. human leukocyte antigen (HLA) immune mediated.

  • Antibodies can be detected years before symptoms/diagnosis
  • Several antigens have been identified that are the targets of autoantibodies in DM type 1 including insulin itself, glutamic acid decarboxylase, protein tyrosine phosphatase (IA-2) and the cation transporter ZnT8.
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7
Q

Explain type 2 Diabetes mellitus

A

More common

Insulin resistance and insufficiency.

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8
Q

Factors leading to type 2 Diabetes mellitus

A

Insulin reduces breakdown of glycogen in the liver;

insulin resistance means that glycogen is broken down and glucose is released into the blood stream

More prevalent with central adiposity i.e. increased waist to hip ratio

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9
Q

What is Doubke Diabetes?

A
  • Type 1 diabetes is diagnosed
  • Use of Insulin can lead to weight gain
  • Development of Type 2 DM: unresponsive to insulin

Some of the symptoms can be reduced by diet and exercise control

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10
Q

Explain Gestational Diabetes

A

Increased insulin resistance due to pregnancy hormones (Oestrogen, Progesterone, Placental Lactogen).

Hormones increase insulin resistance in the mother

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11
Q

What are the Risks of Gestational Diabetes: prenatal?

A
  • Miscarriage
  • Stillbirth
  • Placental insufficiency
  • Polyhydramnios
  • Pre eclampsia
  • Premature birth
  • Growth retardation (IUGR)
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12
Q

What are the Risks of Gestational Diabetes: perinatal?

A

•Large baby:
birth complications
Shoulder dystocia

  • Newborn Jaundice
  • Newborn Hypoglycaemia
  • Respiratory Distress Syndrome (prem)
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13
Q

What is Alzheimer’s Diabetes ?

A

Insulin resistance specific to the brain

  • People with diabetes more likely to develop Alzheimer’s then those without
  • Damage to blood vessels in brain
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14
Q

You are more prone to diabetes if you have depression (60% increase)

True or false?

A

True

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15
Q

What is the Role of insulin in metabolism?

A

Stimulates uptake of glucose by the cell
➢ translocates glucose transporters from cytosol to plasma membrane

➢ Stimulates glycogen production (glycogenesis)
activation of glycogen synthase

➢Stimulates fatty acid and triglyceride production in the liver:
Removes fats and glucose from the bloodstream

➢Inhibits adipose cell lipase (fat breakdown) in adipose

➢Moves amino acids into cells
Increases RNA transcription and protein synthesis (anabolic effect)
Prevents use of protein as a fuel source (protein degradation) by increasing glucose availability as a fuel

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16
Q

What causes Type 1 Diabetes?

A

Insulin deficiency due to destruction of Beta cells in pancreas. Treatment by insulin injections/pumps ie insulin replacement.

17
Q

What causes Type 2 Diabetes?

A

Insulin deficiency due to increased bloodstream glucose ie demand (type 2 diabetes is associated with obesity – increasing the risk by 80-100 fold).
OR/AND

Insulin resistance

18
Q

Endocrine signalling in Glucose metabolism

A

Endocrine signalling:
•Hormone travels within blood vessels to act on a distant target cell
•Insulin produced in the pancreas acts on the liver, muscle cells and adipose tissue

19
Q

Paracrine signalling in Glucose metabolism

A

Paracrine signalling:

  • Hormone acts on an adjacent cell
  • α and β cells: Glucagon and Insulin release acts as paracrine signalling on each other.
20
Q

How does Homeostasis control Hypoglycaemia?

A

●Glucagon is secreted by the alpha- cells of the Islets of Langerhans within the pancreas
●Glucagon stimulates glycogenolysis and gluconeogenesis within the liver, thereby increasing blood glucose levels
●It also inhibits Insulin secretion

21
Q

How does Homeostasis control Hyperglycaemia?

A

●When blood glucose levels increase, insulin is secreted by the beta- cells within the Islets of Langerhans
●It has an endocrine effect on the liver
●Insulin also has a paracrine effect, inhibiting glucagon secretion

22
Q

Explain the action of insulin on target cells : muscle and fat cells

A
  • Binding of insulin to the insulin receptor on the plasma membrane of muscle and fat cells
  • mobilisation of GLUT4 glucose transporters from inside the cytoplasm to the cell surface
  • glucose transported into the cell
  • stored as triacylglycerol (adipocytes) or glycogen (striated muscle).
23
Q

What are Incretins ?

A

Incretins are peptide hormones produced in the intestine which are released on intake of food and they stimulate insulin release.

24
Q

Action and role of GLUT 1

A

Acts on:

  • Fetal tissue
  • Blood Brain Barrier
  • Transport of glucose to fetal and brain tissues

Role:

Transport of glucose to fetal and brain tissues

25
Q

Action and role of GLUT 2

A

Acts on:

  • Liver
  • Pancreas beta-cells
  • Kidney

Role:

Bidirectional to allow uptake and release of glucose
Necessary for accurate sensing of serum glucose

26
Q

Action and role of GLUT 3?

A

Acts on:

  • neurons
  • placenta
27
Q

Action and role of GLUT 4

A

Acts on:

  • Adipocytes
  • Striated muscle

Role:

10% of insulin stimulated glucose uptake. Glucose stored as triacylglyceride (TAG).
Majority of insulin-stimulated glucose uptake occurs in muscle. Glucose is stored as glycogen.

28
Q

What are the Glucose Transporters?

A

GLUT 1
GLUT 2
GLUT 3
GLUT 4

29
Q

Explain how Insulin is released from beta-cell?

A

• Glucose is transported into the cell via a transporter (GLUTs)

  • ATP is produced, which leads to closure of the potassium channel
  • Presence of Sufonylureas enhances this
  • Depolarisation opens Calcium channels
  • Insulin is released
30
Q

Insulin Regulation in T2 diabetes?

A

Insufficient insulin secretion: Loss of first phase of normal biphasic response to intravenous glucose.

  • Onset of DM is associated with hypersecretion of insulin.
  • Circulating insulin levels are higher than in healthy controls but still insufficient to restore glucose homeostasis
  • Hypersecretion leads to β-cell “burn-out”
31
Q

Treatments for Diabetes

A

Insulin:
•Replaces insulin lost through beta cell damage or destruction. Type 1 diabetes and late stage diabetes type 2

GLP-1 (Glucagon-like peptide 1) analogue (exenatide):
•promotes insulin release, inhibits glucagon release reduces appetite and delays gastric emptying thus blunting the rise in glucose levels after eating.
•Side effects: Nausea and acute pancreatitis (concerns are being raised). Used as an alternative to insulin in the early stages of type 2 diabetes.

DPP4 inhibitors:
•DPP4 is involved in the turnover of incretins and so by inhibiting this enzyme the action of the incretins is extended. Moderately effective in the early stages of type 2 diabetes.

Moderation of diet and exercise:
•Low carbohydrate to decrease glucose load
•Exercise (stimulates Glut4 movement to the cell surface)

Short term low calorie diet (800 calories): 8-20 weeks
•Decreases fat store in liver, restores insulin production
•May have long term restorative effect
•Remission- but keep intake of carbohydrates low.
•Must be done in conjunction with the healthcare team.

32
Q

Signs of Diabetes

A
  • Blood Glucose
  • Loss of body fat and muscle
  • Polyuria
  • Polydipsia
33
Q

Type 1 Diabetes mellitus complications

A

Diabetic ketoacidosis:

➢Lack of insulin leads to increased amounts of glucagon which stimulates production of glucose by glycogenolysis / gluconeogenesis in the liver and muscle cells
➢Breakdown of fatty acids in adipocytes to ketones.
➢↓pH → hyperventilation

Usually happens in type 1 rather than type 2 DM.

NEURO-ENDO (21 decks)

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