Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 - LCRS - Endocrinology > Type 2 Diabetes Mellitus > Flashcards

Type 2 Diabetes Mellitus Flashcards

1
Q

Definition of diabetes (in particular T2)

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

T2DM is not ketosis prone (much less likely to have ketones than in T1)
T2DM is not mild
T2DM often involves weight, lipids and blood pressur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the biochemical markers of diabetes?

A

Fasting Glucose above 7 (6-7 is impaired fasting glucose)
2h Glucose above 11 (7.8-11 is impaired glucose tolerance)
Random Glucose above 11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which type of diabetes is more common?

A

T2DM (More genetic than T1. It is not a disease of lifestyle, it is a genetic condition It is accelerated by lifestyle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Prevalence of diabetes

A

10% at 60yrs

  • > prevalence is increasing and is now also seen more in children and young individuals
  • > prevalence varies enormously
  • > Greatest in ethnic groups that move from rural to urban lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

MODY

A
  • Several hereditary forms (1-8)
  • Autosomal dominant
  • Ineffective pancreatic B cell insulin production
  • Mutations of transcription factor genes, glucokinase gene
  • Positive FH, no obesity
  • Specific treatment for type
  • monogenic diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathophysiology of T2DM?

A
  • MODY relatively uncommon but gives useful metabolic insights
  • Genes and intrauterine environment and adult environment. (IU environment: predicts adult environment and it can accelerate given a particular diet/exercise.)
  • Insulin resistance and insulin secretion defects
  • Fatty acids important in pathogenesis and complications (some FAs seem particularity important for insulin resistance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do twin studies in diabetes show?

A

there is a higher genetic link in T2DM than in T1DM

i.e. identical twins 35% both T1, 70% both T2; nonidentical twins 10% both T1, 40% both T2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diabetes Type 2 summarised

A
  • Genetics: can make you prone to obesity and FAs as well as Insulin resistance with adipocytokines -> inflammation
  • there is interplay between genetics and intrauterine growth restriction (e.g. not enough food)
  • obesity and fatty acids process the development of Insulin resistance
  • Insulin resistance has metabolic effects: mitogenic and metabolic dyslipidemia which causes microvascular complications such as stroke or MI
  • eventually the insulin resistance wears down the beta cells and causes beta-cell failure
  • beta cell failure causes hyperglycaemia which has microvascular complications
  • beta cell failure also makes dyslipidamiea and metabolic defects worse
  • at a certain point the beta-cell-failure may become absolute and the person has insulin requirement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the connection between baby weight and diabetes?

A

Babies with lower weight at 1yr of age had a higher (22%) chance of having blood sugar problems later than babies that had a higher weight (6%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Relationship between Insulin resistance and insulin production

A
  • at some point everyone becomes insulin resistant, for some people it is at the age of 50 and for others at a potential age of 110
  • insulin resistance increases with age
  • T2DM is a balance between the 2
  • insulin resistance increases and insulin production decreases over time in T2DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Metabolism and presentation of T2DM

A
  • Heterogeneous
  • Obesity
  • Insulin resistance and insulin secretion deficit
  • Hyperglycaemia and dyslipidaemia
  • Acute and chronic complications
  • more cholesterol carried in a harmful way
  • there are preventable and dilatable complications but some people now show up when it has already progressed so far that e.g. their eyesight is harmed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Can NEFAs be used to make glucose?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is insulin release impaired in someone with diabetes or prediabetes?

A
  • there is a big loss in first phase insulin production in both cases, it is the first thing that goes.
  • there is also a generally reduced. insulin release.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some chemical released by adipocytes?

A

Adipose tissue = endocrine organ

  • TNF-alpha, IL-6
  • Leptin (elevated in obesity)
  • Resistin (elevated in obesity and T2DM)
  • Apelin
  • Visfastin
  • Adiponectin
  • Endocannabinoids
  • Glucocorticoids (increase 11beta-hsd1 in fat)
  • Fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Obesity and T2DM

A
  • More than a precipitant
  • Fatty acids and adipocytokines important
  • Central or omental obesity (Central adipocytes (in omentum) are more active (more turnover also more active from endocrine perspective), drain directly into the liver)
  • 80% T2DM are obese (at diagnosis, more than gen pop and T1)
  • Weight reduction useful treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Preturbations in gut microbiota

A
  • Obesity, insulin resistance T2DM (more ass. with obesity than diabetes but not necessarily causation)
  • Host signaling
  • Bacterial lipopolysaccharides fermentation to short chain FA, bacterial modulation bile acids
  • Inflammation, signaling metabolic pathways (altering them)
  • Most studies correlative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a common side effect of diabetes treatments?

A

Weight gain (metformin excluded)

18
Q

What are the mechanisms behind weight gain in the different types of drugs for diabetes?

A
  • in secretagogues (sulphonylureas and glinides) increased insulin reverses the catabolic effects of diabetes
  • thiazolidinediones: increased adipocyte proliferation as. well as fluid retention
19
Q

How can patients with T2DM present?

A
  • acute: hyperosmolar coma

- chronic: Ischameic heart disease, retinopathy

20
Q

complications of T2DM

A

Macrovascular: IHD, renal artery stenosis, cerebrovascular, PVD
Microvascular: retinopathy, neuropathy, nephropathy
Metabolic: lactic acidosis, hyperosmolar (metabolic complications are less likely than in T1)
of Treatment: hypoglycaemia

21
Q

What are the basics of management of T2DM?

A
  • Education
  • Diet (healthy human diet)
  • Pharmacological treatment
  • Complication screening -> before there is irreversible damage
22
Q

Why do we treat T2DM?

A
  • Symptoms
  • Reduce chance of acute metabolic complications (unlikely in T2DM)
  • Reduce chance of long term complications; good evidence base (UK prospective diabetes study or UKPDS)
  • EDUCATION
23
Q

What should an individual with T2DM eat?

A
  • 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)
24
Q

Treatment and monitoring of T2DM

A

Weight
Glycaemia
Blood pressure
Dyslidiaemia

25
Q

Options for weight loss in T2DM

A
  • healthier diet
  • exercise
  • orlistat - intestinal lipase inhibitor (fat is removed via faeces) – only drug for weight loss in the country
  • gastric bypass surgery (diabetes could go into remission but would return later, not much known about long term effects atm)
26
Q

Metformin

A
  • Biguanide, insulin sensitiser -> makes insulin more effective
  • if overweight patient with T2DM where diet alone has not succeeded
  • Reduces insulin resistance
  • Reduced HGO
  • Increases peripheral glucose disposal
  • GI side effects
  • do not use if severe liver, severe cardiac or mild renal failure

-> just about everyone with T2DM should be taking metformin, it is very effective and safe

27
Q

Incretin effect

A

Oral glucose has a stronger effect on insulin production than i.v. glucose

28
Q

How do sulphonylureas work?

A

They stimulate the remaining beta cells to make more insulin (bind, steps cause the blockage of K channel and Ca2+ influx causing insulin release)

29
Q

What mefdications can be used in diabetes?

A
  • metformin
  • insulin
  • suplphonylureas (make remaining beta cells produce insulin)
  • thiazolidinediones -> act on central and peripheral insulin resistance
  • GLP1
  • DPP4 inhibitor (also has an anti-glucagon effect)
  • SGLT2 inhibitor (increases amount of sugar excreted in urine)
30
Q

Acarbose

A
  • Alpha glucosidase inhibitor
  • Prolongs absorption of oligosaccharides
  • Allows insulin secretion to cope, following defective first phase insulin -> for patients with not enough first phase insulin
  • As effective as metformin
  • Side effects flatus (causes fermentation of sugar in the bowel)
31
Q

Thiazolidinediones

A
  • Peroxisome proliferator-actived receptor agonists PPAR-γ
  • Pioglitazone
  • Insulin sensitizer, mainly peripheral
  • Adipocyte differentiation modified, weight gain but peripheral not central
  • Improvement in glycaemia and lipids
  • Evidence base on vascular outcomes
  • Side effects of older types hepatitis, heart failure

(they cause increased storage of FAs in adipocytes and therefore there are less of them in the circulation and cells become more dependant on the use of carbs (i.e. glucose) as their energy source)

  • > redistribute fat from momentum to arms and legs
  • > don’t only decrease glucose levels but also stops people from having heart attacks.
32
Q

GLP-1 as treatment for diabetes

A
  • Secreted in response to nutrients in gut
  • 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 (DPPG-4 inhibitor)
33
Q

What are glistens?

A

DPP4 inhibitors

34
Q

What are the effects of GLP1 agonists?

A 
Exenatide, liraglutide
Injectable
Long acting GLP-1 agonist
Decrease [glucagon]
Decrease [glucose]
Weight loss

-> very effective for sugar and also causes weight loss

35
Q

What are the effects of gliptins (DPPG-4 inhibitors)?

A 
Increase half life of exogenous GLP-1
Increase [GLP-1]
Decrease [glucagon]
Decrease [glucose]
Neutral on weight

-> oral not as effective and also doesn’t cause weight loss

36
Q

Empaglifozin

A
  • Inhibits Na-Glu transporter, increases glycosuria = SGLT inhibitor
  • N=7200, 206 weeks
  • HbA1c lower
  • 32% lower all cause mortality
  • 35% lower risk heart failure

-> this may not be due to the sugar effect but due to the

37
Q

What are other aspects of control in T2DM?

A

Blood Pressure

  • possibly 90% in T2DM
  • clear benefits to treatment

Dyslipidaemia

  • increased cholesterol
  • high triglycerides
  • low HDL cholesterol
  • clear benefits to treatment

=> increases life span

38
Q

Why is diabetes in pregnancy important?

A
  • think about the intrauterine environment of the baby

- if the baby has IUGR the baby can have a higher risk of developing T2DM

39
Q

Screening for diabetes

A

Problem?
- Mortality, morbidity, cost

Screen?
- Specifics of program unclear, which test how often in who?

Diagnosis?

  • Glucose, fasted or stimulated?
  • High risk?

Treatment?
- All aspects of control

40
Q

What is more effective in treatment of T2DM - lifestyle or metformin?

A

Lifestyle intervention is more effective than metformin in treatment of diabetes over years.

41
Q

What are the most common types of diabetes?

A
  • T1
  • T2
  • MODY (maturity onset diabetes of the young)
  • LADA (latent autoimmune diabetes of adulthood)
42
Q

What should you treat in diabetes T2?

A

glucose
weight
BP
dyslipidamia

Year 2 - LCRS - Endocrinology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions