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Phase 2 3. Endocrinology > PBL 1 - T1DM > Flashcards

PBL 1 - T1DM Flashcards

1
Q

What are the cell types within the islet of langerhans and what do they secrete?

A

β cells → produce Insulin

α cells → produce Glucagon

delta-cells → produce Somatostatin

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2
Q

Describe the structure of insulin

A

polypeptide hormone

- two short chains (A and B) linked by disulphide bonds

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3
Q

What is proinsulin?

A

insulin + c peptide

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4
Q

What is pre-proinsulin?

A

precursor synthesised by the ribosomes of the beta cells from insulin mRNA

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5
Q

How is pre-proinsulin converted to proinsulin?

A

cleaved in the golgi apparatus

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6
Q

Where is insulin stored?

A

in secretory granules

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7
Q

What factors can increase insulin release?

A
  • hyperglycaemia
  • growth hormone
  • cortisol
  • beta agonists
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8
Q

What factors can decrease insulin release?

A
  • hypoglycaemia
  • somatostatin
  • alpha agonists
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9
Q

Why is growth hormone said to have anti-insulin activity?

A

it supresses the abilities of insulin to stimulate uptake of glucose in peripheral tissues and enhance glucose synthesis in the liver.

However, administration of growth hormone stimulates insulin secretion, leading to hyperinsulinemia

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10
Q

What triggers insulin secretion?

A

β-cells sense changes in plasma glucose concentration an responds

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11
Q

How is glucose levels detected in the beta cells?

A

Glucose enters β cells via the GLUT-2 receptor.
○ Glucose transporter 2 (GLUT2), constitutively expressed in β-cells, is the first encountered glucose sensor in β-
cells
○ mobilization of GLUT2 to the plasma membrane is insulin-independent and the transporter protein shows a low
substrate affinity, ensuring high glucose influx

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12
Q

What is the mechanism of insulin secretion?

A

● Metabolism of the glucose generates ATP => closes the ATP-sensitive Potassium (K+) channels in the membrane

● Closure of these K+ channels causes a depolarisation in the membrane (since K+ is not moving out of the cell).

● Depolarisation causes voltage-gated Calcium channels to open, causing Ca2+ influx.

● Increased intracellular calcium causes fusion of insulin granules with the cell membrane, releasing insulin by exocytosis.

● Insulin is released into the portal circulation and is carried to the liver, its primary target organ

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13
Q

Where does insulin bind?

A

Insulin binds to Insulin Receptors on the surface of target tissues

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14
Q

Describe the insulin receptors

A
  • tyrosine kinase receptors

- made up of 2 alpha and 2 beta units

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15
Q

Where are insulin receptors mainly found?

A
  • liver
  • striated muscle
  • adipocytes
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16
Q

How does insulin bind to the insulin receptor?

A

insulin binds to

the α-unit

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17
Q

What changes occur on insulin binding to the insulin receptor?

A

conformational change in the β-units, causing autophosphorylation and an intracellular cascade of events.

Insulin-receptor complex is internalised by the cell
> Insulin is degraded
> Receptor is recycled to the cell surface

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18
Q

What is the effect of insulin on the liver?

A

○ Increases glycogen synthesis
○ Increases fatty acid synthesis
○ Inhibits gluconeogenesis (PEPCK & G6Pase)

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19
Q

What is the effect of insulin on the muscle?

A

○ Increases glucose transport (GLUT4 translocation to membrane)
○ Increases glycogen synthesis

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20
Q

What is the effect of insulin on the adipose tissue

A

○ Increases glucose transport (GLUT4)
○ Suppresses lipolysis
○ Increases fatty acid synthesis

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21
Q

What is the effect of insulin on electrolytes?

A

increases the permeability of many cells to potassium, magnesium and phosphate ions.

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22
Q

How does insulin effect potassium levels?

A

Insulin activates sodium-potassium ATPases in many cells, causing a flux of
potassium into cells.

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23
Q

What is glycogen synthesised from?

A

glucose

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24
Q

What is the function of glycogen?

A

in liver = storage for blood glucose maintenance

in muscle = storage for local energy production (only used by muscle itself)

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25
Q

How is glucagon synthesied?

A
  • synthesized as proglucagon

- processed in alpha cells of pancreatic islets into glucagon

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26
Q

Where is glucagon secreted?

A

alpha cells in the islet of the pancreas

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27
Q

What is the major stimulus for glucagon secretion?

A

hypoglycaemia

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28
Q

What causes inhibition of glucagon secretion?

A

hyperglycaemia (major inhibition)

also inhibited by somatostatin

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29
Q

What can trigger glucagon secretion?

A
  • hypoglycaemia
  • elevated blood levels of amino acids
  • exercise
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30
Q

Describe glucagon signalling

A

Glucagon binds to the Glucagon Receptor, a G-protein coupled receptor (GPCR) found in hepatocytes.

○ Increases cyclic AMP (cAMP)
○ cAMP stimulates cAMP-dependent protein kinase (PKA)

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31
Q

What is the effect of glucagon on target tissues?

A

Only acts on the liver (only site of receptors), to increase blood glucose

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32
Q

How does glucagon increase blood glucose levels?

A

○ Glucagon stimulates breakdown of glycogen stored in the liver - acts on hepatocytes to activate the enzymes that
depolymerize glycogen and release glucose.

○ Glucagon activates hepatic gluconeogenesis - pathway by which non-hexose substrates such as amino acids are
converted to glucose

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33
Q

What effect does glucagon have on lipolysis?

A

appears to have a minor effect of enhancing lipolysis of triglyceride in adipose tissue, which could be viewed
as an addition means of conserving blood glucose by providing fatty acid fuel to most cells.

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34
Q

What is the normal range of glucose?

A

3.5-8.0 mmol/L

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35
Q

Which tissues are more dependent on glucose than others?

A
  • erythrocytes (no mitochondria)
  • brain (FA cannot cross BBB)
  • retina
  • testes - BTB
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36
Q

What is the response of insulin levels in a fasted state?

A

Insulin concentration is low

  • Main action is to regulate glucose release by the liver
    > Acts as a hepatic hormone, modulating glucose production – insulin inhibits gluconeogenesis
    > Hepatic glucose production rises as insulin levels fall
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37
Q

What is the response of insulin levels in a postprandial state?

A

Insulin concentrations are high
○ Promote glucose uptake into peripheral tissues (increased glucose utilisation)
○ Suppresses glucose production in the liver

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38
Q

Why is diabetic insulin injection not equivalent to

A

1 - insulin is secreted directly into the portal circulation and reaches the liver in high concentration

2 - Subcutaneous soluble insulin takes 60-90 minutes to achieve peak plasma levels - onset and offset of action are too slow

3 - Absorption of subcutaneous insulin into the circulation is variable

4 - Basal insulin levels are constant in healthy people. In contrast, insulin injections causes peaks and declines in plasma insulin
levels, causing swings in metabolic control

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39
Q

Describe the factors that influence the aetiology of T1DM

A
  • polygenic genetic susceptability
  • environmental factors
  • viruses
  • geographical factors
  • dietary factors
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40
Q

What gene polymorphisms increase susceptibility to T1DM

A

DR4-DQ8 and DR3-DQ2 are considered susceptibility genes

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41
Q

What gene polymorphisms provide protection from T1DM

A

DR15-DQ6 considered protective

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42
Q

What is the link between viruses and T1DM?

A

In a genetically susceptible individual, viral infection may stimulate the production of antibodies against a viral
protein that trigger an autoimmune response against antigenically similar beta cell molecules

○ congenital rubella syndrome
○ human enteroviruses.

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43
Q

What geographical factors are involved in the aetiology of T1DM?

A

geographical variation in disease prevalence

increasing worldwide incidence

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44
Q

What dietary factors are involved in the aetiology of T1DM?

A

Potential increased risk with exposure to cow’s milk in infancy, early introduction of cereals, or maternal vitamin
D ingestion increase type 1 diabetes risk.

infant supplementation with vitamin D may be protective.

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45
Q

What autoimmune diseases is T1DM associated with?

A

○ Autoimmune thyroid disease
○ Coeliac disease - shares the HLA-DQ2 genotype, more common in DM1 patients
○ Addison’s disease (adrenal insufficiency)
○ Pernicious anaemia

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46
Q

What is the main cause of T1DM?

A

autoimmune pancreatic beta-cell destruction in genetically susceptible individuals.

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47
Q

What antigens are T1DM most likely to produce antibodies against?

A

○ glutamic acid decarboxylase (GAD)
○ Insulin
○ islet auto-antigen- 2 (IA-2) - a tyrosine-phosphatase- like molecule

48
Q

How does beta-cell destruction occur?

A

proceeds sub-clinically for months to years as insulitis (inflammation of the beta cell).

49
Q

What is insulitis?

A

inflammation of the beta cell due to the infiltration of mononuclear cells into beta cells

50
Q

Which molecules damage the beta cells?

A

Predominantly CD8 + , but also some CD4 + (and some neutrophils/macrophages)

Inflammatory cells release cytokines, including IL-1, IL-6, IFN-alpha and NO, causing further beta cell injury

51
Q

When does hyperglycaemia occur in onset of T1DM?

A

Once 80-90% of beta cells destroyed

52
Q

How is T1DM treated?

A

Patients need exogenous insulin to reverse this catabolic condition, prevent ketosis, decrease hyperglucagonemia, and normalize lipid and protein metabolism

53
Q

What is the effect of insulin deficiency on energy production?

A

the body metabolises fat preferentially over glucose for energy

Oxidation of fat over produces ketone bodies:
> Acetoacetic acid
> Beta hydroxybutyric acid

These are released from the liver into the blood, and lead to metabolic acidosis

54
Q

How does insulin deficiency result in hyperglycaemia

A

unsuppressed hepatic glucose output
> Insulin normally inhibits gluconeogenensis/glycogenolysis, but these processes are no longer inhibited

reduced glucose deposition in skeletal muscle and adipose tissue

55
Q

What hormones are stimulated during hyperglycaemia?

A

○ Glucagon
○ Adrenaline
○ Cortisol
○ growth hormone

56
Q

What processes are triggered by the counter-regulatory hormones secreted in hyperglycaemia?

A

○ Gluconeogenesis
○ Glycogenolysis
○ Ketogenesis

57
Q

What is the result of insulin deficiency in the body?

A

As a result, patients present with hyperglycaemia and anion gap metabolic acidosis.

Leads to:
○ Glycosuria
○ Dehydration from the loss ofbody water in urine

If uncorrected, progressive acidosis and dehydration lead to coma and ultimately death

58
Q

What is DKA?

A

Diabetic ketoacidosis

59
Q

How and why are ketone bodies produced in diabetes?

A

absence of insulin leads to the release of free fatty acids from adipose tissue (lipolysis), which are converted by
beta oxidation into ketone bodies (acetoacetate and β-hydroxybutyrate).

60
Q

What is the purpose of ketone bodies?

A

β-Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery (protective mechanism in case of starvation)

ketone bodies have a low pKa and therefore turn the blood acidic (metabolic acidosis).

61
Q

How does the body respond to increasing ketone levels in diabetes?

A

The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and
other mechanisms must work to compensate for the acidosis.

One such mechanism is hyperventilation to lower the blood carbon dioxide levels
(in its extreme form, may be observed as Kussmaul respiration)

62
Q

What is the effect of high glucose levels on the urine?

A

High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis

63
Q

What is osmotic diuresis?

A

when substances in the blood accumulate in the tubules of the kidney, reducing reabsorption of water in the kidneys, thereby increasing urine output

64
Q

What is the result of osmotic diuresis?

A

polyuria, dehydration, and polydipsia.

65
Q

What is the consequences of DKA?

A

mechanisms, the average adult with DKA has a total body water shortage of about 6 liters (or 100
mL/kg), in addition to substantial shortages in sodium, potassium, chloride, phosphate, magnesium and calcium.
Glucose levels usually exceed 13.8 mmol/L

66
Q

What can trigger DKA?

A

includeinfection, not takinginsulincorrectly,stroke and certain medications such assteroids

67
Q

What are the symptoms of DKA?

A

rapid onset:

o Excessive thirst
o Frequent urination
o Nausea and vomiting
o Abdominal pain
o Weakness or fatigue
o Shortness of breath
o Fruity-scented breath
o Confusion
68
Q

How is DKA confirmed?

A
  • Hyperglycaemia

- Presence of ketones in urine

69
Q

What are the long-term complications of T1DM and how do they occur?

A

vascular complications due to:

  • glycosylation of proteins in tissue and serum
  • production of sorbitol
    > normally involved in osmoregulation
    > formation requires NADH => excess sorbitol production = reduced NADH for production of molecules
    like NO => increased blood pressure
  • free radical damage.
70
Q

What are the microvascular complications of T1DM?

A

○ Retinopathy
○ Neuropathy
○ Nephropathy

71
Q

What are the macrovascular complications of T1DM?

A

○ Cardiovascular disease
○ Cerebrovascular disease
○ peripheral vascular disease.

72
Q

What effect does hyperglycaemia have on cells?

A

known to induce oxidative stress and inflammation.

○ Oxidative stress can cause endothelial dysfunction by neutralising nitric oxide.

○ Dysfunctional endothelium allows entry of LDL into the vessel wall, which induces a slow inflammatory process
and leads to atheroma formation

73
Q

What is T1DM?

A

is a metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency.

= results in the inability to maintain blood glucose levels.

= lifelong

74
Q

How does T1DM occur?

A

due to destruction of pancreatic beta cells, mostly by immune-mediated mechanisms.

75
Q

How is autoimmune T1DM characterised?

A

Characterised by absolute insulin deficiency and the presence of antibodies to pancreatic beta cells

76
Q

How is idiopathic T1DM characterised?

A

○ Uncommon form that is characterised by absence of antibodies.
○ Increased likelihood in patients of African or Asian ancestry and has a strong genetic component.
○ Presentation of idiopathic type 1 diabetes does not differ from that of autoimmune type 1 diabetes.

77
Q

What are the classic symptoms of T1DM?

A
  • polyuria
  • polydipsia
  • polyphagia
  • unexplained weight loss
  • fatigue
  • blurred vision
  • nausea
78
Q

Describe the T1DM symptom of polyuria

A

caused by osmotic diuresis secondary to hyperglycemia
○ Glucose and ketones are freely filtered at the glomerulus and not all of it can be reabsorbed as it exceeds the
renal threshold.

○ An increased solute concentration in the tubular lumen causes an osmotic gradient, resulting in increased water,
sodium and potassium loss in the urine.

79
Q

Describe the T1DM symptom of polydipsia

A
  • thirst is a response to the hyperosmolar state and dehydration
    ○ due to the resulting loss of fluid and electrolytes (dehydration, dry mouth)
    ○ Hyperaldosteronism exacerbates renal potassium loss.
    ○ Since K+ is lost in large quantities during osmotic diuresis, there will be an extracellular migration of K+ from cells
    into the blood, therefore serum K+ is usually normal or elevated due to the resulting loss of fluid and electrolytes
    (dehydration, dry mouth)
80
Q

Describe the T1DM symptom of weight loss

A

due to fluid depletion and accelerated muscle/fat breakdown.

81
Q

Describe the T1DM symptom of fatigue

A

caused by muscle wasting from the catabolic state of insulin deficiency, hypovolemia, and hypokalemia
○ Muscle cramps are caused by electrolyte imbalance

82
Q

Describe the T1DM symptom of blurred vision

A

effect of the hyperosmolar state on the lens and vitreous humor. Glucose and its metabolites cause
osmotic swelling of the lens, altering its normal focal length.

83
Q

What tests are performed to confirm T1DM

A
  • blood glucose levels
  • glycated haemoglobin
  • autoantibodies
84
Q

What are the blood glucose levels in a normal individual?

A

■ Fasting plasma glucose level <7.0 mmol/L (Fasting = no caloric intake for 8 hours)

■ Plasma glucose 2hrs after glucose should be < 7.8mmol/L

85
Q

What are the blood glucose levels in a T1DM patient?

A

■ Fasting plasma glucose level >7.0 mmol/L

■ Plasma glucose > 11.1 mmol/L following glucose tolerance test (2hrs after 75g oral glucose)

86
Q

What is glycated haemoglobin?

A

gives an accurate measure of glycemic control. Haemoglobin A1c (HbA1c) is an integrated
measure of an individual’s prevailing blood glucose concentration over several weeks.

87
Q

What HbA1c level is indicative of T1DM?

A

HbA1c > 6.5% (48mmol/L)

88
Q

What autoantibody tests should be performed?

A

Test for C-Peptide deficiency can help determine the decline in β cell function.

(During insulin production, the C-peptide is cleaved off from pre-proinsulin, leaving A & B peptides)

89
Q

How is DKA treated?

A

Treating symptoms:

For Hypovolaemia → IV fluids

For Insulin deficiency → IV Insulin
(most essential treatment for switching off ketogenesis)

For hypokalaemia → IV potassium

90
Q

What is the preferred diet in T1DM?

A

● Low in sugar
● High in starchy carbohydrates (with a low GI)
● High in fibre
● Low in fat (especially saturated fats)

91
Q

What are the different forms of insulin

A
  • animal
  • human (recombinant - produced synthetically)
  • analogues:
    > long - acting
    > short-acting
92
Q

What is the effect of short-acting insulin on glucose control?

A

little effect on overall glucose control because improved postprandial glucose is balanced by higher
levels before the next meal

93
Q

When is short-acting insulin used?

A

● Used for pre-meal injection in multiple dose regimens
● Used for continuous IV infusion in labour or medical emergencies
● Used in patients using insulin pumps

94
Q

What is the disadvantage of human insulin?

A

Human insulin is absorbed slowly, reaching a peak 60-90 minutes after subcutaneous injection
○ Absorption delayed because soluble insulin is in the form of a stable hexamer
○ Needs to dissociate into monomers/dimers before it can enter the circulation

Action tends to persist after meals → predisposing patients to HYPOGLYCAEMIA

95
Q

What is the effect of long-acting insulin?

A

● Structurally modified to delay absorption or prolong duration of action
● Action of human insulin can be prolonged by the addition of zinc or protamine.

96
Q

When is long-acting insulin used?

A

● Tend to be injected once or twice a day to provide background insulin lasting approximately 24 hours.
● They don’t need to be taken with food since they don’t have a peak action.

97
Q

What is the advantage of long-acting insulin?

A

Useful in patients on intensified therapy or with troublesome hypoglycaemia

98
Q

How is insulin administered?

A

● Insulin is usually administered via a pen injection

● Injections are given into subcutaneous fat on the abdomen, thighs or upper arms

99
Q

What factors influence the rate of insulin absorption?

A

depends on local subcutaneous blood flow

Accelerated by:
■ Exercise
■ Local massage
■ Warm environment

Absorption is more rapid from the abdomen, and slowest from the thigh

100
Q

What are insulin pumps?

A

CSII (continuous subcutaneous insulin infusion) is delivered by a small pump strapped around the waist that infuses a
constant trickle of insulin via a needle in the subcutaneous tissues.

The insulin pump uses regular or rapid-acting insulin

Provides a basal rate of insulin and delivers mealtime bolus dosing.

101
Q

What are the advantages of insulin pumps?

A

○ may reduce hypoglycaemia, especially when combined with continuous glucose monitoring systems (CGMS) and
threshold suspend features
○ May improve A1C
○ provides greater flexibility.

may reduce anxiety and
help achieve better glycaemic control in selected patients.

102
Q

How is glucose monitored with insulin pumps?

A

patient must still measure blood glucose frequently to adjust the pump to deliver the appropriate amount of insulin.

103
Q

What is the aim of intensive insulin therapy?

A

aims to mimic physiological insulin release by combining basal insulin with bolus dosing at mealtime

104
Q

What is a continuous glucose monitoring system?

A

measures subcutaneous interstitial fluid glucose every 5 minutes.

105
Q

What are the disadvantages of continuous glucose monitoring systems?

A

The glucose sensors used in CGMS are not reliable at lower ranges of glucose, and thus do not eliminate the need for
fingersticks.

CGMS are also less accurate than traditional capillary blood glucose-monitoring methods.

106
Q

What are the advantages of CGMS?

A

Real time CGMS, worn by a patient on a regular basis, may help improve glycaemic control.

they provide glucose trends, provide alarms to impending hypo- or
hyperglycaemia, and reduce episodes of hypoglycaemia.

107
Q

What are sensor-augmented insulin pumps?

A

Insulin pumps with glucose sensors integrated into the same unit

108
Q

What are the complications of insulin therapy?

A
  • At the injection site:
    ○ Painful, reddened lesions, possibly scarring
    ○ Injection site abscesses are rare
    ○ Local allergic responses can occur early in therapy
    ○ Lipohypertrophy (= fatty lumps) can occur with overuse of a single injection site
  • Insulin resistance
  • Weight gain
  • Hypoglycaemia
109
Q

What times of the day poses the greatest risk of hypoglycaemia?

A

○ Before meals
○ At night
○ During exercise

110
Q

What can episodes of hypoglycaemia be precipitated by?

A

○ Irregular eating habits
○ Unusual exertion
○ Alcohol excess
○ Can also be caused by variation in insulin absorption

111
Q

What causes hypoglycaemia?

A

Results from an imbalance between insulin injection and patient’s diet, activity and basal insulin requirement

112
Q

What are the symptoms of hypoglycaemia?

A

(blood glucose <3mmol/L)

adrenergic features:

  • sweating
  • tremor
  • palpitations
  • hunger
  • anxiety
  • pallor
  • cold sweat
  • coma
113
Q

What is nocturnal hypoglycaemia?

A

basal insulin requirement falls during the night but increase from about 4am onwards, at a time when levels of injected insulin are falling.

As a result, many patients wake with high blood glucose levels, but find that injecting more insulin at night increase the risk of hypoglycaemia in the early hours of the morning

Dinnertime NPH is a frequent cause of symptomatic and asymptomatic nocturnal hypoglycaemia, and can be
taken at bedtime so that the peak effect is closer to the early morning increase in cortisol.

114
Q

How is hypoglycaemia treated?

A

Give glucose (15-20g of a fast acting carbohydrate)
○ sugary fizzy drink (cola, lemonade)
○ 3 or more glucose tablets
○ five sweets e.g. jelly beans

115
Q

How do you treat hypoglycaemia in a person with reduced consciousness?

A

give intramuscular glucagon
○ glucagon will facilitate the release of stored glucose back into the bloodstream, raising the blood glucose level.
○ Intravenous Dextrose - form of sugar.
○ Long acting carbohydrate may be required to prevent a further drop in blood sugar.

Phase 2 3. Endocrinology (25 decks)

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