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phase 2a > Introduction to diabetes > Flashcards

Introduction to diabetes Flashcards

1
Q

where does all glucose come from?

A

liver ( bit from kidney)

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2
Q

what occurs in the liver ?

A

breakdown od glycogen, gluconeogenesis

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3
Q

where is glucose delivered to?

A

insulin dependant tissues, brain and red blood ells

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4
Q

what do muscles use for fuel?

A

FFA

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5
Q

describe what happens post feeding

A

1.Rising glucose (5-10 min after eating) stimulates insulin secretion and suppresses glucagon
2. 40% of ingested glucose goes to liver and 60% to periphery, mostly muscle
3. Ingested glucose helps to replenish glycogen stores both in liver and muscle
4.High insulin and glucose levels suppress lipolysis and levels of non-esterified fatty acids (NEFA or FFA) fall

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6
Q

what is the islet of lagerhans

A

the site of insulin and glucagon secretion in the endocrine pancreas

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7
Q

what microstructures of islets have important physiological effects

A

beta cells
alpha cell
paracrine crosstalk

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8
Q

what do beta cels do in islets?

A

secrets insulin

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9
Q

what do alpha cells do in iselts?

A

secrete glucagon

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10
Q

describe paracrine crosstalk

A

between alpha and beta cells is physiological .ie local insulin release inhiivrs glucagon - an effect lost in diabetes

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11
Q

insulin secretion by beta cell

A
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12
Q

insulin action in muscle and fat cells

A
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13
Q

what does insulin suppress?

A

Supresses hepatic glucose output
 Glycogenolysis
 Gluconeogenesis
Suppresses
Lipolysis
Breakdown of muscle

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14
Q

what does insulin increase?

A

Increases glucose uptake into insulin sensitive tissues (muscle, fat)

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15
Q

what does glucagon increase?

A

Increases hepatic glucose output
 Glycogenolysis
 Gluconeogenesis

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16
Q

what does glucagon reduce?

A

Reduce peripheral glucose uptake

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17
Q

what does glucagon stimulate?

A

Stimulate peripheral release of gluconeogenic precursors (glycerol, AAs)
Lipolysis
Muscle glycogenolysis and breakdown

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18
Q

what is diabetes mellitus a disorder of?

A

A disorder of carbohydrate metabolism characterised by hyperglycaemia

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19
Q

what does diabetes mellitus cause?

A

causes morbidity and mortality through
Acute hyperglycaemia which if untreated leads to acute metabolic emergencies diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
Chronic hyperglycaemia leading to tissue complications (macrovascular and microvascular)
Side effects of treatment- hypoglycaemia

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20
Q

what other serious complications is diabetes associated with?

A

diabetic retinopathy
diabetic nephropathy
stroke
cardiovascular disease
diabetic neuropathy

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21
Q

what re the types of diabetes?

A

Type 1
Type 2
Includes gestational and medication induced diabetes
Maturity onset diabetes of youth (MODY), also called monogenic diabetes
Pancreatic diabetes
“Endocrine Diabetes” (Acromegaly/Cushings)
Malnutrition related diabetes

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22
Q

definitions of diabetes

A

Symptoms and random plasma glucose > 11 mmol/l
Fasting plasma glucose > 7 mmol/l
No symptoms - GTT (75g glucose) fasting > 7 or 2h value > 11 mmol/l (repeated on 2 occasions)
HbA1c of > 48mmol/mol (6.5%)

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23
Q

describe the pathogenesis of type 1 diabetes

A

An insulin deficiency disease characterised by loss of beta cells due to autoimmune destruction
Beta cells express antigens of HLA histocompatability system perhaps in response to an environmental event (?virus)
Activates a chronic cell mediated immune process leading to chronic ‘insulitis’

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24
Q

what does failure of insulin secretion lead to?

A
  1. Continued breakdown of liver glycogen
  2. Unrestrained lipolysis and skeletal muscle breakdown providing gluconeogenic precursors
    3.Inappropriate increase in hepatic glucose output and suppression of peripheral glucose uptake
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25
Q

what does rising glucose concentration result in?

A

increased urinary glucose losses as renal threshold (10mM) is exceeded

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26
Q

what does failure to treat insulin lead to?

A
  1. Increase in circulating glucagon (loss of local increases in insulin within the islets leads to removal of inhibition of glucagon release), further increasing glucose
  2. perceived ‘stress’ leads to increased cortisol and adrenaline
  3. progressive catabolic state and increasing levels of ketones
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27
Q

what is type 2 diabetes a consequence of?

A

A consequence of insulin resistance and progressive failure of insulin secretion (but insulin levels are always detectable)

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28
Q

what does impaired insulin action lead to ( 3 things)

A
  1. Reduced muscle and fat uptake after eating
  2. Failure to suppress lipolysis and high circulating FFAs
    3.Abnormally high glucose output after a meal
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29
Q

what does low levels of insulin prevent ?

A

prevent muscle catabolism and ketogenesis so profound muscle breakdown and gluconeogenesis are restrained and ketone production is rarely excessive

30
Q

define type 2 diabetes

A

Insulin resistance and impaired insulin secretion due to a combination of genetic predisposition and environmental factors (obesity and lack of physical activity)

31
Q

define type 1 diabetes

A

Severe insulin deficiency due to autoimmune destruction of the  cell (initiated by genetic susceptibility and environmental triggers)

32
Q

what are the principles of treatment of diabetes?

A

Control of symptoms
Prevention of acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states
Identification and prevention of long-term microvascular complications

33
Q

what treatment is used for type 2 diabetes?

A

weight loss
exercise
- if substantial can reverse hyperglycaemia
Control of symptoms
Prevention of acute emergencies, ketoacidosis, hyperglycaemic hyperosmolar states
Identification and prevention of long-term microvascular complications

34
Q

what does Sulphonylureas (gliclazide, glibenclamide) do?

A

stimulate insulin release by binding to beta-cell receptors
Improve glycaemic control (1-2% in HbA1c) at the expense of significant weight gain
Can cause hypoglycaemia (occasionally prolonged and fatal, particularly in the elderly and when renal function is impaired)
Use gliclazide in most people

35
Q

what does thiazolidinediones bind to?

A

bind to the the nuclear receptor PPARy- peroxisome proliferator- activated receptor

36
Q

what does thiazolidinediones activate?

A

Activate genes concerned with glucose uptake and utilisation and lipid metabolism

37
Q

what does thiazolidinediones improve

A

insulin sensitivity

38
Q

what would an ideal drug in type 2 diabetes include?

A

Reduce appetite and induce weight loss
Preserve -cells and insulin secretion
Increase insulin secretion at meal time
Inhibit counterregulatory hormones which increase blood glucose such as glucagon
Not increase the risk of hypoglycaemia during treatment

39
Q

what do SGLT2 inhibitors block?

A

SGLT2 inhibitors block the reabsorption of glucose in the kidney, increase glucose excretion, and lower blood glucose levels

40
Q

what specific benefit may SGLT2 have?

A

in reducing CV mortality

41
Q

side effects of SGLT2 inhibitors?

A

Side effects, genital thrush, increased risk of euglycaemic ketoacidosis including in type 2 diabetes, now licensed in type 1 diabetes

42
Q

what oral agent is the first line?

A

metmorfin

43
Q

Why doesn’t DKA occur in Type 2 diabetes?

A

It is rare because the low insulin levels are sufficient to suppress catabolism and prevent ketogenesis. It can occur if hormones such as adrenaline rise to high levels (eg during an MI)

44
Q

Why does obesity cause Type 2 diabetes?

A

Obesity (particularly central) impairs insulin action. In those, already insulin resistant due to genetic factors and who have progressive impairment in insulin secretion this brings out diabetes at an early stage.

45
Q

What are the presenting features of diabetes?

A
  • thirst
    -polyuria
    -weight loss and fatigue
    -hunger
    -pruritis vulvae and balanitis
    -blurred vision
46
Q

what are the suggestive features of type 1 diabetes?

A

Onset in childhood / adolescence
Lean body habitus
Acute onset of osmotic symptoms
Prone to ketoacidosis
High levels of islet autoantibodies

47
Q

what are the suggestive features of type 2 diabetes?

A

Usually presents in over-30s
Onset is gradual
FH is often positive
Almost 100% concordance in identical twins
Diet, exercise and oral medication can often control hyperglycaemia; insulin may be required later in the disease

48
Q

how to differentiate between 1 or 2?

A

Can be difficult
Type 2 is diagnosed in younger patients, including childhood
Type 1 patients can be obese
Uncontrolled Type 2 can present with weight loss and ketouria

IF IN DOUBT – TREAT WITH INSULIN

49
Q

what does reduced insulin lead to in fat metabolism ?

A

Reduced insulin leads to fat breakdown and formation of glycerol (a gluconeogenic precursor) and free fatty acids

50
Q

what happens to the free fatty acids produced in fat metabolism?

A

Impair glucose uptake
Are transported to the liver, providing ‘energy’ for gluconeogensis
Are oxidised to form ketone bodies (beta hydroxy butyrate, acetoacetate and acetone)

51
Q

what does the Absence of insulin and rising counterregulatory hormones lead to in ketoacidosis?

A

to increasing hyperglycaemia and rising ketones
Glucose and ketones escape in the urine but lead to an osmotic diuresis and falling circulating blood volume
Ketones (weak organic acids) cause anorexia and vomiting
Vicious circle of increasing dehydration, hyperglycaemia and increasing acidosis eventually lead to circulatory collapse and death

52
Q

define DKA ( diabetic ketoacidosis)

A

Hyperglycaemia (plasma glucose usually <50 mmol/l)
Raised plasma ketones (urine ketones > 2+)
Metabolic acidosis – plasma bicarbonate < 15 mmol/l

53
Q

what causes DKA ( diabetic ketoacidosis)

A

Intercurrent illness
infection
myocardial infarct
Treatment errors – stop/reduce insulin dose
Previously undiagnosed diabetes
Unknown

54
Q

what are the symtoms of DKA

A

develop over days
polyuria and polydipsia
nausea and vomiting
weight loss
weakness
abdominal pain (confused with surgical abdomen)
Drowsiness / confusion

55
Q

what are the signs of DKA?

A

hyperventilation (Kussmaul breathing)
dehydration (average fluid loss 5-6 litres)
hypotension
Tachycardia
coma

56
Q

what is the biochemical diagnosis. of DKA

A

hyperglycaemia (<50 mmol/l)

K+ – high on presentation despite total body K+ deficit (due to acute shift of K out of cell with acidosis), subsequently fall with insulin and rehydration, anticipate fall in K+

HCO3- <15 mmol/l

urea and creatinine - raised due to pre-renal failure

urinary ketones dipstix >2+ ketones
blood ketones >3.0

57
Q

How is DKA managed?

A

rehydration (3L first 3 hrs)

insulin (inhibits lipolysis, ketogenesis, acidosis, reduces hepatic glucose production, increase tissue glucose uptake)

replacement of electrolytes (K+)

treat underlying cause

Treatment must be started without delay

Follow DKA protocol in hospital

58
Q

what are possible complications of DKA?

A

cerebral oedema (deterioration in conscious level)
children more at risk

adult respiratory distress syndrome

thromboembolism – venous and arterial

aspiration pneumonia (in drowsy/comatose patients)

death

59
Q

what are the aims of treatment in type 1 diabetes?

A

-Relieve symptoms and prevent ketoacidosis
-Prevent microvascular and macrovascular complications
-On average, people with Type 1 diabetes lose 8 years of life (mostly from cardiovascular disease)

60
Q

what microvascular complications can arise with diabetes

A

Around 30% in the UK will develop diabetic nephropathy
Those with nephropathy tend to develop proliferative retinopathy and severe neuropathy with major effect on quality of life

61
Q

how is type 1 diabetes treated?

A

To restore the physiology of the beta cell
Insulin treatment
Twice daily mixture of short/medium acting insulin
Basal bolus, (once or twice daily medium acting insulin plus pre meal quick acting insulin)
Ability to judge CHO intake
Awareness of blood glucose lowering effect of exercise

62
Q

what do inappropriately high insulin levels indicate?

A

high risk of hypoglycaemia

63
Q

what does acute deprivation of glucose within the brain leads to?

A

to cerebral dysfunction (loss of concentration, confusion, coma

64
Q

what are the physiological defences to hypoglycaemia?

A

Release of glucagon, adrenaline
Symptoms of
Sweating, tremor, palpitations (autonomic activation)
Loss of concentration, ‘hunger’

65
Q

at glucose level- 4.6 mM- what should happen?

A

inhibition of insulin secretion

66
Q

at glucose level- 3.8 mM- what should happen?

A

counter-regulatory hormone release (glucagon and adrenaline)

67
Q

at glucose level- 3.8-2.8 mM- what should happen?

A

autonomic symptoms
sweating, tremor, palpitations

68
Q

at glucose level <2.8 mM- what should happen?

A

neuroglycopenic symptoms
confusion, drowsiness, altered behaviour, speech difficulty, incoordination

69
Q

at glucose level <1.5 mM- what should happen?

A

severe neuroglycopenic
convulsions, coma, focal neurological deficit ie hemiparesis

70
Q

What is the dilemma for those with type 1 diabetes?

A

Setting higher glucose targets will reduce the risk of hypoglycaemia but increase the risk of diabetic complications

Setting lower glucose targets will reduce the risk of complications but increase the risk of hypoglycaemia

71
Q

what are the factors making it difficult for people with diabetes to sustain effective self management?

A

-Risk of hypoglycaemia
-Too arduous a treatment
-Risk of weight gain
-Interference with lifestyle
-Lack of sufficient training from -diabetes teams

phase 2a (67 decks)

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