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diabetes Flashcards

1
Q

what is diabetes?

A

it is a group of disorders that is characterised by hyperglycaemia which is high blood glucose and reduced action or lack of insulin

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2
Q

what is the anatomy of the pancreas?

A

around the pancreas head is the duodenum with the common bile duct joining it and going behind the pancreas head and the pancreatic duct coming in from two branches with a common origin that runs through the centre of the longitudinal pancreas. The pancreas itself is made of a head, body and tail, with lobules in. The lobules contain pancreatic islets which are islets of langerhans and pancreatic acini which are exocrine cells

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3
Q

what are the subtypes of islet cells?

A

there are F cells which make pancreatic polypeptides, delta cells which are around 5% and make somatostatin, alpha cells which make glucagon and are around 25% and beta cells which make insulin and comprise around 75%

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4
Q

what is the structure of insulin?

A

it is a soluble protein with two chains - alpha and beta

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5
Q

how is insulin made?

A

it is made first in the nucleus as preproinsulin INS gene and the this makes preproinsulin mRNA. From this it goes to the RER to make preproinsulin and then the trans-golgi network to make proinsulin. From here insulin is made by immature secretory granules and then mature secretory granules make the insulin hexamer or crystals

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6
Q

what are the three layers of insulin action?

A

firstly metabolic actions
then paracrine effects
finally there are vascular, fibrinoloysis and growth and cancer effects

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7
Q

what are the four types of diabetes diagnosis and their values?

A

HbA1c - >48mmol/mol
fasting glucose - >7mmol/L
random glucose - >11.1mmol/L
two hour reading after OGTT - >11.2mmol/L

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8
Q

how is the OGTT done?

A

this is the oral glucose tolerance test - take fasting glucose, then ingest 75g anhydrous glucose and then do a two hour reading

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9
Q

what is a IGT and IFG result of the OGTT?

A

it will be a fasting result of 6.1-6.9 and then after ingesting will be impaired glucose tolerance with a result of 7.8-11.1

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10
Q

what is prediabetes?

A

it is a state previous to diabetes where you use the HbA1c criteria - it reflects the average plasma glucose over the past 8-12 weeks. If it is 48mmol/mol or over then it is diabetes, if it is between 41 and 48mmol/mol then this is pre diabetes.

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11
Q

what are the types of diabetes?

A

there is T1, 2, gestational or specific types

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12
Q

what are specific types of diabetes?

A

these are genetic, endocrinopathies, disease of the exocrine pancreas

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13
Q

what is the epidemiology of T1DM?

A

there is equal sex incidence but after 15 years of age the risk for males increases two fold. It can occur at any age but peaks at puberty, and it is highest in european origin with incidence increasing by 3-4%

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14
Q

what is T1DM?

A

it is autoimmune destruction of the insulin producing beta cells in the islets of langerhans

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15
Q

what is the pathophysiology of T1DM?

A

there are genetics - the HLA class II which comprises DR3-DQ2 and DR4-DQ8, there is exposure to triggers or environmental factors and there is autoimmunity

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16
Q

what are the risk factors of T1DM?

A

there are viral infections, diet such as cows milk, perinatal complications such as a low birth weight and family history which gives a genetic susceptibility

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17
Q

what is the process of T1DM?

A

there are three stages. Stage 1 is when there is trigger of beta cell immunity but no symptoms. Stage 2 is when there is loss of beta cell secretory function and development of antibodies, with slight glucose elevation but no symptoms and stage 3 is loss of beta cell capacity and symptoms

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18
Q

how does T cell activation occur?

A

there is an APC with costimulatory proteins that has an MHC class II with an antigen on. This binds to the T cell receptor which has CD3 and CD4 on it which is on the surface of a CD4+ T cell, which also has costimulatory proteins. There is also an interleukin 2 receptor on this T cell

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19
Q

what is the result of humoral autoimmunity?

A

autoantibodies

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20
Q

which is more common in T1DM Gad65 or 67 autoantibodies?

A

Gad65

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21
Q

what autoantibodies are there in diabetes?

A

there are insulin, islet antigen 2, ZnT8 transporter and glutamic acid decarboxylase autoantibodies as well as Gad65 and 67 autoantibodies

22
Q

what is the presentation of T1DM?

A

there is rapid onset of a few weeks with weight loss, abdo pain, osmotic symptoms, low energy, slimness and diabetic ketoacidosis

23
Q

what is the management of T1DM?

A

always need insulin at the start of diagnosis but there is no role for an oral agent as the body is unable to produce insulin at all

24
Q

what is the presentation of T2DM?

A

often overweight with symptoms present for a few months and minimal weight loss unless they are left for a long period. They can present with complications such as loss of vision, foot ulcers or fungal infections and can also present in a state of HONK or hyperosmolar hyperglycaemia

25
Q

which complications occur first?

A

macrovascular first and then microvascular

26
Q

what is the Mx of T2DM?

A

three stages - first is lifestyle with exercise and weight loss - may be bariatric surgery and change in diet. The second is oral therapy with metforminin, and then DDP4 inhibitor, SGLT1 inhibitor, GLP1 agonist or sulphonylureas (up to three agents). The third stage is insulin - once a day and then numerous times

27
Q

what is gestational diabetes?

A

it is diabetes in pregnancy that was not present prior to pregnancy. There is hyperglycaemia that is first detected in pregnancy and a fasting glucose over 5.6mmol/L and a 2 hour of over 7.8mmol/L

28
Q

what is the diagnosis procedure for gestational diabetes?

A

oral glucose tolerance test - but use a different criteria from normal diabetes, if they have previous gestational diabetes then ask to self monitor using capillary blood glucose, test at 12 week scan and then if normal at 24 and 28 weeks
DO NOT USE HBA1C

29
Q

what are the risk factors for gestational diabetes?

A

previous history of gestational diabetes, family history of diabetes, ethnic minority, previous macrosomic baby and BMI of over 30

30
Q

what are the short term risks of gestational diabetes?

A

macrosomia, stillbirth, morbidity of neonate and pre-eclampsia

31
Q

what are the long term risk of gestational diabetes ?

A

obesity of child, development of T2DM in mother

32
Q

what is the management of gestational diabetes?

A

if mild then diet, majority will require insulin but only during pregnancy. There is limited oral options - these would be glibenclamide or metformin

33
Q

what happens post pregnancy in gestational diabetes?

A

there is repeat of HbA1c or fasting glucose 13 weeks after pregnancy as there is an increased risk of diabetes, annual diabetes screening required

34
Q

what are the types of genetic diabetes?

A

there is MODY - mature onset diabetes of the young, mitochondrial diabetes and maternally inherited diabetes and deafness

35
Q

what is disease of exocrine?

A

it is secondary diabetes or essentially any condition that damages the pancreas - pancreatitis, pancrectomy for cancer or trauma, CF or haemochromatosis

36
Q

what is drug induced diabetes?

A

it comes from many drugs such as prolonged high doses steroids, atypical antipsychotics, immunotherapy such as nivolumab (melanoma treatment) and protease inhibitors in HIV treatment

37
Q

what endocrinopathies can cause diabetes?

A

glucagonoma (glucagon secreting tumour), stomatostatin secreting tumour (somatostatinoma), cushing syndrome and acromegaly

38
Q

what are counter regulatory hormones?

A

they are hormones that usually oppose the action of insulin and are secreted as a result of stress response. These are adrenaline, noradrenaline, glucocorticoid, growth hormones and glucagon

39
Q

what are the stimuli for insulin release?

A

drugs for diabetes treatment, prostaglandins, fatty acids, ketones and glucose , gut hormones and vagal nerve stimulation

40
Q

what are stimuli for the inhibition of insulin release?

A

alpha adrenergic agents such as adrenaline, serotonin, dopamine, beta blockers, somatostatin, sympathetic stimulation

41
Q

what is glucagon?

A

it is a polypeptide of 29 AAs that is rapidly degraded in tissues especially liver and kidney

42
Q

what are the stimuli for glucagon release?

A

gastrin, CCK and cortisol, exercise, fasting and hypoglycaemia, amino acids and beta adrenergic stimulation

43
Q

what are the stimuli for inhibition of glucagon release?

A

ketones, glucose, insulin, somatostatin and free fatty acids

44
Q

what are the actions of glucagon?

A

increases glucose levels through glycogenolysis, gluconeogenesis and lipolysis
increases secretion of insulin and growth hormones
reduces the intestinal motility and gastric acid secretion

45
Q

what are the effects of insulin?

A

decreases glucose production, increases glucose utilisation and decreases lipolysis

46
Q

what are the effects of adrenaline, growth hormone and cortisol?

A

increases glucose production and lipolysis and decreases glucose utilisation

47
Q

what are the effects of FFAs?

A

increase glucose production but decrease utilisation

48
Q

what happens when there is low blood sugar?

A

this promotes glucagon release from the pancreas which stimulates glycogen breakdown into glucose in the liver and raises the blood sugar

49
Q

what happens when there is high blood sugar?

A

promotion of insulin release from the pancreas which stimulates glucose uptake from the blood into tissue cells and stimulates the conversion of glucose to glycogen in the liver to lower blood sugar

50
Q

where is glucagon produced?

A

the alpha cells of the pancreas whereas insulin in the beta cells of the pancreas

51
Q

what does the hypothalamus act on ?

A

in hyperglycaemia the beta and the alpha cells, in hypo the medulla for adrenaline, the cortex for cortisol and the pituitary gland for growth hormone

CP (38 decks)

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