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Z YEAR 1 BRS Endocrinology > Introduction to Diabetes Mellitus > Flashcards

Introduction to Diabetes Mellitus Flashcards

1
Q

What is the action of insulin?

A
  • Glucose
  • decrease HGO
  • increase muscle uptake
  • decrease proteolysis
  • decrease lipolysis
  • decrease ketogenesis
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2
Q

What are the clinical implications of insulin?

A
  • Type 1 diabetes mellitus
  • Hypoglycaemia
  • Insulin Resistance
  • Type 2 diabetes mellitus
  • Management
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3
Q

What is Glut-4?

A
  • Common in myocytes (muscle) and adipocytes (fat)
  • Highly insulin-responsive
  • Lies in vesicles
  • Recruited and enhanced by insulin
  • 7-fold increase glucose uptake
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4
Q

How does insulin effect cell metabolism in fed state?

A
  1. In fed state, insulin inhibits the breakdown of protein in the muscle and reduce oxidation of amino acids
  2. Converts amino acids to proteins
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5
Q

How does insulin effect cell metabolism in fasting state?

A
  1. Cortisol can increase breakdown of protein which can release Amino acids out of muscle (these are called gluconeogenic amino acids AAs e.g. alanine)
  2. GH stimulates protein synthesis
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6
Q

What happens in gluconeogensis in the liver?

A
  1. Gluconeogenic AAs and pyruvate and lactate are taken up by the liver with glucagon
  2. In fed state insulin increase protein synthesis
  3. In fed state Insulin inhibits gluconeogensis
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7
Q

What is your fuel source from?

A
  1. Carbohydrate (most from)
  2. Protein (20%)
  3. Fat (30-40%)
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8
Q

What does lipoprotein lipase (LPL) enzyme do?

A

Breaks down triglycerides that would otherwise be unable to leave the circulation

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9
Q

What happens to triglycerides in the blood stream?

A
  1. Triglycerides broken down by LPL which needs insulin
  2. Therefore the triglycerides is broken down in glycerol and NEFAs and these are taken up by fat cell (adipocyte)
  3. If really eaten then glucose can also be take up by the adipocyte so in fed state insulin increase glucose uptake into the fat cell and the insulin converts the glycerol and NEFA into triglycerides to store it
  4. In fed state insulin inhibits breakdown of triglycerides in fat cell
  5. In fasting cell GH and cortisol help to break down triglycerides to form NEFA and glcycerol in the fat cell which are related from fat cell to use as a fuel source
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10
Q

What is the hepatic portal circulation?

A
  • Blood from the heart to the gastrointestinal system where take to liver to be processed/stored
  • Insulin from pancreas related into hepatic portals circulation so quick response
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11
Q

What happens to glycerol in the liver?

A
  1. Glycerol into liver by transporter to form Gly-3P then stored as triglycerides or converted into glucose by gluconeogensis
  2. This glucose then released as hepatic glucose
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12
Q

How much is hepatic gluconeogensis occur?

A

25% HGO after 10 hour fast

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13
Q

What can the brain use as fuel?

A
  1. Glucose (its no1)
  2. Ketone bodies
  3. NOT fatty acids (NEFA)
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14
Q

What happens to NEFA in liver?

A
  1. NEFA in liver taken up
  2. Converted to fatty acid CoA
  3. In fed state, insulin will inhibit acetyl CoA into ketone bodies but glucagon stimulates it
  4. Abnormal when high glucose and still have high ketone bddies
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15
Q

What is hepatic glycogenolysis?

A

-The generation of glucose from stored glycogen in the liver

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16
Q

What happens to glucose in the liver?

A
  1. Glucose enter liver by transporter and converted to Glucose 6 phosphate
  2. Insulin stimulates it to convert it to glycogen
  3. Glucagon stimulates formation of glucose 6 phosphate form glycogen
  4. Glucose then related from liver and this is NOT new glucose just stored glucose as glycogen
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17
Q

What happens in muscle cell in fed state?

A
  1. Insulin encourages glucose uptake to muscle (GH and glucagon inhibit this)
  2. If Glucose not needed in muscle cell at that time this is covered to glycogen (and stored in muscle cell) and if needed converted to acetyl CoA
  3. NEFA can be taken up by muscle and the nEFA and acetyl CoA oxidised and used as energy source (mitochondria0
18
Q

What is difference of glycogen in liver and glycogen in muscle?

A
  • Glycogen in liver can be converted to glucose and be released
  • Glucose can not be released from muscle
19
Q

What happens in fasted state?

A
  • Low insulin-to-glucagon ratio
  • [Glucose] 3.0-5.5mmol/l
  • increase [NEFA]
  • decrease [amino acid] when prolonged
20
Q

Whats happening in the body in fasted state?

A 
-Increase  Proteolysis
•increase Lipolysis
•increase HGO from glycogen and gluconeogenesis
•Muscle to use lipid
•Brain to use glucose, later ketones
•increase Ketogenesis when prolonged
21
Q

What happens in fed state?

A
  • Stored insulin released then 2nd phase

* High [insulin] to [glucagon] ratio

22
Q

What happens in body in fed state?

A
  • Stop HGO
  • ↑ Glycogen
  • ↓ gluconeogenesis
  • ↑ protein synthesis
  • ↓ proteolysis
  • ↑ Lipogenesis
23
Q

What does the diagnosis of diabetes Mellitus involve?

A 
•Fasting glucose >7.0 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 requires 2 positive tests or 1 positive test + osmotic symptoms
24
Q

Describe the pathophysiology of type 1 Diabetes?

A
  • Autoimmune condition (produces autoantibodies which attack insulin secreting beta cells)
  • Absolute insulin deficiency
    1. Increase proeinolysis
    2. Increase HGO
    3. increase lipolysis
  • If prolonged lead to production of ketone bodies
25
Q

What is diabetic ketoacidosis?

A

pH.7.3 stones +3 HCO3-<15, gluc>11

serious acute complication

26
Q

What is the presentation of T1DM?

A
  • Weight loss
  • Hyperglycaemia
  • Glycosuria with osmotic symptoms (polyuria, nocturia, polydipsia)
  • Ketones in blood and urine
27
Q

What are some useful diagnostic tests of T1DM?

A
  • Antibodies: GAD, IA2
  • C-peptide
  • Presence of ketones
28
Q

What happens if too much insulin administered?

A
  • Switch off hepatic gluconeogensis
  • Reduced glucose output
  • With glucose in the system glucose uptake by muscle if too much insulin more and more glucose taken up and nothing can really be done to stop in
29
Q

What is the counter-regulatory response to hypoglycaemia?

A

-Increase Glucagon
-Increase Catecholamines
-Increase Cortisol
-Increase Growth hormone
THIS CAUSES:
1. Increase hepatic glucose output with glycogenolysis and gluconeogensis
2. Increase lipolysis

30
Q

What is impaired awareness of hypoglycaemia?

A
  • Reduced ability to recognise symptoms of hypoglycaemia
  • Due to loss of counterregulatory response
  • Recurrent hypoglycaemia
31
Q

What are the autonomic symptoms and signs of hypoglycaemia?

A
  • Sweating
  • Pallor
  • Palpitations
  • Shaking
32
Q

What are the neurolycopenic symptoms and signs of hypoglycaemia?

A
  • Slurred speech
  • Poor vision
  • Confusion
  • Seizures
  • Loss of consciousness
33
Q

What is severe hypoglycaemia?

A

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

34
Q

What happens in type 2 diabetes?

A

-Insulin resistance resides in liver muscle and adipose tissue
-All metabolic sites and all arms of intermediary metabolism
•Glucose
•Fatty acids
-Enough insulin to suppress
•Ketogenesis
•Proteolysis

35
Q

What is insulin resistance?

A
  1. Pancreas still produces inulin and insulins still binds to insulin receptor
  2. This activates PI3K-Akt pathway which activates metabolic actions from insulin
  3. Increased insulin produced
  4. Another pathway is also activated form insulin binding: MAPK pathway which stimulates growth and proliferation (so increased growth in smooth arteries, and abnormal lipid profile in blood)
36
Q

What happens in insulin resistance?

A 
•High [TG]
•Low [HDL]
•Insulin resistance
•Adipocytokines
•Inflammatory state
•Energy expenditure
-Hypertension
•BP >135/80 mmHg
-Waist circumference
•Men >102 cm 
•Women >88 cm
-Fasting glucose
•>6.0 mmol/L
37
Q

What is the presentation of T2DM?

A
  • Hyperglycaemia
  • Overweight
  • Dyslipidaemia
  • Less osmotic symptoms
  • With complications
  • Insulin resistance
  • Later insulin deficiency
38
Q

What are the risk factors of T2DM?

A 
Age 
PCOS
Increase BMI 
Family Hx 
Ethnicity 
Inactivity
39
Q

What are some complications of diabetes/

A

-Eye disease
-Renal failure
-Diabetic foot
-Nerve disease
-Stroke, heart disease
•Retinopathy
•Neuropathy
•Nephropathy
-Cardiovascular

40
Q

What are the dietary recommendations and education for diabetes?

A 
Healthy eating or diet
•Total calories control
•Reduce calories as fat 
•Reduce calories as refined carbohydrate
•Increase calories as complex carbohydrate
•Increase soluble fibre
•Decrease sodium
41
Q

What is the management of T1DM?

A 
•Exogenous insulin (basal-bolus regime)
•Self-monitoring of glucose
•Structured education
•Technology (insulin pumps)
-Monitoring and preventing long term diabetes related complications
42
Q

What is the management of T2DM?

A 
•Diet
•Oral medication
•Structured education
•May need insulin later
-Monitoring and preventing long term diabetes related complications

Z YEAR 1 BRS Endocrinology (8 decks)

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