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Phase 2 3. Endocrinology > PBL 2 - T2DM > Flashcards

PBL 2 - T2DM Flashcards

1
Q

What is T2DM?

A

progressive disorder characterised by hyperglycaemia that accompanies a relative insulin
deficiency

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2
Q

What do T1DM and T2DM have in common?

A

both lead to hyperglycaemic states, and both
share common macrovascular (coronary heart, cerebrovascular, and peripheral vascular disease) and microvascular
(retinopathy, nephropathy, and neuropathy) complications.

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3
Q

What features are unique to T2DM?

A

● Patients are usually overweight (85% are obese, BMI > 30)
● Patients are usually older (although many teenagers are now presenting with T2DM)
● Usually present with a longer history, with slowly progressing symptoms or with chronic complications.
● Hyperglycaemia is less marked than Type 1 DM
● No ketoacidosis
● Islet cell antibodies not present
● Weight loss is minimal

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4
Q

What symptoms are shared between T1DM & T2DM

A

● Polyuria - due to osmotic diuresis when blood glucose levels exceed the renal threshold.
● Thirst - due to the resulting loss of fluid and electrolytes (dehydration, dry mouth)
● Tiredness, impaired consciousness, impaired visual activity
● Muscle weakness and muscle wasting
● Skin - more prone to infections
● Tachycardia, hypotension

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5
Q

What are the 4 main determinants of T2DM?

A

○ Obesity and physical inactivity
○ increase age
○ ethnicity
○ family history

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6
Q

Describe normal insulin secretion

A

beta cell exhibits a biphasic insulin secretory response to a continuous glucose infusion

● First-phase insulin release begins immediately, peaks in 10 minutes, and is over at 20 minutes.
● A second (delayed) response begins at about 15 to 20 minutes, rises to a maximum over the next 20 to 40 minutes, and
remains constant for the duration of the infusion

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7
Q

Describe the pathogenesis of T2DM

A

ordinarily involves the development of insulin resistance associated with
compensatory hyperinsulinemia, followed by progressive beta-cell impairment that results in decreasing insulin secretion
and hyperglycemia.

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8
Q

What is insulin resistance?

A

the failure of target tissues to respond to insulin. I.e. a normal amount of insulin fails to lead to normal
glucose regulation

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9
Q

What is the result of insulin resistance in the muscles?

A

decreased glucose uptake (and therefore decreased glucose clearance from the blood)

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10
Q

What is the result of insulin resistance in the liver?

A

impaired suppression of glucose production, causing elevated fasted plasma glucose levels

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11
Q

How is insulin resistance compensated in the early stages of disease?

A

by increased insulin secretion (causing hyperinsulinemia), which allows glucose metabolism to remain normal

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12
Q

What abnormalities manifest in T2DM patients?

A

manifest abnormalities both in tissue (muscle, fat, and liver) sensitivity to insulin and in pancreatic insulin secretion.

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13
Q

What happens when the body cannot compensate for insulin resistance?

A

β cells are unable to compensate adequately and blood glucose rises, producing hyperglycaemia

> Beta cells are unable to meet the body’s increased demand for insulin
Initially a failure in the first phase of insulin secretion
Later, the second phase of insulin secretion is also impaired
Over time, there is a gradual loss of beta cell mass
DM2 patients also have a markedly reduced incretin effect

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14
Q

What is the T2DM response to different feeding states with decreasing beta cell function?

A

resistance first develops postprandial hyperglycemia and subsequently develops fasting hyperglycemia.

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15
Q

How does hyperglycaemia effect T2DM?

A

Hyperglycemia itself causes additional inhibition of insulin secretion and more insulin resistance (glucose toxicity), which further accentuates the hyperglycemia.

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16
Q

What 3 abnormalities characterise T2DM?

A

1) Insulin resistance
2) Increased glucose production by the liver
3) deficient insulin secretion by beta cells.

= targets of therapeutic interventions

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17
Q

What is the most common cause of insulin resistance?

A

Obesity - not only absolute amount of body fat, but also its distribution is important (central obesity has a greater risk)

Increased general sugar uptake correlates with obesity, leading to hyperinsulinaemia and downregulation of insulin receptors

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18
Q

What is the correlation between physical activity and insulin sensitivity?

A

Inactivity is associated with down regulation of insulin-sensitive kinases and may promote accumulation of FFAs in skeletal muscle

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19
Q

How does T2DM arise?

A

By itself, insulin resistance is not a disease.
● For disease to arise = combination of insulin resistance and another defect.
● The occurrence of disease can thus be thought of as ‘2 hit’, with insulin resistance being first hit.

It is the decreasing beta-cell function that accounts for the progression from impaired glucose tolerance (IGT) to type 2
diabetes, and increasing severity of hyperglycemia.

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20
Q

How does visceral obesity cause insulin resistance?

A
  • resistance starts with increase in body fat
  • exaggerated by decrease in physical activity

-Visceral obesity unique -intraperitoneal fat drains directly to the liver via the portal circulation and is metabolically
more active than subcutaneous adipose tissue.

FFA and TAG accumulate in sites that do not normally store fat, e.g. the liver, skeletal muscle, heart and pancreatic beta bells

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21
Q

What are the effects of elevated FFA?

A
  • lipotoxicity
  • inhibit glucose uptake & glycogen storage in peripheral tissues
  • decreased hepatic insulin sensitivity
  • Reduced adiponectin production
  • incresed leptin, pro-inflammatory cytokines
  • Adipose tissue releases inhibitory mediators
  • intracellular accumulation of TAG and acyl CoA derivatives,
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22
Q

Describe lipotoxicty

A

chronic FFA elevation has a direct toxic effect on pancreatic beta cells

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23
Q

What is the consequence of reduced adiponectin production?

A
  • normally promotes insulin action on target tissues
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24
Q

What is the consequence of adipose tissue releasing inhibitory mediators

A

(NEFA and TNF-alpha)
interfere with insulin signalling by disrupting
the propagation of protein-tyrosine phosphorylation

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25
Q

What is the outcome of NEFA overload?

A

lead to intracellular accumulation of TAG and acyl CoA derivatives, especially diacylglycerol
○ These molecules activate intracellular signalling pathways (serine kinase pathways) that block insulin signalling by
blocking the insulin receptor tyrosine kinase signalling cascade

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26
Q

How does hyperinsulinaemia occur and what is the outcome?

A

Caused by insulin resistance

Can down-regulate the number of insulin receptors on the plasma membrane, further causing cellular insulin resistance

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27
Q

Describe the mitochondrial abnormalities in T2DM

A

Abnormal intracellular accumulation of TAG in liver and skeletal muscle suggests a defect with mitochondrial lipid oxidation

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28
Q

What is metabolic syndrome?

A
  • insuli resistance
  • hypertension => heart disease
  • high serum lipids
  • obesity (central, abdominal)
  • non-alcoholic fatty liver albuminurea
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29
Q

Which body systems are insulin independent?

A
  • brain

- nervous system

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30
Q

How is glucose transported?

A

GLUT 3 actively transports glucose across the cell membrane of nervous tissue in the presence of low or high plasma
glucose levels and in the presence or absence of insulin.

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31
Q

What is the body’s energy source in the presence of insulin?

A

preferentially uses glucose by actively taking it up and metabolising it or storing it as glycogen in the muscle or as fat in the adipose tissue, effectively lowering postprandial plasma glucose.

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32
Q

What is the body’s energy source in the absence of insulin?

A

switches to ketone/free fatty acid metabolism, reducing uptake of glucose and instead
using circulating free fatty acids for energy.

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33
Q

What are the major causes of death in T2DM?

A
  • cardiovascular complications
  • renal failure
  • infections
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34
Q

Which consequences of hyperglycaemia may play a role in onset of damage?

A
  • non-enzymatic glycosylation (glycation)
  • polyol pathway
  • abnormal microvascular blood flow
  • haemodynamic changes
  • other
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35
Q

How does glycation occur?

A

Many proteins, e.g. haemoglobin, collagen and LDL and tubulin (in peripheral nerves), become glycosylated due to high
levels of plasma glucose (glucose binds covalently)

Glycation occurs roughly in proportion to hyperglycaemia severity

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36
Q

What is the result of glycation

A

accumulation of advanced glycosylated end products (AGEs)

permanently alters the structure & potentially affecting function

Unstable bonds in proteins containing AGEs result in physical cross-linking of nearby proteins - this may
contribute to thickening of the vascular BM in diabetes

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37
Q

What is the polyol pathway?

A

two-step process that converts glucose to sorbitol to fructose

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38
Q

Why is the polyol pathway activated?

A

Hyperglycaemia increases glucose uptake into insulin-independent tissues.

Some glucose enters aldose reductase pathway

39
Q

What is the aldose reductase pathway

A

Glucose + NADPH → Sorbitol + NADP

catalysed by aldose reudctase (has a low affinity for glucose, it generates significant amounts of sorbitol when glucose levels
are elevated)

40
Q

What is the outcome of the aldose reductase pathway

A

depletes cellular reducing agents, thereby altering redox status

Sorbitol accumulates and alters cell homeostasis

41
Q

What are the consequences of sorbitol accumulation?

A

This causes changes in vascular permeability, cell proliferation, and capillary structure via stimulation of protein kinase C
and transforming growth factor beta

in the eye -> excess sorbitol creates an osmotic gradient that causes influx of fluid and consequent swelling

42
Q

How does abnormal microvascular blood flow cause damage in T2DM?

A

● Impairs blood supply of nutrients and oxygen
● Microvascular occlusion occurs due to vasoconstrictors - e.g. endothelins and thrombogenesis
● Leads to endothelial damage

43
Q

What other factors cause damage in T2DM?

A

● Formation of ROS and stimulation of growth factors - TGF-beta and VEGF by ischaemic tissues
● Stimulates endothelial cell proliferation

44
Q

What are macrovascular complications?

A

refer to the larger arteries as opposed to pathology of the smaller capillaries in microvascular
complications.

45
Q

What are type 2 diabetic patients are at a very considerable risk of excessive morbidity and mortality from?

A 
○ Ischaemic Heart Disease
○ Myocardial infarction (MI) - 2-4x more likely
○ Peripheral Vascular Disease (PVD)
○ Claudication
○ Ischaemia
○ Ulceration/Gangrene in feet
(Amputation of a foot for gangrene is 50x more likely)
○ Cerebrovascular Disease
○ Stroke - 2x more likely
○ Transient ischaemic attack
46
Q

How does hyperglycaemia affect larger blood vessels?

A

atherosclerosis

47
Q

In what ways can a T2DM patient develop macrovascular complications?

A

● Direct effects of hyperglycaemia on the arterial wall
● Side effects of diabetic therapy
● Exacerbation of general risk factors for atherosclerosis (associated with metabolic syndrome)

48
Q

How are macrovascular complications managed?

A
  • smoking cessation
  • hypertension treatment
  • low dose aspirin
  • statins to lower cholesterol
49
Q

How can cardiovascular risk in diabetes be minimised?

A
  • control of BP
  • management of dyslipidaemia
  • antiplatelet therapy
  • antihyperglycaemic pharmacotherapy
  • lifestyle changes
  • exercise
  • nutrition therapy
50
Q

What are the main classes of drugs used in T2DM

A
  • Biguanides
  • Sulphonylureas
  • Thiazolidinediones
  • Incretin Based Therapies
  • SGLT2 Inhibitors
51
Q

Describe the biguanides

A 
Metformin
- blood glucose-lowering treatment 
- weight-neutral
- does not cause hypoglycaemia 
- established benefits in
microvascular disease

First line therapy

Mechanism of action is not fully understood. It is thought to the reduce hepatic gluconeogenesis.

52
Q

Describe sulphonylureas

A

Mechanism of Action: inhibits ATP-sensitive K+ channels
● Closed potassium channels cause a depolarisation and subsequent Ca2+ influx causing
insulin release.

● Glibenclamide, Gliclazide, Glimepiride, Tolbutamide, Glipizide used clinically.

53
Q

Describe thiazolidinediones

A

Ligand for peroxisome proliferator-activated receptor-Ɣ (PPARƔ).
● PPARƔ is a transcription factor, stimulating expression of genes involved in triglyceride storage.
● Stops inappropriate deposition of lipid in non-adipose tissues (which leads to insulin resistance) – therefore improves
insulin sensitivity.
● Pioglitazone

54
Q

What are the incretins and why are they targeted?

A

Incretins are peptide hormones that are released in the GI tract in response to food, and potentiates insulin secretion. They
are:
○ Glucagon-like Peptide 1 (GLP-1)
○ Gastro-Intestinal Peptide (GIP)

These incretins are rapidly broken down by DPP-4.
In type 2 diabetes, this is diminished, thus you don’t get the insulin effect required.

55
Q

What are the different types of incretin based therapies?

A
  • incretin mimetics

- DPP-4 inhibitors

56
Q

Describe incretin mimetcs

A

Exenatide, Liraglutide
● Mimic incretins (GLP-1)
● Engineered for slower breakdown - not cleaved by DPP-4
● Injected – improve endogenous insulin secretion

57
Q

Describe DPP-4 inhibitors

A

Sidagliptin, Vildagliptin
● Inhibit DPP-4 - enzyme that breaks down endogenous incretins
● Increase endogenous incretin-mediated increase in insulin secretion
● Oral drugs

58
Q

Describe SGLT2 inhibitors

A

● These inhibit the reuptake of glucose by blocking the action of the SGLT2 transports in the kidney PCT.
● As a result, it reduces hyperglycaemia.
● About 25% of the filtered glucose is not reabsorbed, however this results in glycosuria (which can increase risk of UTIs)
● Dapagliflozin

59
Q

Why do microvascular complications occur in T2DM?

A

due to damage to smaller capillaries.

due to thickening of the basement membrane, alongside increased vascular permeability throughout the body.

60
Q

How can diabetes effect the eye?

A

○ Cataracts → denaturation of the protein and other components of the lens, rendering it opaque

○ External ocular palsies → affect nerves 3 and 6, normally resolve spontaneously within 3-6 months

○ Diabetic retinopathy → damage to the retina and iris, which can lead to blindness

61
Q

What is the pathogenesis of diabetic retinopathy?

A

Hyperglycaemia causes intramural pericyte death, and thickening of the basement membrane of small blood vessels in the
retina
● This initially increases vascular permeability, increasing retinal blood flow, and disrupts intracellular metabolism in retinal
endothelial cells
● This leads to impaired vascular autoregulation, increased production of vasoactive substances and endothelial cell
proliferation.
● The resulting capillary hypoperfusion and closure cause chronic retinal ischaemia, stimulating growth factors (VEGF) that
increases vascular permeability (causing retinal leakage and exudation).

62
Q

What are the different stages of diabetic retinopathy?

A

non-proliferative (early stages) and proliferative (late stage)

63
Q

Describe the main features of the non-proliferative stage of diabetic retinopathy

A
  • microaneurysms
  • dot haemorrhages
  • hard exudates
  • cotton wool spots
64
Q

How do microaneurysms occur in the non-proliferative stage?

A

result from damage to the wall of small vessels

65
Q

How do dot haemorrhages occur in the non-proliferative stage?

A

superficial haemorrhages occur in the outer layers and ganglion cell when vessel walls are breached

66
Q

How do hard exudates form in the non-proliferative stage?

A

(proteins and fluid left behind)
○ Damaged blood vessels leak fluid into the retina
○ The fluid is cleared into retinal veins, leaving behind protein and lipid droplets → form hard exudates
○ These are eventually cleared by macrophages

67
Q

How are cotton wool spots formed in the non-proliferative stage?

A

○ Caused by micro-infarcts within the retina due to occluded vessels
○ The spot itself is due to the accumulation of debris within cytoplasm of axons
○ Debris is removed by macrophages
○ As this occurs, there may be white dots (cytoid bodies) where the cotton wool spot used to be

68
Q

What are the main features of the peroliferative stage of diabetic retinopathy?

A
  • venous blleding
  • blockage of blood vessels
  • fibrotic bands
  • retinal detachment
  • macular oedema
69
Q

Describe venous bleeding in the proliferative stage of diabetic retinopathy

A

damage to the walls of veins causes their calibre to vary and elongation to occur (formation of venous
loops)

70
Q

Describe blockage of blood vessels in the proliferative stage of diabetic retinopathy

A

leads to areas of capillary non-perfusion
○ Ischaemia in these regions causes release of VEGF and other growth factors - stimulate neovascularization in the
retina
■ Growth of new blood vessels on optic disc or retina.
○ While some of these new blood vessels inside the retina are helpful, others emerge through the retina and lie on
its surface
○ The normal shearing stresses that occur within the eye causes these vessels, which are often flaccid and
abnormal, to bleed
○ Small haemorrhages give rise to pre-retinal haemorrhages
○ Further bleeding leads to vitreous haemorrhage and sudden loss of vision

71
Q

Describe how fibrotic bands form in the proliferative stage

A

form later as collagen tissue grows along the margins of the new vessels

72
Q

Describe how retinal detachment occurs in the proliferative stage

A

fibrotic bands may contract and pull on the retina, causing further haemorrhage and retinal
detachment

73
Q

Describe how macular oedema occurs in the proliferative stage

A

○ Fluid leaking from vessels is cleared poorly from the macular areas because its anatomy differs to the rest of the
retina
○ When clearance fails, this leads to macular oedema.
○ Thickens and distorts the retina at the macula
○ Sustained distortion causes a loss of central vision

74
Q

What is the treatment and management for diabetic retinopathy

A

● Good glycaemic control
● Stop smoking
● Good blood pressure control
● Address risk factors
● Ophthalmic review (laser, vitrectomy, VEGF inhibitors).
○ Diabetic patients are checked annually from the age of 12 years for evidence of retinopathy.
○ Patients are referred to opthamologists if there are any threatening signs.

75
Q

What is diabetic nephropathy

A

Diabetic nephropathy is damage to your kidneys caused by diabetes. In severe cases it can lead to kidney failure. But not everyone with diabetes has kidney damage.

76
Q

What are the early signs of diabetic nephropathy?

A

In the first few years, there is hyperfiltration, which later declines steadily.
○ This is due to renal hypertrophy (at the glomerulus), leading to an increase in GFR.

77
Q

What are the middle stages of diabetic nephropathy?

A

As the kidney becomes more damaged, the afferent arteriole dilates more than the efferent arteriole
○ This increases glomerular pressure, further damaging glomerular capillaries
○ Increased glomerular pressure also increases the shear stress on endothelial cells.
○ This causes mesangial cell hypertrophy and increased ECM secretion, resulting in eventual thickening of the
glomerular basement membrane (glomerular sclerosis)
○ There is also disruption of the protein cross-linkages that normally make the kidney an effective filter → the end
result is the leakage of large molecules (particularly protein) into the urine → microalbuminuria.

78
Q

What is microalbuminuria

A

small traces of albumin in the urine that normally cannot be detected on a dipstick.

79
Q

Why is screening for microalbuminuria useful

A

it is an independent predictor of macrovascular disease in type 2
diabetes

80
Q

What are the later stages of diabetic nephropathy?

A

Later there is progressive glomerulosclerosis (hardening of the glomerulus) and glomerular destruction.
○ This further increases the leakage of proteins → macroalbuminuria.
● Ultimately glomerulosclerosis worsens until glomeruli are progressively lost and renal function deteriorates → end-stage
renal failure.

81
Q

How is diabetic nephropathy treated?

A

Progression to end stage renal failure can be slowed primarily by ensuring good blood pressure and glycaemic control.
Blockade of the renin-angiotensin system using ACE inhibitors or AII-RAs is also of proven benefit.
● Detection of microalbuminuria or overt nephropathy (macroalbuminuria) should prompt vigorous efforts to reduce
progression of nephropathy or cardiovascular disease:
○ Aggressive cardiovascular risk reduction (ACEi, statins, stop smoking etc)
○ Improve glycaemic control → there is strong evidence to suggest that good glycaemic control prevents
microalbuminuria.
○ Patients must be referred to the renal clinic if eGFR < 30 and/or develop CKD

82
Q

What is diabetic neuropathy?

A

Diabetic neuropathy is nerve damage that is caused by diabetes. Over time, high blood glucose levels, also called blood sugar, and high levels of fats, such as triglycerides, in the blood from diabetes can damage your nerves

83
Q

Where does diabetic neuropathy mainly manifest?

A

peripheral nervous system, but can sometime affect the CNS

84
Q

How does diabetic neuropathy occur?

A

secondary to metabolic disturbance, and prevalence is related to the duration of diabetes and the degree of metabolic control

capillary damage, including occlusion in the vasa
nervorum
○ Reduced blood supply to the neural tissue results in impairments in nerve signalling that affect both sensory and
motor function
■ Axonal degradation of nerve fibres, with thickening of the schwann cell basal lamina

85
Q

How is diabetic neuropathy characterised?

A

by slowed nerve conduction with axonal loss and demyelination.

86
Q

What is the pathogenesis of diabetic neuropathy

A

○ impaired blood flow due to the changes in the capillaries
● Capillary damage
● Structural changes
● Axonal degradation due to ischaemia.

○ direct toxicity via the polyol pathway/ low myoinositol, free radicals, nitric oxide and glycation of neuronal
proteins.

87
Q

What are the symptoms of diabetic neuropathy?

A

○ Numbness or loss of feeling
○ Prickling/Tingling
○ Aching/Burning pain
○ Unusual sensitivity or tenderness when feet are touched.

88
Q

What are the signs of diabetic neuropathy?

A

○ Diminished vibratory perception
○ Decrease knee and ankle reflexes
○ Reduced protective sensation such as pressure, hot and cold,
and pain

12

○ Diminished ability to sense position of toes and feet.

89
Q

What is the diabetic foot a combination of?

A

○ Ischaemia
○ ulceration
○ infection

90
Q

How does foot ulceration occur?

A

Foot ulceration is often due to trauma, in the presence of neuropathy and peripheral vascular disease (PVD).

91
Q

Where are common sites of ulceration?

A

Most ulcers develop at the site of a plaque of callus skin, beneath which tissue necrosis occurs and eventually breaks
through to the surface.

92
Q

Why do diabetic patients present late with ulceration?

A

Due to the peripheral nerve dysfunction associated with diabetes (diabetic neuropathy), patients have a reduced ability to
feel pain. This means that minor injuries may remain undiscovered for a long while.

93
Q

What are the effects of hyperglycaemia on capillaries?

A

● Hyperglycaemia causes:
○ increased blood flow to capillaries
○ advanced glycosylation end products and oxidative stress
○ thickening and altered composition of the basement membrane
○ loss of pericytes that regulate vessel calibre.
● basement membrane thickening
○ Basement membrane thickening causes increased vascular permeability causing capillaries to become leaky.
● Capillary closure
○ causes the tissue beyond the obstruction to become starved of blood and oxygen.
○ this causes ischaemic damage to the tissue in question.

Phase 2 3. Endocrinology (25 decks)

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