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Molecular Basis of Disease > 20- Diabetes and Hypoglycaemia > Flashcards

20- Diabetes and Hypoglycaemia Flashcards

1
Q

what are the main sources of glucose maintenance in the body?

A

dietary carbohydrates
glycogenolysis - breakdown of glycogen to release glucose in the liver
gluconeogenesis - production of glucose from non-glucose sources in the liver

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2
Q

define gluconeogenesis

A

production of glucose from non-glucose sources in the liver, such as lactate, alanine, and fatty acids

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3
Q

describe the regulation of blood glucose levels in a fed state

A

food breakdown increases blood glucose levels, detected by the pancreas

insulin released from pancreatic beta cells which:
- increases glucose uptake into tissues, especially muscle and adipose tissue
- converts some glucose into glycogen, stored in the liver
reduces peripheral catabolism
- prevents breakdown of glycogen and other macromolecules

these actions decrease blood glucose levels, maintaining them within the 4-6mmol range

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4
Q

explain the regulation of blood glucose levels in a fasting state

A

not eating for some time leads to a decrease in blood glucose levels, detected by the pancreas

glucagon released from pancreatic alpha cells, which:
- increases gluconeogenesis and glycogenolysis in the liver = releases glucose into the blood
- induces breakdown of lipids and proteins/ lipolysis for energy

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5
Q

what is the function of insulin?

A

promotes storage of glucose, decreases blood glucose levels

promotes growth

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6
Q

what major metabolic actions does insulin stimulate?

A

increases glucose uptake into tissues – especially muscle and adipose tissue

promotes lipogenesis, inhibits lipolysis = more lipid production

converts some glucose into glycogen for storage in liver & muscle

prevents gluconeogenesis

promotes protein synthesis in the muscles

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7
Q

name the 4 counter-regulatory hormones for insulin

A

glucagon
adrenaline
cortisol
growth hormone

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8
Q

what is the function/functions of glucagon?

A

mobilises fuel

maintains BGL during fasting by increasing glucose release

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9
Q

what major metabolic actions does glucagon stimulate?

A

activates gluconeogenesis and glycogenolysis by the liver

activates fatty acid release = used in gluconeogenesis

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10
Q

what is the function of adrenaline in glucose regulation?

A

mobilises fuels in acute stress, part of the flight-or-fight response

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11
Q

what major metabolic actions does adrenaline stimulate?

A

stimulates glycogenolysis and fatty acid release = increases glucose

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12
Q

what is the function of cortisol in glucose regulation?

A

long-term changes to glucose levels, decreasing blood glucose

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13
Q

what major metabolic actions does cortisol stimulate?

A

amino acid mobilisation for gluconeogenesis

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14
Q

what is the function of growth hormone in glucose regulation?

A

inhibits insulin

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15
Q

what major metabolic actions do growth hormones stimulate?

A

stimulates lipolysis, production of fatty acids for gluconeogenesis

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16
Q

define diabetes mellitus

A

a metabolic disorder characterised by chromic hyperglycaemia, glycosuria and associated abnormalities in lipid and protein metabolism

can be insulin dependent (type 1) or non-insulin dependent (type 2)

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17
Q

list and describe the 4 classifications of diabetes mellitus?

A

type 1 = deficiency in insulin secretion

type 2 = insulin secretion is retained, but target organs resist its actions (insulin resistance

secondary = pancreatic health issues affecting insulin secretion (e.g., chronic pancreatitis)

gestational = occurs during pregnancy

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18
Q

describe the onset of type 1 diabetes mellitus

A

predominantly in children and young adults, but can occur at any age

sudden onset within days or weeks

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19
Q

what is the cause, and related factors of type 1 DM?

A

cause: autoimmune destruction of pancreatic beta cells

related factors:
- genetic = strong link with HLA genes on chromosome 6
- environmental = viruses such as mumps and rubella, drugs, stress - can trigger beta cell destruction

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20
Q

explain the pathogenesis of type 1 DM

A

autoantigens as components of pancreatic beta cells are presented to antigen-presenting T lymphocytes = triggers an immune response

activates Th1 and Th2 lymphocytes - different pathways:

  • Th1 lymphocytes can release interferon-gamma, activates macrophages which release IL-1 and TNF-alpha
  • Th1 lymphocytes can release IL-2, activates autoantigen specific T-cytotoxic CD8 cells
  • Th2 lymphocytes release IL-4, activates B-lymphocytes which produce islet autoantibodies

these all result in beta-cell destruction

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21
Q

why are infections a particular risk factor in the pathogenesis of type 1 DM?

A

infections can activate the immune system, triggering or accelerating beta-cell destruction

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22
Q

what is an autoantigen?

A

molecule/protein recognised by immune system as foreign to the body

in type 1 DM – autoantigens are components of pancreatic beta cells

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23
Q

examples of autoantigens in type 1 DM

A

glutamic acid decarboxylase
tyrosine-phosphatase-like molecules
islet autoantigens

components of pancreatic beta cells

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24
Q

what is an autoantibody?

A

antibody produced by immune system that targets and reacts with the body’s own tissues/ self-antigens

in type 1 DM = circulating autoantibodies formed in response to autoantigens present on the surface of pancreatic B-cells

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25
Q

what is the most commonly detected antibody associated with type 1 DM?

A

islet autoantigens

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26
Q

what is amylin?

A

a glucoregulatory peptide hormone co-secreted with insulin; works to lower BGL

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27
Q

how does amylin work to lower BGL?

A

slows gastric emptying - fewer dietary carbohydrates released into small intestine, prevents sudden increase in BGL

suppresses glucagon output from pancreatic cells

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28
Q

what are the metabolic complications of an absence of insulin?

A

increased hepatic glucose output = glycosuria

impaired glucose uptake into cells = high blood glucose remains/ hyperglycaemia which causes increased hunger/ polyphagia

increased glucose has an osmotic effect - causes diuresis, increases urination frequency and water loss, dehydration and affects fluid balance = can lead to diabetic coma

increased lipolysis = increased fatty acid production = beta-oxidation producing ketone bodies = diabetic ketoacidosis

29
Q

describe the metabolic complication of insulin deficiency triggering hyperglycaemia

A

without insulin, glucose can’t enter tissues = blood glucose remains high/ hyperglycaemia = triggers polyphagia

high conc of glucose passes through kidneys and the PCT can’t reabsorb all the glucose = some glucose is urinated out = glycosuria

presence of high glucose in urine draws more water into the nephron = increased frequency of urination and fluid loss = excessive thirst/ polydipsia

impairment of fluid balance can lead to volume depletion = leads to diabetic coma

absence of insulin also triggers lipolysis, producing fatty acids = oxidised by beta-oxidation into ketone bodies = excessive ketone bodies can lead to diabetic ketoacidosis

30
Q

how can diabetic ketoacidosis occur from type 1 DM?

A

insulin suppresses lipolysis, absence of insulin increases lipolysis

breakdown of lipids into fatty acids

lots of fatty acids produced, oxidised into ketone bodies by beta-oxidation

high levels of ketone bodies can lead to diabetic ketoacidosis

31
Q

what is the onset of type 2 DM?

A

slow onset over months to years

affects middle-aged to elderly individuals; prevalence increases with age

32
Q

what is the cause and related risk factors of type 2 DM?

A

cause: uncertain pathogenesis involving insulin resistance and B-cell dysfunction

related factors: strong family history association

33
Q

describe the diagnostic criteria for type 2 DM in the presence of symptoms - four tests

A

random plasma glucose greater than 11/ ≥ 11.1mmol/l

fasting plasma glucose greater than 7/ ≥ 7.0 mmol/l after at least 8hrs of no caloric intake

oral glucose tolerance test (OGTT) plasma glucose greater than 11/ ≥ 11.1 mmol/l

HbA1c ≥6.5% (48mmol/mol)

34
Q

describe the diagnostic criteria for type 2 DM in asymptomatic individuals

A

two abnormal values on separate days needed for T2DM diagnosis

35
Q

what is the OGTT?

A

oral glucose tolerance test

used in individuals with a fasting plasm glucose of above 7mmol/L to determine glucose tolerance status

carried out to check the body’s ability to metabolise glucose

recommended for those with impaired fasting glycaemia, unexplained glycosuria, and clinical features of diabetes with normal plasma glucose values

36
Q

what is the HbA1c test? what is its diagnostic criteria for diabetes?

A

glycated haemoglobin test, measures average blood sugar level over three months, performed at any time of day

measures covalent linkage of glucose to Hb residue

diagnostic threshold is HbA1c greater than/ ≥ 6.5% (48 mmol/mol)

may be affected by genetic and hematologic disorders (e.g., hemoglobinopathies, certain anaemias like sickle cell disease, malaria)

37
Q

what can affect the HbA1c test?

A

genetic and hematologic disorders = e.g., hemoglobinopathies, certain anaemias like sickle cell disease, malaria

38
Q

what two tests are performed to determine pre-diabetes?

A

impaired glucose tolerance
impaired fasting glycaemia

39
Q

how is the impaired glucose tolerance/IGT test conducted?

A

administer 75 grams of oral glucose, collect blood samples at 0 minutes and 120 minutes after digestion

results = fasting plasma glucose >7mmol/L, OGTT value of 7.8-11.1mmol/L

40
Q

what results for the impaired fasting glycaemia test would indicate pre-diabetes?

A

fasting plasma glucose between 6.1 to 6.9 mmol/L

OGTT value of <7.8 mmol/L

41
Q

list 5 types of drug treatments for type 2 DM

A

metformin
sulfonylureas
thiazolidinediones
DPP-4 inhibitors
alpha-glucosidase inhibitors

42
Q

describe metformin as a treatment for type 2 DM - effect and actions?

A

effect: counteracts insulin resistance and lowers blood glucose

actions: reduces hepatic glucose production, increases glucose uptake into muscle

43
Q

describe sulfonylureas as a treatment for type 2 DM - effect and actions?

A

effect: stimulates insulin secretion from beta cells to lower BGL

actions: enhances insulin secretion, risks hypoglycaemia without careful monitoring and diet changes

44
Q

describe thiazolidinediones as a treatment for type 2 DM - effect and actions?

A

effect: increases insulin sensitivity

action: has a slow onset glucose lowering effect

45
Q

describe DPP-4 inhibitors as a treatment for type 2 DM - effect and actions?

A

effect: prevents breakdown of natural incretin hormones. incretin stimulates insulin release; has a short half-life and is broken down by DPP-4

action: raises circulating concs of endogenous incretin hormones, prolongs half-life and stimulates insulin secretion

46
Q

describe alpha-glucosidase inhibitors as a treatment for type 2 DM - effect and actions?

A

effect: slows digestion of carbohydrates and inhibits intestinal alpha-glucosidase

action: delays glucose absorption, less of a sudden spike in BGL

47
Q

describe the three methods used for monitoring glycaemic control in diabetes

A
  • self-monitoring through capillary blood measurements or urine analysis to detect glucose in urine
  • regular assessments every 2-3 months involving glycated haemoglobin/ HbA1c tests
  • measuring urinary albumin to assess risk of nephropathy
48
Q

what are the two main types of complications from type 2 DM?

A

microvascular = affecting small vessels

macrovascular = affecting larger vessels

49
Q

what are the microvascular complications associated with type 2 DM?

A

retinopathy = affecting vision
nephropathy = impairing kidney function
neuropathy = nerve damage, particularly to the feet

50
Q

what is the mechanism behind microvascular complications in T2DM?

A

hyperglycaemia leads to:
- glycation of proteins
- increased sorbitol production
- formation of advanced glycation end products (AGE)

these cause structural changes in microvasculature

51
Q

how does retinopathy manifest in individuals with T2DM?

A

retinopathy involves damage to blood vessels in the retina, making them weak and leaky due to prolonged exposure to high glucose levels

ultimately affects vision

52
Q

how does nephropathy relate to T2DM?

A

nephropathy occurs from high glucose levels damaging renal microvasculature = impairs kidney function = causes protein leakage into urine

53
Q

how does neuropathy and diabetic foot occur in T2DM?

A

changes in microvascular nerve structures impair blood flow = leads to nerve damage affecting peripheral nerves

reduced blood flow to the lower limbs and nerve damage contribute to poor wound healing, more susceptible to infections

54
Q

what are the macrovascular complications associated with T2DM?

A

abnormalities in serum lipids contribute to a higher risk of CV events

formation of atherosclerotic plaques increase the risk of heart attacks and stroke

55
Q

define hypoglycaemia

A

a plasma glucose level below 4.0 mmol/L

56
Q

common causes of hypoglycaemia in diabetes

A

exogenous insulin and diabetes medications - seen more often in types 1 and 2

57
Q

common causes of hypoglycaemia unrelated to diabetes

A

drugs (quinolones, quinine, beta-blockers, ACE inhibitors)

alcohol consumption

endocrine diseases (e.g. cortisol disorders),

inherited metabolic disorders (e.g. hereditary fructose intolerance)

insulinomas

sepsis

chronic kidney disease

58
Q

what is reactive hypoglycaemia?

A

recurrent drops in blood glucose levels after eating, typically occurring within 4 hours

also called postprandial hypoglycaemia

59
Q

what are the potential causes of reactive hypoglycaemia?

A

benign pancreatic tumours causing insulin overproduction

tumour consumption of glucose

deficiencies in counter-regulatory hormones - e.g. glucagon

60
Q

name the two classes of symptoms for hypoglycaemia

A

neurogenic/ autonomic
neuroglycopenic/ CNS

61
Q

what are the neurogenic/autonomic symptoms of hypoglycaemia? mechanism behind them?

A

triggered by falling glucose levels

symptoms:
- shaking, cold sweats, anxiety, nausea, palpitations, and numbness

cause: activated by the autonomic NS, mediated by sympathoadrenal release of catecholamines and acetylcholine

62
Q

what are the neuroglycopenic symptoms of hypoglycaemia?

A

a result of neuronal glucose deprivation leading to CNS glucose deprivation

symptoms:
- confusion, difficulty speaking, ataxia, paraesthesia, seizures, coma, death

63
Q

define ataxia

A

disorders affecting co-ordination, balanced and speech

64
Q

define paraesthesia

A

feeling of tingling, numbness/ pins and needles – can be caused by affected nerve supply to neurons

65
Q

LO: Revise the homeostasis of blood glucose, its distribution, control by insulin, counter-regulatory hormones

A
66
Q

LO: Understand hyperglycaemia (DM)

A
66
Q

LO: Define Hypoglycaemia and its causes

A
67
Q

LO: Understand the sign and symptoms of hypoglycaemia

A

Molecular Basis of Disease (27 decks)

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