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Clinical biochemistry > Diabetes and hypoglycaemia > Flashcards

Diabetes and hypoglycaemia Flashcards

1
Q

What is glucose?

A

Glucose is a major energy substrate

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2
Q

What is blood glucose levels maintained through?

A

○ Maintenance of blood glucose levels through (4-6mmol):
○ Dietary carbs eaten and then absorbed
○ Glycogenolysis in liver
○ Gluconeogenesis

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3
Q

What is the role of the liver after a meal?

A

stores glucose as glycogen

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4
Q

What is the role of the liver during a fast?

A

makes glucose available through glycogenolysis and gluconeogenesis

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5
Q

Why is it important to regulate glucose?

A

○ Brain and erythrocytes require continuous supply: – therefore avoid deficiency
○ Brain and RBCs cannot metabolise glucose themselves
○ High glucose and metabolites cause pathological changes to tissues;

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6
Q

What is diabetes mellitus?

A

Metabolic disorder characterised by chronic hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism

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7
Q

What is hyperglycemia a result of?

A

Hyperglycaemia result of increased hepatic glucose production and decreased cellular glucose uptake

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8
Q

What is glycosuria and at what level does it occur?

A

Glucose in urine

Blood glucose > ~ 10mmol/L

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9
Q

What is involved in the diagnosis of diabetes mellitus?

A

○ In the presence of symptoms: (polyuria, polydipsia & weight loss for Type I)
○ Random plasma glucose ≥ 11.1mmol/l (200 mg/dl)
▪ Random is defined as any time of day without regard to time since last meal OR
• Fasting plasma glucose ≥ 7.0 mmol/l (126 mg/dl) Fasting is defined as no caloric intake for at least 8h
OR
• Oral glucose tolerance test (OGTT): plasma glu ≥ 11.1 mmol/l
○ In the absence of symptoms:
-test blood samples on 2 separate days

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10
Q

What are the value range of patients with impaired glucose tolerance(IGT) of:

  • Fasting plasma glucose
  • OGTT value
A

○ Fasting plasma glucose 6.1-6.9mmol/L

○ OGTT value of 7.8 – 11.1 mmol

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11
Q

What are the value range of patients with impaired fasting glycaemia(IFG) of:

  • Fasting plasma glucose
  • OGTT value
A

○ Fasting plasma glucose ‹ 7.0 mmol/L and

○ OGTT value of < 7.8

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12
Q

What individuals is OGTT used . in and to determine what?

A

OGTT used in individuals with fasting plasma glucose of ‹ 7.0 mmol/L to determine glucose tolerance status.

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13
Q

In what patients should oral glucose tolerance test(OGTT) be carried out in?

A

○ In patients with IFG
○ In unexplained glycosuria
○ In clinical features of diabetes with normal plasma glucose values
○ For the diagnosis of acromegaly (excess GH results in excess glucose)

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14
Q

Steps involved in OGTT

A
  1. Check blood glucose first
  2. 75g oral glucose and test after 2 hour
  3. Blood samples collected at 0 and 120 mins after glucose
  4. Subjects tested fasting after 3 days of normal diet containing at least 250g carbohydrate
    - If blood glucose >8.1 = diabetes
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15
Q

What is type 1 diabetes?

A

Insulin secretion is deficient due to autoimmune destruction of b-cells in pancreas by T-cells

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16
Q

What is type 2 diabetes?

A
  • Insulin secretion is retained but there is target organ resistance to its actions
  • Insensitivity of receptors
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17
Q

What is secondary diabetes caused by?

A

• Chronic pancreatitis, pancreatic surgery, secretion of antagonists

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18
Q

What does gestational diabetes occur due to and when?

A
  • Occurs for first time in pregnancy due to placental hormones i.e. HPL
  • Happens between 18-24 weeks
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19
Q

What are all the classifications of diabetes?

A
  1. Type 1
  2. Type 2
  3. Secondary
  4. Gestational
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20
Q

Who is type 1 DM predominantly in?

A

○ Predominantly in children and young adults; but other ages as well

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21
Q

What is the onset of type 1 DM?

A

Sudden onset

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22
Q

What is the most common cause of type 1 DM?

A

Most common cause is autoimmune destruction of B-cells

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23
Q

What strong genetic link is there for type 1 DM?

A

○ Strong link with HLA genes within the MHC region on chromosome 6

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24
Q

Pathogenesis of type 1 DM?

A

○ HLA class II cell surface presents as foreign and self-antigens to T-lymphocytes to initiate autoimmune response
○ Circulating autoantibodies to various cell antigens against:
○ Glutamic acid decarboxylase
○ Tyrosine-phosphatase-like molecule
○ Islet auto-antigen
○ The most commonly detected antibody associated with type 1 DM is the islet cell antibody

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25
Q

What does destruction of pancreatic beta cells cause?

A

Destruction of pancreatic ß-cell causes hyperglycaemia due to absolute deficiency of both insulin & amylin

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26
Q

What is amylin?

A

A glucoregulatory peptide hormone co-secreted with insulin

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27
Q

How does amylin lower blood glucose?

A

Lowers blood glucose by slowing gastric emptying, & suppressing glucagon output from pancreatic cells

28
Q

What does amylin reduce in the intestines?

A

○ Reduces amount of glucose that can be absorbed from the intestine

29
Q

What happens to amylin when islet cells are destroyed?

A

○ When islet cells are destroyed: amylin is deficient (which usually inhibits glucagon)

30
Q

What is the presentation of type 2 DM?

A

○ Slow onset (months/years)
○ Patients middle aged/elderly – prevalence increases with age
○ Strong familiar incidence
○ Pathogenesis uncertain – insulin resistance; β-cell dysfunction:
-May be due to lifestyle factors - obesity, lack of exercise

31
Q

What are the metabolic complications of type 2 DM?

A
  1. Hyper-osmolar non-ketotic coma

2. Hyperosmolar hyperglycaemic state

32
Q

Why are there no ketone bodies in hyper osmolar non-ketotic coma?

A

○ No ketone bodies

-Because lipolysis is not occurring so no production of ketone bodies

33
Q

What happens in hyperosmolar hyperglycaemic state?

A 
○ Development of severe hyperglycaemia
○ Extreme dehydration
○ Increased plasma osmolality
○ Impaired consciousness
○ No ketosis
○ Death if untreated
34
Q

What is the treatment of type 2 DM, stepwise?

A
  1. Diet and exercise
  2. Oral monotherapy
    • Metformin
  3. Oral combination
  4. Insulin +/- oral agents
    • Sulphonylureas
    • Gliptins
    • GLP-1 analogues
35
Q

What do sulfonylureas do?

A

○ Bind and close KATP channels, depolarize B cell releasing insulin

36
Q

What do metformin do?

A

○ Decreases gluconeogenesis

○ Increases uptake of glucose from blood

37
Q

What do thiazolidinediones do?

A

○ Activate PPARγ receptor (controller of lipid metabolism), which (somehow) reduces insulin resistance

38
Q

What do SGLT2 inhibitors do?

A

Promote glucose excretion via kidney

39
Q

What do incretin targeting drugs do?

A

○ Potentiate insulin release in response to rising plasma glucose

40
Q

What are DPP-4 inhibitors also known as?

A

Also known as gliptins

41
Q

What do DPP-4 inhibitors do ?

A

○ DPP4 usually destroys incretin so DPP4 inhibitors prevent this destruction and incretin stimulate insulin secretion

42
Q

What are the aims of monitoring glycaemic control?

A

Prevent complications or avoid hypoglycaemia

43
Q

What are long term complications that occur in both type 1 and type 2 DM?

A
  • Micro-vascular disease

- Macro-vascular disease

44
Q

What is hypoglycemia defined as?

A

Defined as plasma glucose < 2.5 mmol/L

45
Q

What are the causes of hypoglycemia?

A
  • Drugs
  • Endocrine diseases
  • Inherited metabolic disorders
  • Insulinoma
  • Severe liver disease
46
Q

What are examples of inherited metabolic diseases?

A
  • Glycogen storage disease type l (von Gierke’s disease)
  • Galactosaemia
  • Hereditary fructose intolerance
47
Q

What is Glycogen storage disease type I a deficiency of?

A

○ Deficiency of G-6-Phosphatase: impaired glucose release from glycogen

48
Q

What is galactosaemia a deficiency of?

A

○ Deficiency of galactose-1-phosphate uridyl transferase: liver damage

49
Q

What is hereditary fructose tolerance a deficiency of?

A

Deficiency of fructose-1-phosphate adolase B: accumulation of fructose-1-phosphate in liver

50
Q

What type of disorder is glycogen storage disease type 1A?

A

Autosomal recessive disorder

51
Q

What synthesis is blocked and from what in glycogem storage disease type 1A?

A

Glucose synthesis from glycogen or by gluconeogenesis is blocked

52
Q

What does accumulation of glycogen cause?

A

Accumulation of glycogen causes hepatomegaly

53
Q

What deficiency is in galactosaemia?

A

○ Galactose-1-phosphate uridyl transferase deficiency

54
Q

What disorder is galactosaemia?

A

○ Autosomal recessive disorder

55
Q

What does the deficiency of G-1-PUT impar in galactosaemia?

A

Deficiency of G-1-PUT impairs conversion of galactose-1-phosphate to glucose-1-P

56
Q

Where does Galactose 1 phosphate accumulate and why’s it bad in galactosaemia?

A

Gal-1-phosphate accumulates in liver - toxicity

57
Q

What is galactose excreted in in galactosaemia?

A

Galactose excreted in urine

58
Q

What disorder is hereditary fructose intolerance?

A

○ Autosomal recessive disorder

59
Q

What deficiency is hereditary fructose intolerance of?

A

Deficiency of fructose 1-phosphate aldolase B

60
Q

What happens to ingested fructose in hereditary fructose intolerance and what does it inhibit?

A

○ Ingested fructose accumulates – inhibits glycogenolysis at phosphorylase step.

61
Q

What is fructose detected in hereditary fructose intolerance?

A

Fructose detected in urine

62
Q

What is benign fructose intolerance due to?

A

Due to absence of fructokinase

63
Q

What is the physiological counter-regulatory response to falling glucose levels in fasting?

A

○ Suppression of insulin release, limiting glucose entry into non-cerebral tissues
○ Secretion of glucagon, adrenaline, noradrenaline, cortisol and growth hormone to raise glucose level

64
Q

What is the glucose counterregulatory hormone response to falling glucose levels in fasting?

A

○ Glucagon
▪ Secreted by a-cells of pancreas in response to hypoglycaemia
▪ Stimulates glycogenolysis and gluconeogenesis
○ Cortisol
▪ Increased gluconeogenesis

65
Q

What are the neurogenic signs and symptoms of hypoglycaemia triggered and activated by?

A

○ Triggered by falling glucose levels

○ Activated by ANS & mediated by sympathoadrenal release of catecholamines and Ach

66
Q

What is neuroglycopaenia due to in hypoglycemia?

A

○ Due to neuronal glucose deprivation

67
Q

What are the signs and symptoms of neuroglycopaenia?

A 
▪ confusion
▪ difficulty speaking
▪ ataxia
▪ paresthesia
▪ seizures
▪ coma
▪ death

Clinical biochemistry (6 decks)

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