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Hormones > Endo 17: Type 2 diabetes > Flashcards

Endo 17: Type 2 diabetes Flashcards

(56 cards)

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1
Q

Define DM

A

Diabetes mellitus can be defined as a state of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues, notably the retina, kidney, nerves, and arteries

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2
Q

T/F T2DM is ketosis prone

A

F: not prone, but can happen

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3
Q

Oral glucose test

A

less than 6 when fasing

2 hrs after oral glucose, should be 7.8 or less

random test shouldn’t be above 11.1

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4
Q

Which diabetes have greater genetic basis

A

T2DM

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5
Q

Greatest diabetes risk

A

Greatest in ethnic groups that move from rural to urban lifestyle

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6
Q

Pathophysiology of T2DM

A
  1. Genes and intrauterine environment and adult environment.
  2. Insulin resistance and insulin secretion defects
  3. Fatty acids important in pathogenesis and complications
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7
Q

What is MODY, how is it different from type 1 and type 2

A

Several hereditary forms (1-8)- i.e. MONOGENIC (so different to T2DM)

Autosomal dominant

Ineffective pancreatic B cell insulin production

+ve FH, no obesity

Due to not enough insulin production/poor insulin sensing by the b cells, NOT autoimmune destruction (like type 1)

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8
Q

Differentiate MODY and T2DM

A

MODY monogenic, T2DM multiple genes contribute to disease

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9
Q

What kind of mutation in MODY

A

Mutations of transcription factor genes, glucokinase gene

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10
Q

What is the relationship between intrauterine environment and T2DM

A

Intrauterine growth restriction…if you’re born light more likely to be diabetic (possible due to epigenetic mechanisms)

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11
Q

Which factors cause macrovascular disease in T2DM

A

Genes leading to insulin resistance MODULATED (not caused by) adipocytokines. Genes can leading to obesity and FAs can affect the insulin resistance. Genes also leading to IUGR which is a risk factor for T2DM.

Insulin resistance leading to MITOGENIC (due to growth protperties of insulin) and METABOLIC DYSLIPIDAEMIA which lead to macrovascular disease.

Insulin resistance can also lead to inflammation but this doesn’t affect macrovascular disease

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12
Q

How can you differeniate between vascular disease in diabetics vs normal people

A

Diabetics have microvascular disease, never normal people have this

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13
Q

What lads to microvacular disease

A

Beta cell falure leads to metabolcic dyslipidaemia (leadingg to macrovasc)

and

HYPERGLYCAEMIA (LADS TO MICROVACULAR)

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14
Q

Rates of concordance in type 1 and type 2 diabetes

A

T1DM: mono= 35%, di=10%

TD2M: monozygous=70%, dizygous= 40%

DOMINANT FOR T2DM!

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15
Q

What else other than genetics is associated with diabetes

A

Intrauterine environment and prebirth weight

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16
Q

Change in insulin prodction and resistance wih age normally

A

Increased resistace

Falling insulin production….

When it gets to a point that the resistance increases above the amount of insulin that can be produced that’s diabetes.

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17
Q

Insulin problems in T2DM

A

Insulin resistance and insulin secretion deficit

`

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18
Q

How does insulin secretion change with impairment of glucose tolerance

A

Insulin Secretion Deteriorates with Progressive Impairment of Glucose Tolerance

The 1st phase of insulin release in response to increased glucose due to a meal is much reduced in those with impaired glucose tolerance, and not increase at all in those with TD2M.

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19
Q

What is the reason for hyperglycaemia in T2DM

A

There is inability to stop the HGO (due to insulin resistance and GLP1)

There is reduced glucose clearance (i.e. reduced ability to drive glucose into muscle and liver)

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20
Q

Effect of insulin resistance on adipocyte vs what happens when insulin resistance

A

Normally switches of lipolysis….

BUT if you have insulin resistance, more TG–> glycerol and NEFA….

NEFA is made into VDLD and glycerol…. glycerol turned into glucose

THIS MOSTLY COMES FROM OMENTAL FAT

See card I wrote for this bit

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21
Q

Effect of insulin on muslce

A

So there is more glucose produced from liver due to glycogenolysis and increased gluconeogenesis from the glycerol but

glucose cannot be taken up intomuscle

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22
Q

Other than the increased lipolysis, how else can adipocytes affect diabetes

A

Hormones are produced by adipocytes= adipocytokines.

E.g. TNF-a can cause lipolysis and VLDL secretion

etc.

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23
Q

Why is central fat more important in diabetes

Study These Flashcards
A

Drains straight to liver… more endocrine function than peripheral

24
Q

Why is obesity important in diabetes

Study These Flashcards
A

Fatty acids and adipocytokines important

25
T/F most obese people develop diabetes
F- but 80% of TD2M people are obese CENTRAL/OMENTAL obesity is most important
26
Involvement of gut microbiome in T2DM -------------- problem with most diabetes treatments, and the exception
It can affect intermediary metabolism Bacterial lipopolysaccharide fermentation short chain FAs, and bacterial modulation of bile acids, Inflammation, signaling metabolic pathways ------------- most cause weight gain, apart from metformin
27
Presentation of T2DM Summarise the complications
Osmotic symptoms (less likely compared to T1DM.... so presents later, high plasma glucose leaks into urine) Infections On screening test at presentation of complication - Acute; hyperosmolar coma, - Chronic; ischaemic heart disease, retinopathy Complications: -Macrovasc: IHD, cerebrovascular disease, renal artery stenosis, PVD - Microvasc: retinopathy, neuropathy and nephropathy - Metabolic: hyperosmolar and lactic acidosis - Due to treatment: hypoglycaemia
28
Microvascular complicaions of diabetes
retinopathy nephropathy neuropathy
29
Metabolic complicaions of diabetes
These are less common than in type 1 Lactic acidosis Hyperosmolar
30
Macrovascular complications of T2DM
Ishcaemic heart disease Cerebrovascular Renal artery stenosis PVD
31
Complication of treatment of diabetes Treatment types
hypoglycaemia Education, diet, pharmacological, complication screening
32
How should T2DM be treated in terms of diet
Control total calories/increase exercise (weight) reduce refined carbohydrate (less sugar) increase complex carbohydrate (more rice etc) reduce fat as proportion of calories (less IR) increase unsaturated fat as proportion of fat (IHD) increase soluble fibre (longer to absorb CHO) Address salt (BP risk)
33
Drugs acting on the liver to reduce sugar output
Metformin and insulin (but this causes weight gain
34
Drugs acting on the pancrease
Sulphonylurease (increase insulin release)
35
How does metformin work
``` insulin sensitiser overweight patient with T2DM where diet alone has not succeeded Reduces insulin resistance Reduced hepatic glucose output Increases peripheral glucose disposal ```
36
What is measured in TD2M for monitoring ------------- What drug works to reduce fat absorption ------------ What drugs work on sugar
Weight Glycaemia Blood pressure Dyslidiaemia ---------- ORLISTAT is a GI lipase inhibitor RIMONABANT is a cabbanoid antagonist (suppress action of GABA on the MCH neurones, and prevent increased orexin production) ----------------- Metformin/insulin (but it would cause weigt gain) reduce HGO Sulphonylureas increase insulin secretion from pancreas (control sugar but cause weight gain) a-glucosidase inhibitor... increasing time to absorb sugar (gets over the reduced 1st phase insulin release) GLP1 anlogue + DPP4 inhibitor (to increase amount of insulin from pancreas) Thiazolidinediones (deal with insulin resistance) SGLT2 inhibitor= increase glucose excretion
37
How does metformin work When is it indicated How does it work Side effects and contraindication
Biguanide, insulin sensitiser overweight patient with T2DM where diet alone has not succeeded Reduces insulin resistance: -Reduced hepatic glucose output -Increases peripheral glucose disposal GI side effects Not in severe heart, liver or MILD renal failure
38
Release of insulin
Glucose comes in, increases ATP, blocks ATP sensitive K+channels, causes Ca2+ influx and insulin release
39
When can sulphonylureas be used
When patient still has some beta cell function
40
How does sulphylureas work and what are they also known as
INSULIN SECRETAGOGUES Blocks the ATP sensitive K+ chanenel, forcing it to close to increase insulin release USED IN TYPE II ONLY (not type I there is no pancreatic function) cause weight gain
41
What is acarbose
Alpha glucosidase inhibitor Prolongs absorption of oligosaccharides Allows insulin secretion to cope, following defective first phase insulin As effective as metformin
42
Side effects of acarbose
Flatus
43
Actio of thiazolidineodione
Peroxisome proliferator-actived receptor agonists PPAR-γ Insulin sensitizer, mainly peripheral Adipocyte differentiation modified, weight gain but peripheral not central Improvement in glycaemia and lipids Evidence base on vascular outcomes Older types cause hepatitis
44
Side effects of thiazolidineodiones
Side effects of older types hepatitis, heart failure
45
What happens if you inject someone with glucose vs get someone to drink glucose orally
If you inject glucos into one patient, and oral administer glucose in another, then you get MUCH more insulin secretion in oral admin.
46
What is the incretin effect
Secreted in response to nutrients in gut Release of hormones from L cells in GI system increase insulin secretion
47
What is GLP1 made from and what is its effect How is it broken down
Transcription product of proglucagon gene, mostly from L cell. Stimulates insulin, suppresses glucagon Increases satiety Restores B cell glucose sensitivity Short half life, rapid degredation from enzyme dipeptidyl peptidase-4
48
Use therapeutically of GLP1
GLP-1 agonist .. INJECTED AND DPPG4 inhibitor = GLIPTINS ... ORAL (but not as effective)
49
Effect of GLP1 on weight
weight loss (due to feeling of satiety)
50
GLP1 example, PK and action
- Exenatide, liraglutide - Injected - Long acting GLP-1 agonist - Decrease glucagon - Decrease glucose - Weight LOSS
51
DPPG-4 inhibitor, example, PK and action
``` GLIPTINS Increase half life of exogenous GLP-1 Increase [GLP-1] Decrease [glucagon] Decrease [glucose] Neutral on weight ```
52
How do SGLT2 inhibitors work
Reduce uptake of glucose from the PCT (block SGLT2, which is a Na/glucose transporter inhibitor) but leads to osmotic symptoms REALLY GOOD for heart failure and also lower mortality
53
Why do lots of patient s eventually need insulin
Because of the beta cell failure that eventually occurs
54
What else should we control in T2DM
Blood pressure Diabetic dyslipidaemia (reduce cholesterol, TGs and increase HDL)
55
Screening for diabetes
Specifics of program unclear Diagnosis on glucose, fasted or stimulated?
56
How to prevent progression to diabtetes
Diet and exercise BETTER than metformin

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