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MBD > Diabetes and hypoglycaemia > Flashcards

Diabetes and hypoglycaemia Flashcards

1
Q

How are blood glucose levels maintained?

A

Dietary carbohydrate

Glycogenolysis, glycogen in liver broken down to release glucose

Gluconeogenesis, use of non-glucose sources to produce glucose

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2
Q

In the fed state what happens when glasma glucose increases?

A

Insulin released

causes decreased glycogenolysis (breakdown of glycogen in liver)

or decrease in production of glucose via glucogenolysis

increase in uptake of glucose into liver, converted to glycogen for storage

increase in peripheral uptake by muscles and adipose tissues

decrease in peripheral catabolism- lipolysis, and proteolysis

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3
Q

Blood glucose falls during fasting state, what happens to insulin?

A

Decrease in insulin production by pancreas

Increase in gluconeogenesis, liver increases production of glucose using non-glucose sources e.g lactic amino acids

peripheral uptake of glucose decreases (decrease in glucose going into muscles and adipose)

peripheral catabolism increases, lipolysis and proteolysis, releases glucose into blood stream

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4
Q

Why do we need to regulate plasma glucose levels?

A

need enough glucose to fuel body, brain and erthryocytes require continuous supply of glucose

too much glucose can cause pathological changes in tissues

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5
Q

what is the role of insulin in the liver?

A

insulin inhibits gluconeogenesis, the production of glucose from non-glucose substance.

Insulin is involved in synthesis of glycogen in the liver

And involved in synthesis of lipids or lipogenesis

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6
Q

What is the role of insulin in striated muscles?

A

Insulin is involved in the uptake of glucose from the bloodstream into the muscle cells, to reduce the plasma glucose level

Involved in synthesis of glycogen and proteins

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7
Q

What is the role of insulin in adipose tissues?

A

Insulin helps uptake of glucose into fat cells, decreasing level of glucose in plasma

Involved in synthesis of lipids, lipogenesis, inhibiting lipolysis

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8
Q

What are the counter-regulatory hormones to insulin?

A

Do the opposite of promoting storage and growth of glucose in muscles nad liver

Glucagon

Epinephrine

Cortisol

Growth hormone

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9
Q

What does glucagon do?

A

Activates gluconeogenesis and glycogenolysis - mobilises fuel

when insulin tries to decrease plasma glucose, glucagon can increase glucose level

activates fatty acid release

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10
Q

What is the function of epinephrine?

A

stimulates glycogenolysis, breaks down glycogen and release glucose into blood stream

stimulates fatty acid release

mobilising fuels in acute stress

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11
Q

What is the function of cortisol?

A

Amino acid mobilisation

gluconeogenesis, blood glucose level can increase when we become stressed

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12
Q

What is the function of growth hormone?

A

inhibits insulin action by stimulating lipolysis

insulin causes lipogenesis in liver and fatty cells, GH inhibits this by stimulating lipolysis

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13
Q

What is diabetes mellitus chracterised by? What causes this?

A

Chronic hyperglycaemia, glycosuria and associated abnormalities of lipid and protein metabolism.

caused by increased glucose level up to 10mmol/l, leading to glycosuria

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14
Q

What are the classifications of diabetes?

A

Type 1: deficiency in insulin secretion due to an autoimmune destruction of beta cells of pancreas by t cells

Type 2: insulin secretion is retained but there is target organ resistant to its actions

Secondary diabetes: due to chronic pancreatitis, pancreatic surgery, there is secretion of antagonists to insulin

Gestational: occurs for first time in pregnancy, disappears after giving birth

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15
Q

Who is type 1 DM common in?

What is the commonest cause?

A

Children, young adult. Sudden onset (days/weeks)

commonest cause is autoimmune destruction of B-cells of pancreas

  • due to interaction between environmental and genetic factors
  • strong link with HLA genes within MHC region of chr 6
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16
Q

What is the pathogenesis of type 1 DM?

A

Destruction of B-cells starts with autoantigen formation.

Auoantigen formed on insulin producing Beta cells.

Autoantigens presented to T-lymphocytes to initiate autoimmune response.

Autoantigens ingested by APCs which activate TH 1 and 2 lymphocytes.

T-H1 secretes IL-2 and IFN-y.

IL2 activates autoantigens specific t-cytotoxic lymphocytes, which destroy islet cells through secretion of toxin, decreasing insulin secretion

Activated TH 2 lymphocyte produces IL4, stimulating b lymphocytes to proliferate and produce islet auto-antibodies and antiGAD45 antibodies - destroy beta cells, decreasing insulin resistance

17
Q

What are the autoantibodies against glutamic acid decarboyxlase that are produced in type 1 DM?

A

Tyrosine-phosphate-like molecule

islet auto-antigen

18
Q

Why does destruction of B cells cause hyperglycaemia?

A

Due to deficiency of insulin and amylin.

Amylin - glucoregulatory peptide hormone co-secreted with insulin

Amylin lowers blood glucose by slowing gastric emptying

and suppressing glucagon output from pancreatic cells.

bringing down glucose levels.

19
Q

What are the metabolic complications of type 1 DM?

Starting with hyperglycaemia

A

Hyperglycaemia causes polyphagia (increased appetite, excessive eating)

High plasma glucose level, kidney threshold exceed, kidney can’t remove/reabsorb glucose from the blood - glycosuria

Causes osmotic diuresis - polyuria, urinate a lot as more water comes into blood and can’t be removed by kidney due to high conc. of sugar

Polydipsia, body compensates for increased urination by drinking more water

Volume depletion can cause diabetic coma

20
Q

How does insulin deficiency affect lipolysis?

A

Increased lipoysis as insulin is supposed to help with lipogenesis, in absence there is breakdown

Increases free fatty acid oxidation

can lead to increase in production of ketone bodies

leading to ketoacidosis

ketoacidosis and volume depletion can lead to diabetic coma

21
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, if someone in your family has it, then the risk of you developing it is higher

Pathogenesis uncertain – insulin resistance; B-cell dysfunction and not secreting enough insulin

22
Q

What is the pathophysiology of type 2 DM?

A

Genetic predisposition and environmental factors (obesity, lifestyle factors) leads to insulin resistance.

Body tries to produce enough insulin, leads to beta cell hyperplasia

B-cells of pancreas increase in size, may be able to produce enough insulin to bring glucose plasma levels to normal

B-cell hyperplasia continues to try to make enough insulin, eventually leads to failure of beta cells

causes impaired glucose tolerance

further failure of B-cells leads to diabetes

23
Q

What are the metabolic complications of type 2 DM?

HONK state

A

Hyperglycaemia, hyperosmolar non-ketonic state

Insulin low due to resistance of insulin to target cells, body feels there is low levels of glucose in circulation as uptake to cells is decreased

causes increased in glucose production by gluconeogenesis and glycogenolysis

leads to further increase in blood glucose - hyperglycaemia

leads to glycosuria

osmotic diuresis, water moving from EC space to blood vessels, loss of water and electrolystes - further dehydration - increased blood viscosity, leading to thrombosis

cerebral dehydration as hyperglycaemia increases plasma osmolarity

impaired conciousness, neurological signs due to decreased cerebral blood flow

24
Q

How is diabetes diagnosed in the presence of symptoms such as polyuria, polydipsia, weight loss (1dm) ?

A

Random plasma glucose test , blood glucose checked at any time > or equal 11.1mmol/l (200mg/dl)

Fasting plasma glucose > or equal 7.0mmol/l (126 mg/dl) Fasting is defined as no caloric intake for at least 8h

Oral glucose tolerance test (OGTT) - plasma glu > or equal to 11.1 mmol/l

In the absence of symptoms:

Test blood samples on 2 separate days

25
Q

What is IGT anf IFG (pre-diabetes) ?

A

Impaired glucose tolerance (IGT), when glucose levels are beyond the normal, person is at risk of developing diabetes and cardiovascular diseases

  • Fasting plasma glucose >7mmol/L and
  • OGTT value of 7.8-11.1 mmol

Impaired fasting glycaemia (IFG), blood glucose levels raised but not high enough to be classified as diabetic

  • Fasting plasma glucose 61. To 6.9 mmol/L and
  • OGTT value <7.8mmol/L
26
Q

When should oral glucose tolerance test be used?

A

To check body’s ability of metabolising glucose

  • In patients with IFG
  • In unexplained glycosuria
  • In clinical features of diabetes with normal plasma glucose values

Patient given 75g oral glucose and tested after 2 hours

Blood samples collected at 0, before glucose is given and 120 mins after glucose is given

IFG - OGTT should be less than 7.8

IGT - OGTT should be between 7.8 - 11.1

27
Q

Type 1 treated with insulin therapy, how is T2D treated?

A

Initial stages:

If blood glucose levels are higher doctor advises lifestyle changes, changes in diet and exercise

If that doesn’t help you are given oral monotherapy, metformin

If that doesn’t help you’re given oral combination of drugs

If that doesn’t help you will be given three drugs plus insulin

28
Q

How does metformin treat T2DM?

A

Decreases gluconeogenesis and increases utilisation of glucose at the periphery

29
Q

How does sulfonylureas work to treat T2DM?

A

Depolarises beta cells of the pancreas, pancreas releases insulin, reducing blood glucose levels.

30
Q

How does Thiazolidinediones work?

A

Activates paroxysm proliferator activated receptor, it reduces insulin resistance

31
Q

How do SGLT2 inhibitors work to treat T2DM?

A

Promote glucose excretion via the kidney, prevents glucose reabsorption in the kidney.

32
Q

How do incretin targeting drugs treat T2DM?

A

Helps body produce insulin when it is needed and reduce the amount of glucose produced by liver

  • DPP-4 inhibitors (prevent breakdown of natural incretins which are important to produce insulin and reduce amount of glucose being produced by liver)
  • Synthetic GLP-1 analogues , glucose like peptide analogue, helps to prevent breakdown of incretin.
33
Q

What are the long term complications of both type 1 and 2 DM?

A

Microvascular disease – retinopathy, nephropathy, neuropathy e.g diabetic foot, ulcer that cant heal. Hyperglycaemia can cause glycation of proteins and increase in sorbitol, this can cause thickening of basement membrane

Macrovascular disease – related to atherosclerosis heart attack/stroke

Exact mechanisms of complications are unclear, important for patient to manage blood glucose levels

34
Q

What is hypoglycaemia and its causes

A

Plasma glucose <2.5mmol/L

Drugs most common cause

Common in type 1 diabetes

Less common in type 2 diabetes taking insulin and insulin secretagogues

not common in patients who have drug treatment - hypoglycaemia may be caused by alcohol, illnesses e.g renal disease

35
Q

What drugs can cause hypoglycaemia in diabetes?

A

Exogenous insulin and insulin secretagogues such as glyburide, glipizide and glimepiride

the more commonly used sulfonylureas that can cause hypoglycaemia.

36
Q

What can cause hypoglycaemia in patients withour diabetes?

A

Drugs such as alcohol may cause hypoglycaemia

  • quinolone, quinine, beta blockers, ACE inhibitors and IGF-1

Endocrines disease e.g cortisol disorder

Inherited metabolic disorders e.g hereditary fructose intolerance

Insulinoma - tumour that start in beta cells in pancreas. When they make too much insulin, it brings blood glucose levels below 2.5mmol/L, resulting in hypoglycaemia

Ethanol: inhibit gluconeogenesis, but not glycogenolysis .

  • The hypoglycaemia follows several days alcohol binge with limited food intake; resulting in hepatic depletion of glycogen

Sepsis: relatively common cause of hypoglycaemia

  • Cytokine accelerated glucose utilisation and induced inhibition of gluconeogenesis in the setting of glycogen depletion

CKD chronic kidney disease: mechanism unclear, likely to involve impaired gluconeogenesis, reduced renal clearance of insulin and reduced renal glucose production

37
Q

What are the counter-regulatory responses to hypoglycaemia?

A

Inhibition of insulin secretion, first defence of response

2nd: stimulate glucagon secretion by alpha cells of pancreas, glucagon stimulates hepatic glycogenolysis

stimulates adrenal gland to release cortisol and epinephrine, epinephrine stimulates hepatic glycogenolysis and gluconeogenesis

prolonged hypoglycaemia - beyond 4hrs, cortisol and GH supports glucose production, limits utilisation of glucose at peripheral

cortisol, epinephrin and glucagon work together, decrease utilisation of glucose in periphery + increase production by gluconeogenesis/glycogenolysis

38
Q

What are the signs and symptoms of hypoglycaemia?

A

Neurogenic (autonomic)

  • triggered by falling glucose levels
  • activated by ANS and mediated by sypathoadrenal release of catecholamines and Ach

symptoms associated with elevated adrenaline levels

  • Trembling
  • sweating
  • paleness
  • mood changes
  • dizziness
  • hunger
  • blurred vision
  • headaches
  1. Neuroglycopenia
    * Due to neuronal glucose deprivation

signs:

  • confusion
  • difficulty speaking
  • ataxia
  • paraesthesia
  • seizures
  • coma
  • death
39
Q
A

MBD (21 decks)

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