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brs (phase 1a) > (endo) intro to diabetes > Flashcards

(endo) intro to diabetes Flashcards

1
Q

where is GLUT-4 found?

A

found in myocytes (muscle) and adipocytes (fat)

  • within vesicles
  • recruited and enhanced by insulin
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2
Q

how does GLUT-4 compare to GLUT-2?

A

while GLUT-4 is highly insulin-sensitive, GLUT-2 is not

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3
Q

what is the function of GLUT-4?

A

increases glucose uptake into cells by 7-fold

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4
Q

describe the structure of GLUT-4 chains

A

outer hydrophobic chains but inner hydrophilic chains (where glucose will pass to enter the cell)

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5
Q

which type of amino acids are used to form glucose?

A

gluconeogenic amino acids (e.g. alanine)

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6
Q

how does insulin act on myocytes and affect proteins in the FED state?

A

insulin stimulates AA conversion into protein (i.e. increases protein synthesis + inhibits proteolysis) for storage

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7
Q

along with insulin, what stimulates protein synthesis in myocytes?

A

IGF-1 and GH

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8
Q

insulin inhibits proteolysis in myocytes in the FED state

what happens in the FASTING state?

A

cortisol (and glucagon) act to increase conversion of stored proteins into the gluconeogenic amino acids that they are made up of

= enable gluconeogenesis in the liver to increase blood glucose levels

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9
Q

which hormone stimulates the uptake of gluconeogenic AAs into hepatocytes for gluconeogenesis?

A

glucagon

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10
Q

what is lipoprotein lipase?

A

an enzyme that breaks down triglycerides that would otherwise be unable to leave the circulation

= broken down into NEFAs and glycerol (that can be taken up by adipocytes)

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11
Q

what happens to the NEFAs and glycerol taken up by the adipocytes?

A

converted into triglycerides again and stored

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12
Q

which hormones stimulate and inhibit hepatic gluconeogenesis?

A

stimulate = glucagon, cortisol

inhibit = insulin

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13
Q

how does insulin act on adipocytes in the FED state?

A

insulin acts

1) to stimulate conversion of NEFAs and glycerol into triglycerides (for storage)
2) to increase glucose uptake via GLUT-4 that will then act to increase NEFA and glycerol conversion into triglycerides
3) inhibits breakdown of stored triglycerides

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14
Q

what acts on adipocytes in the FASTING state?

A

both cortisol + GH will act on triglycerides to break them down into NEFAs and glycerol again

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15
Q

what happens with glycerol in the FASTING state?

A

glycerol is taken up by hepatocytes and converted into glycerol-3-phosphate

gly-3p then undergoes gluconeogenesis to form glucose

= increases HGO

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16
Q

what happens with glycerol in the FED state?

A

glycerol is taken up by hepatocytes and converted into glycerol-3-phosphate

the gly-3p is then converted into triglycerides for storage

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17
Q

how are cerebral energy requirements met?

A

glucose (preferred)
ketone bodies

(!! but cannot metabolise NEFAs !!)

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18
Q

what happens with gluconeogenic amino acids in the FED state?

A

insulin acts to

1) reduce/inhibit hepatic gluconeogenesis
2) promote protein synthesis from gluconeogenic AAs

= reducing HGO

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19
Q

what happens with gluconeogenic amino acids in the FASTING state?

A
  • glucagon only acts to:

1) increase uptake of AAs into hepatocytes
2) promote proteolysis to produce more gluconeogenic AAs for gluconeogenesis

  • cortisol + glucagon act to
    1) increase hepatic gluconeogenesis

= increasing HGO

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20
Q

explain the process of ketogenesis

A
  • NEFAs are taken up into hepatocytes
  • NEFAs are converted into fatty acyl-coAs
  • fatty acyl-coAs are converted into ketone bodies
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21
Q

where does ketogenesis take place?

A

hepatocytes

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22
Q

which ketone bodies are made in hepatocytes during ketogenesis?

A
  • acetyl CoA
  • acetoacetate
  • acetone + 3 OH-B
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23
Q

what stimulates and what inhibits ketogenesis?

A

stimulates ketogenesis = glucagon

inhibits ketogenesis = insulin

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24
Q

define hepatic glycogenolysis

A

the generation of glucose from stored glycogen in the liver

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25
Q

describe the process of hepatic glycogenolysis

A

stored glycogen in the liver is converted into glucose-6-phosphate

glucose-6-phosphate is converted into glucose

glucose then released from hepatocytes into the bloodstream

26
Q

what stimulates and what inhibits hepatic glycogenolysis?

A

stimulates glycogenolysis = glucagon

inhibits glycogenolysis = insulin

27
Q

what are the two possible fates of glucose once it is taken up by myocytes?

A

either

1) stored as glycogen

OR

2) combined w NEFAs will form acetyl CoA which in turn can be used to produce ATP via the TCA cycle

28
Q

what stimulates and inhibits glucose uptake into myocytes via the GLUT-4 receptor?

A

stimulates uptake = insulin

inhibits uptake = glucagon, GH

29
Q

summarise the body’s response to the fasting state

A

1) increased proteolysis
2) increased lipolysis (to release more glycerol + NEFAs for ketogenesis if prolonged)
3) increased HGO (from glycogenolysis + gluconeogenesis)

= reduced insulin:glucagon ratio

30
Q

in the fasted state, which substrates are used by myocytes and the brain?

A

myocytes = use lipids

the brain = use glucose, or ketones (but not NEFAs!)

31
Q

summarise the body’s response to fed state

A

1) increased glycogenesis + less hepatic gluconeogenesis = reduces HGO
2) reduced proteolysis + increased protein synthesis
3) reduced lipolysis + increased lipogenesis

= high insulin:glucagon ratio

(stored insulin released then 2nd phase)

32
Q

how is diabetes mellitus diagnosed?

A

either two positive tests OR one positive test + symptoms

possible tests:

  • fasting glucose >7 mmol/L
  • random glucose >11.1 mmol/L
  • oral glucose tolerance test
  • HbA1c >48 mmol/L
33
Q

which possible tests can be done to diagnose diabetes mellitus and what results are expected?

A

(need two positive tests OR one positive test + symptoms)

1) fasting glucose (>7 mmol/L)
2) random glucose (>11.1 mmol/L)
3) HbA1c (>48 mmol/L)
4) oral glucose tolerance test

34
Q

what is the pathophysiology of type 1 diabetes mellitus?

A

less insulin

autoimmune T cell-mediated destruction of beta cells of Islets of Langerhans in pancreas = absolute insulin deficiency

1) increased proteolysis (increases gluconeogenic AAs for GNG)
2) increased lipolysis to release more NEFAs and glycerol (to increase ketogenesis and GNG)
3) increased HGO due to increased gluconeogenesis (AA + glycerol) and glycogenolysis
=
increased blood glucose

35
Q

what is diabetic diuresis?

A

occurs when there is glucose lost in the urine
= subsequent dehydration causes increased volume of water loss in the urine
= increased uptake of water

36
Q

how does diabetic ketoacidosis occur?

A

a serious acute complication of diabetes where due to prolonged insulin deficiency

= increased compensatory lipolysis
= increase concentration of NEFAs
= increased hepatic ketogenesis
= when this occurs in excess, DKA results

37
Q

what is diabetic ketoacidosis?

A

when

1) pH < 7.3
2) HCO3- < 15
3) glucose > 11
4) ketones +++

= a serious acute complication of prolonged, uncontrolled diabetes

38
Q

how do patients with type 1 diabetes mellitus present?

A
  • glycosuria
  • osmotic symptoms (polydipsia, nocturia, polyuria)
  • weight loss
  • hyperglycaemia
  • ketones in the blood + urine
39
Q

which diagnostic tests are useful in type 1 diabetes mellitus?

A

1) C-peptide
2) presence of ketones
3) antibodies = GAD; IA2

40
Q

what is a possible complication of insulin-controlled T1DM?

A

insulin-induced hypoglycaemia

41
Q

what is insulin-induced hypoglycaemia?

A

occurs when too much exogenous insulin is administered to manage the T1DM + to make up for the lack of endogenous insulin (exogenous less well controlled compared to endogenous)

too much insulin
= continued glucose uptake by myocytes
= potential hypoglycaemia

42
Q

what is the counterregulatory response to hypoglycaemia?

A

hypoglycaemia
= stimulates release of glucagon + catecholamines + GH + cortisol

=

1) increase HGO by increasing gluconeogenesis + glycogenolysis
2) increase lipolysis (and therefore ketogenesis)
3) increase proteolysis

43
Q

when can you get recurrent hypoglycaemia?

A

loss of counterregulatory response
= reduced ability to recognise symptoms of hypoglycaemia
= recurrent hypoglycaemia

44
Q

what are the autonomic signs of hypoglycaemia?

A
  • sweating
  • pallor
  • palpitations
  • shaking
45
Q

what are the neuroglycopenic signs of hypoglycaemia?

A
  • confusion/loss of consciousness
  • poor vision
  • slurred speech
  • seizures

(tip: from head to toe)

46
Q

what is severe hypoglycaemia?

A

defined as an episode where a person needs third party assistance to treat

47
Q

what is a CBG?

A

capillary blood glucose

= bedside test done to monitor a patient’s blood glucose levels

48
Q

summarise the pathophysiology of T2DM

A
  • insulin resistance exists in the liver, adipocytes and muscle tissue
  • in severe cases, can lead to insulin deficiency but usually sufficient amounts of insulin are present to inhibit proteolysis and ketogenesis
49
Q

what does insulin bind to and what does this trigger?

A

insulin binds to the insulin receptor, triggering one of two pathways:

1) MAPK pathway = growth, proliferation
2) PI3K-Akt pathway = glucose/fat metabolism

50
Q

which pathway is linked to insulin resistance?

A

insulin resistance lies in the PI3K pathway
= so in T2DM, increased release of proliferal insulin that acts via the MAPK pathway
= for increased growth and proliferation

51
Q

how is insulin resistance T2DM initially overcome?

A

insulin resistance initially overcome w increased insulin production
= from the beta cells of the islets of Langerhans that have undergone hyperplasia + hypertrophy to increase insulin secretion

52
Q

how do patients with T2DM present?

A
  • hyperglycaemia
  • insulin resistance (and maybe later, insulin deficiency)
  • overweight
  • dyslipidaemia
  • complications (e.g. retinopathy, neuropathy, nephropathy)
53
Q

what are the risk factors for T2DM?

A
  • age
  • ethnicity
  • family history
  • increased BMI
  • inactivity
  • PCOS
54
Q

what are the possible complications of T2DM?

A
  • retinopathy
  • stroke/CVD/atherosclerosis
  • peripheral neuropathy
  • nephropathy
  • diabetic foot
55
Q

what dietary recommendations are made to people with type 2 diabetes mellitus?

A
  • control total calories
  • increase calories as complex carbohydrates and reduce those as fats
  • increase soluble fibre
  • decrease sodium
56
Q

summarise how T1DM is managed

A
  • exogenous insulin (basal-bolus regime)
  • self-monitoring of glucose
  • structured education
  • technology
57
Q

summarise how T2DM is managed

A
  • lifestyle changes (i.e. diet, exercise)
  • oral medication
  • structured education
  • technology (may need insulin later)
58
Q

insulin stimulates uptake of glucose into which cells and how?

A

stimulates the uptake of glucose by the adipose and muscle cells through GLUT4receptors

59
Q

what effect does insulin release have on glucagon?

A

increased insulin release

= inhibits glucagon release

60
Q

what are the implications of insufficient insulin?

A

glucose accumulation in the blood
= reduced glucose uptake into skeletal,cardiac and smooth muscle, and adipose tissue

= increased glycogenolysis + gluconeogenesis + glucagon release
= increased lipolysis + ketogenesis
= increased proteolysis

brs (phase 1a) (7 decks)

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