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Human Disease > Diabetes and its treatment > Flashcards

Diabetes and its treatment Flashcards

1
Q

What do alpha cells make?

A

glucagon

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2
Q

What do beta cells make?

A

insulin

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3
Q

What do delta cells make?

A

somatostatin

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4
Q

What contributes to glucose in the blood?

A

Food and Liver

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5
Q

What takes up glucose from the blood?

A

Muscle and kidney (and liver)

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6
Q

When does blood glucose peak throughout the day? (which would then normally be followed by insulin release)

A

Post prandial (roughly 8am, 1pm and 7 pm)

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7
Q

What is diabetes?

A

Metabolic disorder characterised by chronic hyperglycemia resulting from defects in inslin sceretion, insulin action or both

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8
Q

What would result in lack of insulin?

A

Reduced production

Insulin cant get to the cell to work

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9
Q

What happens when there is no insulin released?

A

The liver releases more glucose

The muscle cannot take much so the kidneys uptake the glucose

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10
Q

How is diabetes diagnosed?

A

High blood glucose and symptoms, Hb test (but this doestn detect young people with rapid onset as it looks at the previous 3 months)

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11
Q

What vessels are affected by retinopathy and arterial disease?

A

Retinopathy - microvessels

Arterial disease - macrovessels

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12
Q

What is HbA1c?

A

glycated haemoglobin. It is a measurement of diabetes management over 2 - 3 months.

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13
Q

What affects HbA1c?

A

renal failure - changes the cells ability to bind glucose

thalassaemia - abnormal Hb which binds to glucose more strongly

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14
Q

When can HbA1c be inaccurate?

A

Abnormally high caused by persistent HbF (thalassaemia)

Low caused by haemolysis or increased red cell turnover (blood loss)

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15
Q

What is the blood glucose level of a diabetic when fasting and 2 hrs after meal?

A

fasting >7mmol/L

post 2 hrs >11.1mmol/L

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16
Q

What is IGF ? (almost diabetes)

A

Impaired glucose fasting. (Pre-type 1 diabetes)
Unknown cause
50% risk of diabetes
Treat with healthy diet, yearly glucose checks

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17
Q

What is IGT? (almost diabetes)

A

Impaired glucose tolerance (Pre-type 2 diabetes)
Cause is insulin resistance
50% risk of diabetes
Increased risk of heart disease
Treat with diabetic diest, yearly glucose checks and treat cardiac risk factors
Prevent progression with exercise and weight loss

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18
Q

Other than type 1 and 2, what is the other form of diabetes?

A

Gestational

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19
Q

Name 3 classifications of diabetes?

A

INSULIN DEFICIENCY - auto-immue destruction of pancreas
INSULIN RESISTANCE - unknown cause related to obesity, receptor abnormalities, excessive hormone
GESTATIONAL

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20
Q

Describe type 1 diabetes mellitus?

A 
Less cells in the pancreas, cant make insulin
Incidence 1/10,000
Often younger with weight loss
M>F
Cause is genetic and environmental
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21
Q

How does type 1 diabetes mellitus present?

A 
Polyuria
Thirst
weight loss
dehrydration (wee 5-8L/day)
ketoacidosis
coma
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22
Q

What are the 2 new delivery systems for insulin?

A

INSULIN PUMP - continuous insulin given, less hypos, less insulin, but high cost
INHALED INSULIN - small trials, only 1/10 dose absorbed, long term safety unkown

23
Q

Describe an islet cell transplant?

A

Islets taken from donor pancreas
Isolate islets of langerhans
infusion of islets which go to the portal vein

24
Q

Describe a pancreas transplant?

A

Donor donates pancreas and duodenum

25
Q

What happens if pt needs a short operation?

A

Half the normal morning dose
First on the list
Monitor symptoms
Cover antibiotics

26
Q

What happens if pt needs a long operation?

A

Needs to be in hospital
First on the list
Iv, glucose and K+
cover with antibiotics

27
Q

Describe type 2 diabetes?

A

Insulin resistance so glucose does not go into cell
Incidence 1/1000
Often older with weight gain
M=F
Cause is genetic and environment (more genetic though)

28
Q

What is the link between birth weight and insulin resistance?

A

Increased birth weight = increased risk resistance
decreased body weight = increased insulin sensitivity
Increased BMI = increased rate type 2 diabetes

29
Q

How does type 2 diabetes present?

A

Non symptomatic
Metabolic - thirst, polyuria
Non metabolic - comlications: blurred vision, CVA, peripheral neuropathy, angina, MI, UTI, foot ulcers

30
Q

How do we treat type 2 diabetes? (in order of stage)

A

IF THIN - diet, exercise, sulphonylureas, metformin, insulin

IF FAT - diet, exercise, weight loss, metformin, sulphylureas, insulin

31
Q

What action do sulphonylureas have?

A

Increased insulin release from pancreas

32
Q

What are the side effects of sulphonylureas?

egs tolbutamide, glibenclamide, glicazide

A

hypoglycaemia, weight gain, nausea, anorexia, vomiting, alcoholic, skin rash

33
Q

What is the action of metformin?

A

Suppresses glucose production by the liver

34
Q

What are the side effects of metformin?

A

nausea, vomiting, diarrhoea, VitB12 malabsorption, lactic acidosis

35
Q

What is the action of thiazolidinediones?

A

Increased insulin sensitivity. Increase muscle and decreases secretion from the liver

36
Q

What are the side effects of thiazolidinediones?

eg rosilitizone

A

Hypoglycaemia, liver damage, fluid retention, weight gain

37
Q

What drugs decrease absorption?

A 
Alpha glucosidase inhibitors (acarbase) - flatulence, no hypo, slow glucose absorption
Lipase inhibitors (orlistat) - weight loss, decreased cholesterol, flatulence, no hypo, omhobots pancreatic and gastric lipase
38
Q

What is GLP -1?

A

Glucagon like peptide 1

Diabetics dont produce as much GLP -1

39
Q

When is GLP - 1 secreted?

A

On the ingestion of food

40
Q

What are the effects of GLP - 1?

A

BETA CELLS - enhances glucose dependant insulin secretion in pancreas
ALPHA CELLS - suppressed postprandial glucagon secretion
LIVER - reduced hepatic glucose output
STOMACH - slows the rate of gastric emptying
BRAIN - promotes satisfaction and decreases apetite

41
Q

What are the 2 incretin based therapies?

A
  1. DPP - 4 inhibitors - protect native GLP -1 from inactivation by DPP-4
    (eg sitagliptin, vildagliptin, alogliptin)
  2. GLP - 1 receptor agonists - mimic native GLP - 1
    (eg exenatide, liroglutide, lixisematide)
42
Q

What is exenatide?

A

A GLP - 1 receptor agonist. It is resistant to DPP-IV degradation. Given subcutaneously
Decreases HbA1c
Augments glucose stimulating insulin secretion, slows gastric emptying, suppresses innapropriately increased glucagon

43
Q

Which two organs play large roles in managing diabetes?

A

Gut and kidney

44
Q

Describe the normal glucose handling of the kidney?

A

80% glucose is reabsorbed by SGLT2
10% glucose reabsorbed by SGLT1
Minimal glucose excreted in urine

45
Q

What is the action of dapagliflozin?

A

stops reabsorption by SGLT2 in the renal proximal tubule so more glucose secreted in urine
Secondary benefit of weight loss

46
Q

What 2 classes of treatment can be used for diabetes?

A

Insulin dependent mechanisms - glucose utilisation

Insulin independent mechanisms - glucose excretion

47
Q

What are the insulin dependent mechanisms? (glucose utilisation)

A

Insulin sensitisers - thiazolidinediones, metformin
Insulin releasers - sulphonylureas, meglitinides
Insulin replacement - insulin

48
Q

What are the insulin independant mechanisms? (glucose excretion)

A

SLGT-2 inhibition - dapagliflozin

GLP - 1 and DDPIV - increase insulin release

49
Q

What is gestational diabetes?

A

Mother has increased glucose which crosses the placenta so the baby produces insulin and this controls its own glucose. But insulin is a growth factor so the baby gets other complications and increased risk of still birth.

50
Q

When is gestational diabetes prone?

A

2nd and 3rd trimester

51
Q

What is the treatment for gestational diabetes?

A

85% diet

15% diet and insulin

52
Q

What are the complications associated with gestational diabetes?

A

Still births, large baby, death for mother

53
Q

What is the chance that a mother who experiences gestational diabetes will have diabetes in the future?

A

50% diabetic in next 5 yrs

15% diabetic in next pregnancy

Human Disease (54 decks)

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