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Clinical Biochemistry > Diabetes and Hypoglycaemia > Flashcards

Diabetes and Hypoglycaemia Flashcards

1
Q
  1. In what three ways can you plasma glucose levels be increased?
A
  1. Intake of dietary carbohydrates
  2. Glycogenolysis (Glycogen breakdown)
  3. Gluconeogenesis ( Glucose production from non-glucose stores eg lactate and fatty acids)
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2
Q
  1. How is glucose stored?

When will the stores of glucose be used?

A

•The liver stores glucose as glycogen after meals and makes glucose available through glycogenolysis and gluconeogenesis during fasting.

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3
Q
  1. Why should glucose levels be regulated?
A
  • Need to avoid deficiency because the brain and erythrocytes require a continuous glucose supply.
  • Need to avoid excess because high glucose and metabolites can cause pathological changes to tissues e.g. macro/microvascular diseases and neuropathy.
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4
Q
  1. What is the difference between :
    - Glycogenolysis
    - Glucogenesis
    - Glycolysis
A
  • Glycogenolysis : Glycogen —> Glycose
  • Gluconeogenesis : non-carbohydrate substances —-> Glucose
  • Glycolysis : Breakdown of glucose—> ATP
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5
Q
  1. What effect does insulin have on Adipose?
A

increased glucose uptake and lipogenesis (fat formation) , reduced lipolysis (to reduce glucose synthesis).

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6
Q
  1. What effect does insulin have on the Liver?
A

increased glycogen synthesis and lipogenesis,

reduced gluconeogenesis.

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7
Q
  1. What effect does insulin have on striated muscle?
A

increased glucose uptake, glycogen synthesis and protein synthesis.

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8
Q
  1. What is diabetes Mellitus?
A

•A metabolic disorder characterised by chronic hyperglycaemia (high blood glucose) , glycosuria (excess sugar in urine) and associated abnormalities of lipid and protein metabolism:

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9
Q
  1. What causes the body to be in a state of “hyperglycaemic “
A

increased hepatic glucose production
decreased cellular glucose uptake
(making glucose but the cells not taking it up)

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10
Q
  1. When do you get glycosuria?
A

when blood glucose > ~ 10mmol/L and exceeds renal threshold (filtration and reabsorption rates are not equal)

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11
Q
  1. What is the prevalence of diabetes Mellitus?
A

o Globally 422 million people currently have diabetes; estimated to increase by 2035 (WHO, 2014)
o In the UK 2018 ~ 3.8 million diagnosed with DM.

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12
Q
  1. What is type 1 diabetes?
A

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

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13
Q
  1. What is Type 2 Diabetes?
A

Insulin secretion is retained but there is target organ resistance to its actions (receptor problems etc).

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14
Q
  1. What is secondary diabetes?
A

chronic pancreatitis, pancreatic surgery, secretion of antagonists

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15
Q
  1. What is gestational diabetes?
A

Occurs for first time in pregnancy.

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16
Q
  1. (Referring to type 1 diabetes)
    What age is it most likely to present in?
    How long is the onset?
A

Present predominantly in children and young adults (but other ages as well)

Onset is sudden (days/weeks).

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17
Q
  1. At first what might the symptoms of Type 1 diabetes be perceived as?
A

•Appearance of symptoms may be preceded by ‘prediabetic’ period of several months.

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18
Q
  1. What is the most common cause of Type 1 diabetes?
A

autoimmune destruction of B-cells but there are interactions between genetic and environment factors.
o strong link with HLA (human leukocyte antigen) genes within the MHC (major histocompatibility complex) region on chromosome 6.

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19
Q
  1. What is the pathogenesis of type 1 diabetes ?
A 
o	HLA class II cell surface present as foreign and self-antigens to T-lymphocytes initiate autoimmune response. 
o	Circulating autoantibodies against various -cell antigens are present: 
-	Glutamic acid decarboxylase (GABA production in pancreas), tyrosine-phosphatase-like molecule, Islet auto-antigen (most commonly associated with Type 1 Diabetes). 
•	More than 90% of newly diagnosed persons with type 1 DM have one or another of these antibodies.
•	Destruction of pancreatic ß-cell causes hyperglycaemia due to absolute deficiency of both insulin & amylin.
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20
Q
  1. What is Amylin?
A

(glucoregulatory peptide hormone co-secreted with insulin) lowers blood glucose by slowing gastric emptying & suppressing glucagon output from pancreatic cells.

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21
Q
  1. What is the pathophysiology of diabetes mellitus Type 1?
A

o Genetic predisposition and environmental factors mean autoantigens form on beta cells which circulate around the body stream/lymphatics.
o Autoantigens are processed and presented by antigen presenting cells which then come into contact with T cells.
1. T helper 1 cells cause the activation of macrophages (release IL-1 and TNF-a) and autoantigen-specific T cytotoxic (CD8) cells.
2. T helper 2 cells activate B lymphocytes to produce autoantibodies.
The macrophages, cytotoxic cells and autoantibodies all cause beta cell destruction leading to decreased insulin
secretion

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22
Q
  1. What is the metabolic complication that follows from insulin deficiency causing increased lipolysis?
A

• Insulin deficiency causes increased lipolysis which produces free fatty acids for the formation of ketone bodies (metabolic acidosis can cause diabetic coma).

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23
Q
  1. What is the metabolic complication that follows from insulin deficiency causing hyperglycaemia?
A

•Insulin deficiency causes hyperglycaemia which causes glycosuria (filtration and reabsorption not equal) and polyuria. This leads to volume depletion which causes diabetic coma.

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24
Q
  1. What is the age range and onset of type 2 diabetes?
A

oSlow onset (months/years) and patients usually middle aged/elderly – prevalence increases with age

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25
Q
  1. Is there a strong familial incidence for type 2 diabetes?
A

yes

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26
Q
  1. What is the pathogenesis of type 2 diabetes?
A

•Pathogenesis uncertain but involved insulin resistance or β-cell dysfunction: may be due to lifestyle factors e.g. obesity, lack of exercise.

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27
Q
  1. What are some metabolic complications of type 2 diabetes ?
A

Hyper-osmolar non-ketotic coma (HONK), [Hyperosmolar Hyperglycaemic State (HHS)]
o Development of severe hyperglycaemia.
o Extreme dehydration – increased plasma osmolality.
o Impaired consciousness and death if left untreated.
o No ketosis (insulin is present so no lipolysis so no ketoacidosis).

28
Q
  1. What are some common symptoms of type II diabetes ?
A

polyuria
polydipsia
weight loss for Type I

29
Q
  1. How would you do tests to diagnose Type II diabetes when the patient IS showing symptoms?
A
  • Random plasma glucose (any time of day) ≥ 11.1mmol/l (200 mg/dl ).
  • Fasting (no caloric intake for at least 8h) plasma glucose ≥ 7.0 mmol/l (126 mg/dl).
  • Oral glucose tolerance test (OGTT) for impaired fasting glycaemia - plasma glu ≥ 11.1 mmol/l
30
Q
  1. How would you do tests to diagnose Type II diabetes when the patient ISN’T showing symptoms?
A

test blood samples on 2 separate days.

31
Q
  1. What does :
    -OGTT
    -IGT
    -IFG
    mean?
A

OGTT = Oral glucose tolerance test

IGT = Impaired glucose tolerance (pre-diabetes )

IFG = Impaired fasting Glycaemia

32
Q
  1. When would you do an impaired glucose test (IGT) ?
A

When Fasting plasma glucose >7mmol/L** and

OGTT value of 7.8 – 11.1 mmol

33
Q
  1. When would you do an Impaired fasting glycaemia (IFG) test?
A

Fasting plasma glucose 6.1 to 6.9 mmol/L, and

OGTT value of < 7.8mmol/L

34
Q
  1. What nmol/L of plasma glucose would you do an OGTT?
A

<7 nmol/L

-to determine glucose tolerance status

35
Q
  1. When would you do an OGTT?
A

in patients with IFG

in unexplained glycosuria

in clinical features of diabetes with normal plasma glucose values

36
Q
  1. How do you carry out an OGTT?
A
  • Given 75g oral glucose and test blood glucose levels after 2 hour (samples taken at 0 and 120mins after glucose).
  • Subjects tested fasting after 3 days of normal diet containing at least 250g carbohydrate.
37
Q
  1. What is the Stepwise Treatment of Type II Diabetes:
A
  1. Exercise and Diet.
  2. Metformin monotherapy for type 2 diabetes: helps insulin to re-uptake glucose from plasma (increased peripheral utilisation) and reduce production by gluconeogenesis.
    • Only works with insulin presence so some residual functioning pancreatic islet cells are required.
  3. Combined therapy e.g. sulphonylureas (increases insulin production) or gliptins (inhibit incretin degrading enzymes DPP-4; incretin normally helps in glucose reuptake) etc.
38
Q
  1. Why should one monitor their glucose ?
A

to prevent complications or avoid hypoglycaemia.

39
Q
  1. You should encourage patients to self-monitor their glucose levels, how can this be achieved?
A

o Capillary blood measurement – prick fingers to check blood glucose levels.
o Urine analysis: glucose in urine gives indication of blood glucose concentration is above renal threshold.

40
Q
  1. Whats a test you can use to monitor your blood glucose levels for the past 3-4 months?
    Hint - people with diabetes have to have this test regularly
A

blood HbA1c test (glycated Hb; covalent linkage of glucose to residue in Hb).

41
Q
  1. Whats something we can test for the presence in urine to monitor glucose levels?
A

urinary albumin (index of risk of progression to nephropathy).

42
Q
  1. What is the difference between microvascular and macrovascular complications
A

Diabetes complications are divided into microvascular (due to damage to small blood vessels) and macrovascular (due to damage to larger blood vessels)
• Exact mechanisms of complications are unclear

43
Q
  1. What are some examples of micro vascular disease complications?
A

retinopathy,
nephropathy
neuropathy

44
Q
  1. What are some examples of macro vascular disease complications?
A

related to atherosclerosis heart attack/stroke

45
Q
  1. What value of plasma glucose is defined as hypoglycaemic?
A

•Defined as plasma glucose < 2.5 mmol/L

46
Q
  1. Is hypoglycaemia seen in diabetes patients or non-diabetic patients ?
A

present in patients with diabetes and without diabetes

47
Q
  1. What is the most common cause of hypoglycaemia?
A

Drugs are the most common cause

48
Q
  1. Out of type 1 and type 2 diabetes , which one is it more common to see hypoglycaemia?
A

o common in type 1 diabetes and less common in type 2 diabetes (taking insulin & insulin secretagogues).

49
Q
  1. Hypoglycaemia is uncommon in patients who dont have drug treated diabetes , in these patients what might the cause of hypoglycaemia be?
A 
alcohol
critical illnesses such as hepatic, renal or cardiac failure
sepsis
hormone deficiency
inherited metabolic dx.(diagnosis)
50
Q
  1. What may cause hypoglycaemia is diabetic patients?
A

• Exogeneous insulin & insulin secretagogues e.g. glyburide, glipizide and glimepiride (common sulfonylureas).
o Endogenous insulin suppresses hepatic and renal glucose production and increase glucose utilisation.

51
Q
  1. What are some drugs that are used to treat early type 2 diabetes that SHOULD NOT cause hypoglycaemia?
A

insulin sensitizers (metformin, Glitazones), glucosidase inhibitors, glucagon-like pepdide-1 (GLP-1) receptor antagonist and DDP-4 inhibitors.

52
Q
  1. What are some drugs that would cause hypoglycaemia in patients WITHOUT diabetes?
A 
quinolone
 quinine
beta blockers
ACE inhibitors 
IGF-1
53
Q
  1. What are two endocrine diseases that might cause hypoglycaemia in patients WITHOUT diabetes?
A

cortisol disorder or Insulinoma (insulin secreting tumour)

54
Q
  1. What is a hereditary metabolic disorder that might cause hypoglycaemia in patients WITHOUT diabetes?
A

hereditary fructose intolerance

55
Q

55 What are some other diseases that might cause hypoglycaemia in patients WITHOUT diabetes?

A

: severe liver disease, non-pancreatic tumours (beta cell hyperplasia), renal disease (metabolic. acidosis, reduced insulin elimination).

56
Q
  1. How does ethanol cause hypoglycaemia?
A

inhibit gluconeogenesis, but not glycogenolysis: hypoglycaemia follows several days when the alcohol binge with limited food take causes hepatic depletion of glycogen.

57
Q
  1. How does sepsis cause hypoglycaemia?

* Relatively common cause*

A

glycogen depletion by cytokine accelerated glucose utilisation and induced inhibition of gluconeogenesis.

58
Q
  1. How does chronic kidney disease cause hypoglycaemia?
A

unclear mechanism that may involve impaired gluconeogenesis, reduced renal clearance of insulin and reduce renal glucose production.

59
Q
  1. What is reactive hypoglycaemia (AKA postprandial hypoglycaemia)
    ??
    (Hypo’s after eating)
A

•Recurrent blood sugar drops (within four hours after eating) in both patients with and without diabetes.

60
Q
  1. Who is most likely to have reactive hypoglycaemia?
A

•More common in overweight individuals or those who have had gastric bypass surgery.

61
Q
  1. What causes reactive hypoglycaemia?
A

o a benign (non-cancerous) tumour in the pancreas that overproduces insulin

o too much glucose may be used up by the tumour itself

o deficiencies in counter-regulatory hormones: e.g. glucagon, epinephrine etc.

62
Q
  1. What is the response to hypoglycaemia in a normal patient?
A

• Reduced plasma glucose levels in fast state cause pancreatic beta-cells secretion of insulin to be decreased (1st defence):
o Increased hepatic glycogenolysis and gluconeogenesis and reduced glucose utilisation of peripheral tissue which induces lipolysis and proteolysis.

63
Q
  1. One of our bodies response to hypoglycaemia is to release regulatory hormones, what are these ?
A

Pancreatic alpha cells secrete glucagon to stimulate hepatic glycogenolysis (2nd defence).
o Epinephrine release from adrenomedullary stimulates hepatic glycogenolysis and gluconeogenesis + renal gluconeogenesis
o Prolonged hypoglycaemia (beyond 4 hours): cortisol and GH support glucose production and limit utilisation.

64
Q
  1. What is the counter-regulatory response to hypoglycaemia?
A

• Inhibition of the endogenous insulin secretion and stimulation of glucagon, catecholamines (norepinephrine, epinephrine), cortisol and growth hormone secretion - stimulate hepatic glucose production and cut down glucose utilization in peripheral tissues - increasing in this way plasma glucose levels.

65
Q
  1. What are the signs and symptoms of neurogenic (nervous system ) hypoglycaemia and what causes them?
A

mood changes, sweating and trembling, headaches, dizziness, extreme tiredness, pale, hunger and blurred vision.
o triggered by falling glucose levels
o activated by ANS & mediated by sympathoadrenal release of catecholamines and Ach

66
Q
  1. What causes neuroglycopenia (shortage of glucose in the brain) and what are the symptoms?
A

o Due to neuronal glucose deprivation.
o Sign & symptoms include confusion, difficulty speaking, ataxia (lack of co-ordination, balance and speech), paraesthesia (tingling/prickling caused by peripheral nerve damage), seizures, coma, death.

Clinical Biochemistry (7 decks)

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