Diabetes Mellutis Flashcards

1
Q

Where is GLUT4 commonly found

A

Myocytes and adipocytes
Highly insulin responsive
Lies in vesicles
Recruited and enhanced by insulin

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2
Q

Look at the diagrams on the effects of insulin on cell metabolism and gluconeogenesis

A

Effects of insulin on cell metabolism and gluconeogenesis

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3
Q

What runs out first as a fuel

A

Carbohydrates followed by protein and fat

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4
Q

What enzymes break down triglycerides

A

Lipoprotein lipas which breaks down triglycerides into NEFA and glycerol

Triglycerides are too big so unless broken down they would not be able to be taken up by adipocytes

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5
Q

Circulation adaptations that allow increased speed of digestion etc

A

From aorta you have an hepatoaorta circulation which allows rapid digestion in gut which then flows to liver so insulin is released quickly into the hepatoporto circulation and allows quick effects

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6
Q

Brain and cerebral energy requirement

A

Brain can use glucose and ketone bodies but the brains inability to utilise fatty acids as a fuel makes it unique among body tissue

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7
Q

Diagnosis of Diabetes Mellitus

A

Fasting state greater than 7 mmol/L

Random glucose >11.1 mmol/L

Oral glucose tolerance test ;
Fasting glucose
75g glucose load
2 hour glucose

HbA1c ( >48mmol/mol)

A diagnosis required 2 positive tests or 1 positive test and symptoms

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8
Q

Presentation of Type 1 diabetes

A

Weight loss due to protein breakdown
Hyperglycaemia
Glucosuria with osmotic symptoms ( polyuria, no Turk and polydipsia )
Ketones in blood and urine

Can cause diabetic ketoacidosis

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9
Q

Useful diagnostic tests for T1D

A

Antibodies ; GAD, IA2 and ZNT8
C peptide
Presence of ketones

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10
Q

Counter-regulatory response to hypoglycaemia

A

Increased glucagon
Increased catecholamines
Increased cortisol
Increased growth hormone

These all increase HGO with glycogenolysis and gluconeogenesis
Increased lipolysis

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11
Q

Impaired awareness of hypoglycaemia

A

Reduced ability to recognise symptoms of hypoglycaemia
Due to loss of counter regulatory response
Recurrent hypoglycaemia

Body gets used to having these episodes and so the threshold for which counterregulatory system kicks in falls below . So previously may have come in at 4 mmol/L but now 2

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12
Q

Autonomic Symptoms and signs of hypoglycaemia

A

Sweating
Pallor
Palpitations
Shaking

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13
Q

Neuroglycopenic symptoms of hypoglycaemia

A
Slurred speech 
Poor vision 
Confusion
Seizures 
Loss of consciousness
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14
Q

Severe hypoglycaemia

A

Defined as an episode where a person needs third party assistance to treat

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15
Q

Pathophysiology of T2D

A

Insulin; resistance resides in liver, muscle and adipose tissue

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16
Q

Important distinct between T1D and T2D in terms of keto genesis and proteolysis

A

T2D has enough insulin to suppress ketogenesis and proteolysis

17
Q

Presentation of T2 Diabetes

A
Hyperglycaemia 
Overweight 
Dyslipadaemia 
Less osmotic symptoms 
With complications
Insulin resistance 
Later insulin deficiency
18
Q

Risk factors of T2D

A
Age 
BMI
Ethnicity 
Family history 
Inactivity 
PCOS
19
Q

Dietary recommendations and education of T2D

A
Total calories control 
Reduce calories as fat
Reduce calories as refined carbs
Increase calories as complex carbs
Decrease sodium 
Increase soluble fibre
20
Q

T1D management

A

Exogenous insulin
Self monitoring of glucose
Structured education
Technology

21
Q

T2D management

A

Diet
Oral medication
Structured education
May need insulin later

22
Q

Long term diabetes related complications

A

Retinopathy
Neuropathy
Nephropathy
Cardiovascular