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Molecular Basis Of Disease > Diabetes And Hypoglycaemia > Flashcards

Diabetes And Hypoglycaemia Flashcards

1
Q

How are blood glucose levels maintained?

A
  • Via dietary carbohydrates, glycogenolysis and gluconeogenesis
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2
Q

Describe what happens in the fasting state?

A
  • The Fasting state is a decrease in glucose levels for a prolonged period of time
  • Insulin levels decrease causing an increase in liver gluconeogenesis
  • This causes an increase in glucose production
  • This causes lipolysis - proteoloysis (catabolism - release of glucose into the blood)
  • Leads to a decrease in peripheral uptake
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3
Q

Describe the plasma regulation with high blood sugar

A

High blood sugar -> Pancreas -> Insulin -> stimulates glycogen formation from glucose in liver -> lowers blood sugar

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4
Q

Describe the plasma regulation of low blood sugar

A

Low blood sugar -> Pancreas -> Glucagon -> Stimulates glycogen breakdown to glucose in liver -> Raises blood sugar

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5
Q

Describe the function and major metabolic paths for Insulin

A
  • Promotes growth and storage
  • Stimulates glucose storage in muscle, liver
  • Stimulates protein & fatty acids synthesis
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6
Q

Describe the function and major metabolic paths for Glucagon

A
  • Mobilises fuel and maintains blood glucose in fasting state
  • Activates gluconeogenesis and glycogenolysis
  • Activates fatty acid release
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7
Q

Describe the function and major metabolic paths for Epinephrine

A
  • Mobilises fuels in Acute stress
  • Stimulates glycogenolysis
  • Stimulates fatty acid release
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8
Q

Describe the function and major metabolic paths for cortisol

A
  • Changing long term
  • Amino acid mobilisation, gluconeogenesis
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9
Q

Describe the function and major metabolic paths for growth hormones

A
  • Inhibits insulin action
  • Stimulates lipolysis
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10
Q

What is diabetes mellitus?

A

Metabolic disorder characterised by chronic hyperglycaemia, glycosuria (glucose in urine) and associated abnormalities of lipid and protein metabolism

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11
Q

State the 4 classifications of diabetes?

A
  • Type 1: Deficiency in insulin secretion
  • Type 2: Insulin secretion is retained but target organ resistant to its actions
  • Secondary: Chronic pancreatitis, pancreatic surgery, secretion of antagonists
  • Gestational: Occurs for first time in pregnancy
  • Gestational diabetes is a condition in which a woman without diabetes develops high blood sugar levels during pregnancy.
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12
Q

Describe the key features of type 1 DM with its most common cause?

A
  • Mostly children and young adults
  • Sudden onset (days/weeks)
  • Appearance preceded via ‘prediabetic period’ of several months
  • CC -> Autoimmune destruction of Beta-cells in pancreas -> interaction between genetic + environmental factors -> strong link with HLA genes within the MHC region on chromosome 6.
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13
Q

Describe the pathogenesis of type 1 DM?

A
  • Destruction of B-cells starts with autoantigen formation
  • AA presented to T-lymphocytes to initiate autoimmune response
  • Circulating AutoAB present to various -cell antigens such as glutamic acid decarboxylase
  • Tyrosine-phosphatase-like molecule, Islet auto-antigen
  • Most common detected antibodies is islet cell antibody
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14
Q

Describe how beta cells are destroyed via autoantodies?

A

VD

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15
Q

What does destruction of the pancreatic beta cells leads to and why?

A
  • hyperglycaemia: Absolute deficiency of insulin & amylin
  • Amylin, a glucoregulatory peptide hormone co-secreted with insulin causes decreased blood glucose
  • Leading to slowing gastric emptying, & suppressing glucagon output from pancreatic cells
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16
Q

State the metabolic complications of type 1 DM?

A
  • Insulin deficiency could lead to either:
  • Increased lipolysis -> Increased free fatty acids -> Increased FFA oxidation -> Ketoacidosis (increase in ketone free bodies -> diabetic coma
  • OR
  • Hyperglycaemia-> Glycouria (Glucose in urine) -> Polyuria (increased urination) -> Volume depletion (more water loss) -> Diabetic coma
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17
Q

Describe key presentations of type 2 DM?

A
  • Slow onset (months/years), Patients middle aged elderly - prevalence increase with age
  • Strong familiar incidence
  • Pathogenesis uncertain - insulin resistance; 3-cell dysfunction:
18
Q

Describe the pathophysiology of type 2 DM?

A
  • Primary beta cell failure (rare) -> Diabetes (first pathway)
  • Genetic predisposition + Obesity lifestyle factors -> Insulin resistance ->
  • Compensatory B cell hyperplasia (leads to normoglycaemia) ->
  • Beta cell failure (leads to impaired glucose intolerance) ->
  • B cell failure (late)
19
Q

Describe the pathogenesis of hyperglycaemic hyperosmolar nonketotic
coma (HONK) state + its diagnosis?

A

VD

20
Q

Describe the diagnosis of type 2 DM when symptoms are presented

A
  • In the presence of symptoms: (polyuria, polydipsia & weight loss for Type I)
  • Random plasma glucose ≥ 11.1mmol/I (200 mg/dl)
  • OR Fasting plasma glucose (no food for 8 hr) ≥ 7.0 mmol/I (126 mg/dl)
  • OR Oral glucose tolerance test (OGTT) - plasma glu ≥ 11.1 mmol/I
21
Q

Describe the diagnosis of type 2 DM when symptoms are aren’t present?

A
  • Absence of symptoms -> test blood samples on 2 separate days
22
Q

State the fasting plasma glucose + Oral glucose tolerance test values for individuals with Impaired Glucose Tolerance (IGT - prediabetic) + Impaired Fasting Glycaemia (IFG)?

A
  • Impaired glucose tolerance: FPG >7 mmol/L + OGTT = 7.8 - 11.1 mmol
  • Impaired plasma glycaemia: FPG = 6.1 to 6.9 mmol/L + OGTT < 7.8mmol/L
23
Q

What is the oral glucose tolerance test?
When should it be carried out?

A
  • Used in FPG ‹ 7.0 mmol/L -> tests glucose tolerance status.
  • OGTT should be carried out -> in patients with IFG, in unexplained glycosuria + in clinical features of diabetes with normal plasma glucose values
24
Q

Describe the oral glucose test

A
  • Process
  • 75g oral glucose
  • test after 2 hour
  • Blood samples collected at 0 and 120 mins after glucose
25
Q

State the drugs used for the treatment of T2 DM?

A
  • Metformin (decreases gluconeogenesis)
  • Sulfonylureas (Increases activity of B cells - Increase insulin release)
  • Thiazolidinediones (reduces insulin resistance)
  • SGLY2 inhibitors (Decrease glucose reabsorption from kidney - increase glucose excretion)
  • Incretin targeting drugs (prevents breakdown of natural incretins)
26
Q

What does incretin do?

A
  • Produces insulin
  • Decreases glucose production in liver
27
Q

Describe how glycaemic control is monitored and its aim?

A
  • Aim: prevent complications or avoid hypoglycaemia
  • Self-monitoring encouraged
  • Capillary blood measurement urine analysis: glucose in urine gives indication of blood glucose concentration above renal threshold
  • 3-4 months: blood HbA1c (glycated Hb; covalent linkage of glucose to residue in Hb
  • Others -> urinary albumin -> index of risk of progression to nephropathy
28
Q

State the long term complications of both type 1 and type 2 DM

A
  • Micro-vascular disease -> retinopathy, nephropathy, neuropathy
  • Macro-vascular disease -> related to atherosclerosis heart attack/stroke
  • Exact mechanisms of complications are unclear
29
Q

Define the plasma glucose range for hypoglycaemia

A

PG < 2.5 mmol

30
Q

State the causes for hypoglycaemia

A
  • Causes of hypoglycaemia
  • Drugs are most common cause
  • Common in type 1 diabetes
  • Less common in type 2 diabetes taking insulin & insulin secretagogues
31
Q

What does Insulin secretagogues do?

A
  • Insulin secretagogues help your pancreas make and release (or secrete) insulin
  • Insulin helps keep your blood glucose from being too high
32
Q

What drugs can cause hypoglycaemia in individuals with diabetes?

A
  • Types of sulfonylureas
  • Exogeneous insulin & insulin secretagogues
  • Glyburide, glipizide + glimepiride
33
Q

What causes hypoglycaemia in individuals without diabetes?

A
  • Drugs: alcohol, quinolone, quinine, beta blockers,
    ACE inhibitors + IGF-1
  • Endocrines disease - cortisol disorder
  • Inherited metabolic disorders, e.g. hereditary fructose intolerance
  • Insulinoma - tumour of pancreatic beta cells
34
Q

State 3 factors which can induce hypoglycaemia?

A
  • Ethanol
  • Sepsis
  • Chronic kidney disease
35
Q

Explain how ethanol can cause hypoglycaemia

A
  • inhibit gluconeogenesis, but not glycogenolysis
  • HG follow several days alcohol binge with limited food intake
  • Leads to Hepatic depletion of glycogen
36
Q

Explain how Sepsis can cause hypoglycaemia

A
  • Cytokine accelerated glucose utilization
  • induced inhibition of gluconeogenesis in the setting of glycogen depletion
37
Q

Explain how Chronic kidney disease can cause hypoglycaemia

A
  • Mechanism not clear
  • Impaired gluconeogenesis
  • Decreased renal clearance of insulin + Decreased renal glucose production.
38
Q

What is reactive hypoglycaemia and describe potential causes (3)?

A
  • Postprandial hypoglycaemia causes decreased blood sugar are recurrent, Occurs within 4 hours after eating..
  • unknown cause - benign tumour in the pancreas
  • Leads to overproduction of insulin, too much glucose used up by tumour, deficiencies in counter-regulatory hormones
39
Q

Describe the signs of hypoglycaemia

A
  • Neurogenic (autonomic) signs
  • triggered by decrease in glucose levels
  • Activated by ANS & mediated by sympathoadrenal release of catecholamines + Ach
40
Q

Describe the symptoms of hypoglycaemia?

A
  • Neuroglycopaenia = neuronal glucose deprivation in brain - Sign & symptoms:
  • Confusion, difficulty speaking, ataxia, paresthesia, seizures, coma, death

Molecular Basis Of Disease (30 decks)

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