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3. Inflammation > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is type 1 diabetes characterised by?

A

Type 1 diabetes, which has an immune pathogenesis and is characterised by severe insulin deficiency

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2
Q

What is type 2 diabetes characterised by?

A

Type 2 diabetes, which results from a combination of insulin resistance and less severe insulin deficiency.

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3
Q

What is the aetiology of type 1 diabetes?

A

Type 1 diabetes belongs to a family of HLA-associated immune-mediated organ-specific diseases.

More than 90% of patients with type 1 diabetes carry HLA- DR3, HLA-DR4 or both

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4
Q

What specific HLA regions are implicated in type 1 diabetes?

A

DR3
DR4
IDDM2
IDDM12

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5
Q

What is the pathogenesis of type 1 diabetes?

A

Destruction of beta cells in the pancreas, caused by islet autoantibodies

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6
Q

Which are specific islet-cell antibodies, as seen in type 1 diabetes?

A

Anti GAD
IA2
ZnT8A

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7
Q

What are the stages of type 1 diabetes?

A
  1. Genetic predisposition: DR3; DR3; IDDM2; IDDM12
  2. Early pre-diabetes: islet-cell antibodies
  3. Late pre-diabetes: progressive loss of insulin release and glucose intolerance
  4. Overt diabetes: C-peptide absence
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8
Q

How does type 1 diabetes often present?

A

Young people often present with a 2–6-week history and report the classic triad of symptoms:

  1. Polyuria – due to the osmotic diuresis that results when blood glucose levels exceed the renal threshold
  2. Thirst – due to the resulting loss of fluid and electrolytes
  3. Weight loss – due to fluid depletion and the accelerated breakdown of fat and muscle secondary to insulin deficiency.
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9
Q

What are clinical cues leading to the type 1 diabetes diagnosis?

A
  • leaner build
  • rapid progression to insulin therapy following an initial response to other therapies
  • the presence of circulating islet autoantibodies
  • insulin-deficient
  • ketosis-prone
  • HLA markers
  • autoimmune
  • onset peak in adolescence
  • weight loss
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10
Q

How is diabetes diagnosed?

A

One abnormal lab in symptomatic individuals, two in asymptotic:

  1. Fasting plasma glucose >7 mmol/L
  2. Random plasma glucose > 11.1 mmol/L
  3. HbA1c > 6.5
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11
Q

What is HbA1c?

A

The termHbA1crefers to glycated haemoglobin. It develops when haemoglobin joins with glucose in the blood, becoming ‘glycated’.

By measuring glycated haemoglobin (HbA1c), clinicians are able to get an overall picture of what our average blood sugar levels have been over a period of weeks/months.

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12
Q

What is a normal HbA1c?

A

<42 mmol/L (below 6%)

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13
Q

What is a HbA1c value indicative of prediabetes?

A

42-47 mmol/L

6.0-6.4%

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14
Q

What is a HbA1c value indicative of diabetes?

A

> 48 mmol/L

>6.5%

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15
Q

How does HbA1c affect clinical outcome?

A

Improving HbA1c by 1% (or 11 mmol/mol) for people with type 1 diabetes or type 2 diabetes cuts the risk of microvascular complications by 25%

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16
Q

What does lifestyle advice for type 1 diabetes include?

A
  1. Low in sugar, but not sugar-free
  2. High in starchy carbohydrates
    • Give advice on counting carbohydrates, do not advice a low GI diet
  3. High in fibre
  4. Low in (saturated) fat
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17
Q

What is the treatment algorithm for type 1 diabetes?

A

Offer twice‑daily insulin detemir with rapid-acting analogues injected before meals (first line)

Once-daily insulin glargine (100 units/ml) if insulin detemir is not tolerated or the person has a strong preference for once‑daily basal injections

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18
Q

What are the glucose aims for type 1 diabetes patients?

A

Fasting plasma glucose level of 5to 7mmol/litre on waking and

Plasma glucose level of 4to 7mmol/litre before meals at other times of the day

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19
Q

How does tight regulation of BG, BP and lipid increase health?

A
  • Tight blood glucose control → less microvascular complications
  • Tight blood pressure control → less macrovascular complications
  • Tight blood lipid control → less cardiovascular events
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20
Q

What are the two main pathological features in type 2 diabetes?

A
  1. Pancreatic beta-cells do not make enough insulin

2. Cells do not respond to insulin

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21
Q

What are the four main risk factors that are implied in type 2 diabetes?

A
  1. Increasing age
  2. Obesity
  3. Ethnicity (Asian, African)
  4. Family history
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22
Q

How does inflammation relate to type 2 diabetes?

A

Subclinical inflammatory changes are characteristic of both type 2 diabetes and obesity

Circulating levels of the pro-inflammatory cytokines TNF-α and IL-6 are elevated in both diabetes and obesity

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23
Q

What causes insulin resistance?

A

Insulin resistance is caused by obesity and lack of physical activity, this leads to increase secretion of insulin from pancreatic beta cells, which leads to beta-cell exhaustion combined with hyperglycaemia

Established diabetes is associated with hypersecretion of insulin by depleted beta-cell mass → cells do not respond

Hyperglycaemia and lipid excess are toxic to beta cells, leading to further damage and decreased insulin levels and increased hyperglycaemia

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24
Q

How does insulin secretion change over the course of diabetes?

A

Goes up initially to make up for unresponsive cells, but then goes down massively and plateaus

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25
Q

How does insulin resistance change over the course of diabetes?

A

Slowly creeps up and plateaus high up

26
Q

With what signs is type 2 diabetes associated?

A
  1. central obesity
  2. hypertension
  3. hypertriglyceridemia
  4. decreased HDL-cholesterol
  5. disturbed haemostatic variables
  6. modest increases in a number of pro-inflammatory markers.
27
Q

How does a type 2 diabetes patient often present?

A

Thirst, polyuria and weight loss are typically present but patients may complain of such symptoms as lack of energy, visual blurring or pruritus vulvae or balanitis that is due to Candida infection

28
Q

How does regular exercise influence disease progression and morbidity of type 2 diabetes?

A

Several trials have shown that regular exercise reduces the risk of progression to type 2 diabetes by 30– 60%, and the lowest long-term morbidity and mortality is seen in those with established disease who have the highest levels of cardiorespiratory fitness.

29
Q

What is the treatment aim for type 2 diabetes?

A

Always aim for HbA1c of <48 mmol or <6.5%

30
Q

What is the treatment algorithm for type 2 diabetes?

A
  1. Metformin is first line
  2. If HbA1c rises to 58mmol/mol or 7.5%, metformin WITH:
    - DDP-4
    - pioglitazone
    - Sulphonylurea
    - SGLT
  3. Triple therapy: metformin + SU + DDP-4/pioglitazone
31
Q

What is the prognosis of type 2 diabetes?

A

When type 2 diabetes is diagnosed at age 40, men lose an average of 5.8 years of life, and women lose an average of 6.8 years of life

32
Q

What is diabetic ketoacidosis?

A

Complex disordered metabolic state due to absolute or relative insulin deficiency with the biochemical triad:

  1. Glucose > 11.1 mmol/L
  2. Blood ketones > 3 mmol/L
  3. pH < 7.3
33
Q

What is a metabolic complication of ketoacidosis?

A

Insulin causes K to move into cells, in insulin deficiency the K leaks OUT of the cells, leading to hyperkalaemia

Hyperkalaemia leads to renal K losses and whole body K depletion

When DKA is treated K+ moves rapidly into cells, and because whole body is K+ deplete, extracellular K+ (reflected in serum K+) falls very quickly

34
Q

What is the main cause of diabetic ketoacidosis?

A

Infection

35
Q

What are signs of diabetic ketoacidosis?

A
  • Kussmaul respiration
  • Ketotic fetor
  • Dehydration
  • Tachycardia
  • Hypotension
  • Mild hypothermia
  • Confusion, drowsiness, coma
36
Q

What are symptoms of diabetic ketoacidosis?

A
  1. Polyuria, polydipsia, thirst
  2. Weight loss
  3. Blurred vision
  4. Vomiting
  5. Abdominal pain
  6. Weakness
  7. Leg cramps
37
Q

How would you treat diabetic ketoacidosis?

A
  1. Fluid replacement with 0.9% saline
  2. Insulin replacement
  3. Potassium replacement
  4. Identify and treat cause
  5. Venous thromboembolism prophylaxis
  6. ICU
38
Q

What is Hyperosmolar hyperglycemia state?

A

State of severe uncontrolled diabetes with sufficient insulin to suppress ketogenesis

More common in type 2 diabetes

39
Q

What biochemical values is a hyperosmolar hyperglycemia state characterised by?

A
  • Hypovolaemia
  • Marked hyperglycaemia (≥30mmol/l)
  • Hyperosmolarity (serum osmolality ≥ 320mosmol/kg)
  • No significant ketonaemia (serum ketones<3mmol/l)
  • No significant acidosis (pH>7.3, bicarbonate>15mmol/l)
40
Q

How would you differentiate HHS from DKA?

A

DKA: type 1, younger, rapid onset, pH < 7.3, ketones high, glucose > 11

HHS: type 2, older, onset days to weeks, pH normal, ketones normal, glucose > 30

41
Q

What is the main cause of hyperosmolar hyperglycemia state?

A

Infection

42
Q

What are the complications of hyperosmolar hyperglycemia state?

A

High mortality (15-20%)

  • Osmotic demyelination syndrome (pontine myelinolysis)
  • Cerebral oedema
  • Seizures
43
Q

What are symptoms of hyperosmolar hyperglycemia state?

A
  1. Thirst, polyuria
  2. Blurred vision
  3. Weakness
44
Q

What are the signs of hyperosmolar hyperglycemia state?

A
  1. Dehydration
  2. Tachycardia
  3. Hypotension
  4. Confusion and drowsiness
  5. Coma
45
Q

How would you manage hyperosmolar hyperglycemia state?

A
  1. Gradually normalise osmolality, fluid status and glucose
  2. Intravenous 0.9% saline (normal saline)
  3. Insulin replacement at a fixed rate
  4. Identify and treat the cause
  5. Venous thromboembolism prophylaxis
46
Q

In diabetic patients, what is defined as low blood glucose?

A

<3.5 mmol/L

47
Q

How would you treat mild hypoglycaemia?

A

Oral fast-acting carbohydrate 15-20g

Once recovered (≥3.5 mmol/l (or 4 mmol/l)), eat 15-20g long-acting/complex carbohydrate

48
Q

How would you treat severe hypoglycaemia?

A

If unconscious: IM glucagon or IV glucose

If conscious: oral fast-acting carbohydrate 15-20g

Once recovered (≥3.5 mmol/l (or 4 mmol/l)), eat 15-20g long-acting/complex carbohydrate

49
Q

What macrovascular complications can arise due to diabetes?

A
  • Stroke
  • CVD (coronary heart disease, ischaemic stroke, congetsive heart dailure)
  • DVT
50
Q

What microvascular complications can arise due to diabetes?

A

Nephropathy
Retinopathy
Neuropathy

51
Q

Through what mediators does high blood glucose damage blood vessels?

A
  1. Advanced glycation
  2. Metabolic Mechanisms Sorbitol Generation
  3. Oxidative stress
  4. Cytokines and growth factors (TGF-beta, VEGF, IGF-I)
52
Q

What are the two types of retinopathy?

A
  1. Pre-proliferative → ischaemia

2. Proliferative → new vessels

53
Q

What happens in ischaemic retinopathy?

A
  1. Basement membrane thickening (due to TGF-beta)
  2. Microaneurysm formation
  3. Microaneurysm complications (oedema in the eye due to venous stasis and exudate formation)
  4. Vascular occlusion (ischaemic lesions with alteration of normal vessel permeability)
54
Q

What happens in proliferative retinopathy?

A

New vessel formation (from pre-existing vessels) anterior to the retina

New vessel is abnormal and will bleed easily, bleeding into the eye and causing vision loss

55
Q

What are cardiovascular, GI and genitourinary autonomic neuropathies?

A
  1. Cardiovascular
    • Resting tachycardia
    • Postural hypotension
    • Risk of cardiac arrhythymias / sudden death
  2. Gastrointestinal
    • Gastroparesis
    • Autonomic diarrhoea
  3. Genitourinary
    • Bladder dysfunction
    • Erectile dysfunction
56
Q

What is the mechanism of deformed diabetic foot?

A
  1. Loss of sensation
  2. Loss of joint position sense
  3. Wasting of small intrinsic muscles
  4. But also:
    1. Unrecognized trauma
    2. Abnormal foot posture
    3. Foot deformity (hard to get into shoe)
57
Q

How can you pick up on diabetic nephropathy?

A
  1. Microalbuminuria (very early stage)

2. Proteinuria (late stage)

58
Q

What are the 5 stages of diabetic nephropathy?

A
  1. Stage 1 → Hyperfiltration, or an increase in glomerular filtration rate (GFR) occurs. Kidneys increase in size
  2. Stage 2 → Glomeruli begin to show damage and microalbuminurea occurs
  3. Stage 3 → Albumin excretion rate (AER) exceeds 200 micrograms/minute, and blood levels of creatinine and urea-nitrogen rise
  4. Stage 4 → GFR decreases to less than 75 ml/min, large amounts of protein pass into the urine
  5. Stage 5 → Kidney failure, or end stage renal disease (ESRD). GFR is less than 10 ml/min
59
Q

During annual diabetic screening, what factors are considered?

A
  • Urine tests → Testing for urinary protein allows detection of nephropathy - detecting microalbuminuria ( ACR >3 mg/mmol/)
  • BP
  • eGFR measurement kidney function
  • Cholesterol
  • Smoking Status
  • Retinal photography
  • Foot check
60
Q

What two medications can lower blood glucose?

A

Insulin

Sulfonylureas

61
Q

What is the mechanism of action of sulfonylureas?

A

Sulfonylureas bind to and close ATP-sensitive K+ (KATP) channels on the cell membrane of pancreatic beta cells, which depolarizes the cell by preventing potassium from exiting. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granules with the cell membrane, and therefore increased secretion of mature insulin

There is some evidence that sulfonylureas also sensitize β-cells to glucose

3. Inflammation (21 decks)

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