Diabetes mellitus Flashcards

1
Q

What happens to insulin and glucose in the normal fasted state?

A

low insulin:glucose ratio

glucose concentration = 3.0-5.5mmol/L

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2
Q

What processes are increased in the fasting state?

A
More lipolysis( increase in  NEFAs)
More proteolysis ( increased amino acid concentration when prolonged)
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3
Q

What does the brain use for energy?

A

glucose, then ketone(needs ketogenesis)

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4
Q

How is diabetes mellitus diagnosed?

A

Fasting glucose is >7.0mmol/L, random glucose >11.1mmol/L
Oral glucose tolerance test
fasting glucose
post prandial =75g glucose load, wait 2 hours
HbA1c (.48mmol/mol)
DIAGNOSIS REQUIRES 2 POSITIVE TESTS OR 1 POSITIVE AND OSMOTIC SYMPTOMS

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5
Q

What is type 1 diabetes?

A
  • autoimmune condition (t cell destruction of beta cells in pancreas)
  • absolute insulin deficiency
  • ketoacidosis occurs
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6
Q

What is an example of an acute complication caused by type 1 diabetes?

A

Insulin-induced hypoglycaemia - too much insulin is administered causing reduced gluconeogenesis in liver and increased glucose uptake by the muscles.
Glucose dim circulation will continue to fall

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7
Q

What are the symptoms of type 1 diabetes?

A

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

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8
Q

What are each of the osmotic symptoms?

A

polyuria - frequent need to urinate
polydipsia - excessive thirst
nocturia - waking up more than once in the night to urinate

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9
Q

What are useful diagnostic tests for type 1 diabetes mellitus?

A

Antibodies: GAD, IA2 (markers)
C-peptide(low)
presence of ketones

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10
Q

Pathophysiology of tpd1

A

No insulin leads to proteinolysis (AA produced)
Increased hepatic glucose output
Increased breakdowns of fat ( into non esterified fatty acids)

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11
Q

How does glucose enter the cells?

A

Via glucose transporters such as GLUT-4

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12
Q

Counterregulatory response to hypoglycaemia

A

Increased glucagon, catecholamins, cortisol,growth hormone

All increase hepatic glucose output w glycogenolysis ams lipolysis

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13
Q

Why is hypoglycaemia bad?

A

Reduced ability to recognise symptoms of hypoglycaemia

Recurrent hypoglycaemia

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14
Q

Symproms and signs of hypo

A

Autonomic: sweating
Pallor
Palpitations
Shaking

Neuroglycopenic:

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15
Q

What are characteristics of GLUT -4

A
Common in myocytes and adipocytes
Highly insulin responsive
Lies in vesicles 
Recruited and enhanced by insulin 
Hphillic and Hphobic components cause a 7 fold increase in glucose uptake
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16
Q

What can be used to treat a capillary blood glucose of 1.5mmol/L

A

1mg glucagon injection

17
Q

Where does insulin resistance reside ?

A

Liver, muscle and adipose tissue

18
Q

Do ketogenesis and proteolysis occur in type 2 diabetes ?

A

Have enough to supress those to begin with

19
Q

What are the consequences of insulin resistance ?

A
High triglycerides 
Low HDLS
Hypertension 
Large waist circumference
High fasting glucose (>6mmol/L)
20
Q

What is the mechanism of glucose uptake via glut4?

A

Insulin binds to insulin receptor
Insulin presence causes Glut4 vesicles to fuse with the plasma membrane
Then Glut4 allows glucose to enter cell.

21
Q

What is a glucogenic amino acid ?

A

Can be converted into glucose through gluconeogenesis

22
Q

What is a ketogenic amino acid?

A

Converted into ketone bodies

23
Q

Triglycerides can’t leave circulation, how is this over come?

A

Lipoprotein lipase (LPL) enzyme breaks them down into glycerol and non-esterified fatty acids which can then enter cells such as adipose tissue.

24
Q

What happens to glycerol in cells?

A

Converted into glucose via gluconeogenesis.
Glycerol -> dihydroxyacetone phosphate-> glyceraldhyde-3-phosphate
(For brain fuel when it’s needed)

25
Q

Does insulin promote or inhibit the conversion of proteins to amino acids?

A

Inhibits