Brainscape's Knowledge GenomeTM

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


See full index

Year 2 - Endocrinology > T2DM > Flashcards

T2DM Flashcards

1
Q

Define diabetes

A

State of chronic hyperglycaemia sufficient to cause long-term damage to specific tissues

Fasting blood glucose >7mmol/L

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

Describe T2DM

A

NOT ketosis prone
NOT mild

Often invovles weight, lipids & BPs

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

What is the space between defining markers for diabetes and being normal called?

A

o Impaired Fasting Glucose
- when measuring fasting blood glucose

o Impaired Glucose Tolerance
- when measuring the 2hr response in a glucose tolerance test

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

Epidemiology of T2DM?

A

o Prevalent and mostly T2DM
o Affects adults (but children becoming affected)
o Varied across ethnic groups - greatest in those moving from rural to urban lifestyle

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

Pathophysiology of T2DM?

A

o MODY relatively uncommon BUT gives mtabolic insights

o Can be influenced by genetics, intrauterine & adult environment
- epigenetic changes in the intrauterine envrion. can affect functioning of developing gene

o Caused by insulin resistance & insulin secretion deficits
- FAs important in the complications of T2DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain MODY?

A

Maturity onset diabetes of the young

o Several hereditary forms - autosomal dominant

o Mutations in TF Glucokinase gene
- produces ineffective beta cell insulin secretion

o Postivie FH but NO OBESITY
- specific treatment for each type of MODY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do genes contribute to risk of insulin resistance?

ONENOTE!!

A

IUGR - intrauterine growth resistriction and greatly increase chances of developing T2DM

Insulin resistance ADIPOCYTOKINES –> DYSLIPIDAEMIA –> increased mitogenic pathway –> hypertrophy & increase in BP –> MACROvascular disease

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

Microvascular and Macrovascular?

A

Diabetes complications

o Dyslipidaemia –> MACROvascular

o Hyperglycaemia –> MICROvascular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What have twin studies shown about T2DM?

A

o Follows an almost AUTOSOMAL DOMINANT pattern

o T1DM on the other hand has LESS genetic input

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

Insulin resistance & insulin secretion link?

A

Insulin production decreases w. age
o become more RESISTANT w. age

At some point the IR and IS line bisect:
o at this point, we CANNOT make enough insulin for our resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Metabolism and presentation of T2DM?

A

o Heterogeneous - many forms/causes of T2DM

o Obesity
o Insulin resistant & secretion deficit
o Hyperglycaemia & dyslipidaemia –> acute & chronic complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens in the body when you give some glucose?

A

They will have TWO phases of insulin secretion

  1. FIRST PHASE
    o STORED insulin ready to be released
  2. SECOND PHASE
    o over a period of time, more insulin produced and secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens to people who are developing T2DM in relation to the glucose-insulin response?

A

Still have SOME insulin production BUT will LOSE their FIRST PHASE response to glucose

o make insulin eventually BUT takes a much longer time!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How can people get around the issue w. T2DM and the glucose-insulin response?

A

Eating COMPLEX CHOs

This is as it will release glucose more SLOWLY thus reducing the need for the FIRST PHASE Response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes increased blood glucose in TDM?

A

o DECREASED glucose disposal

o INCREASE HGO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Normal link between HGO and insulin and how is this impaired in T2DM?

A

Insulin LOWERS blood glucose via. REDUCING HGO

  1. When you have NOT eaten, HGO maintains blood glucose at 4mmol/L
  2. AFTER you’ve eaten, insulin STOPS HGO as do not need this output anymore!
  3. Insulin instead drives the glucose from the meal into muscle & adipose tissue

These affects are ABSENT in T2DM so:
o cannot inhibit HGO
o cannot move glucose into muscle/fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Relationship between insulin sensitivity and insulin secretion

A

As you age, insulin sensitivity DECREASES

SO the secretions must INCREASE to compensate
BUT
those with diabetes cannot compensate enough

18
Q

Effect of Insulin Resistance on body?

A
  1. TGs on adipocytes can be broken down to glycerol & NEFAs which is transported to the liver
    o marker for OMENTAL ADIPOCYTES - hence why waist circumference predicitive of IHD
  2. In liver gluconeogensis & glycogenolysis occurs
    o hence increased HGO and decreased glucose uptake
  3. FAs go to liver where they CANNOT be used to make glucose
    o made into VLDL-TGs instead
    o these contribute to the ATHEROGENIC risk!
19
Q

Link between obesity and T2DM?

A

Appears to be a part of the mechanism of T2DM

o more than a precipitant
o FAs and Adipocytokines are important (modulate insulin resistance)

o Central/omental obesity common
- 80% of T2DM

o Weight reduction is useful treatment

20
Q

Gut Microbiota link with T2DM?

A

Appears to be associated w.
o obesity, insulin resistance, T2DM, inflammation & adipocytokine pathways
- via. possible host signalling

Various lipopolysaccharides are fermented by gut bacteria to SHORT CHAIN FFAs
o these enter the host circulation
o modulate bile acids

Possible treatment in the future might involve microbiota transplants

21
Q

What is a common SE of diabetes treatment?

A

WEIGHT GAIN!!

As it reduced blood glucose BUT increases appetite

Note - only METFORMIN reduces weight!

22
Q

Only diabetic drug that reduces weight?

A

Metformin

23
Q

How does T2DM progress?

A

o Intrauterine envrion. may influence insulin resistance in later life

o Late T2DM can make the pancreas produce IMMATURE insulin

  • they don’t have FIRST PHASE insulin
  • SO insulin does NOT work properly

Eventually there is an ABSOLUTE insulin deficiency

24
Q

How can T2DM present?

A

o Osmotic symptoms
o Infections
- hyperglycaemic envrion. is favourable for certain bacteria

o Presentation of complications e.g. acute (hyperosmolar coma) OR chronic (IHD)

  • Microvascular - retino/nephro/neuropathy
  • Macrovascular - IHD, cerebrovascular, renal artery stenosis, PVD
  • Metabolic (rarer than for T1DM)
  • From treatment - e.g. hypo attack
25
Q

Basis of T2DM management?

A

o Education
o Diet
o Pharmacological treatment
o Complication screening

26
Q

How should diet of T2DM be controlled?

A

Control total calories/increase exercise (weight)

o reduce refined CHOs (less sugar)
o increase complex CHOs
o reduce fat as proportion of calories (less IR)
o increase unsaturated fat as proportion of fat (IHD)
o increase soluble fibre (longer to absorb CHO)
o address salt (BP risk)

27
Q

What are the main things treated and monitored in T2DM?

A

o Weight
o Glycaemia
o BP
o Dyslidiaemia

28
Q

Overview of pharmacological interventions for T2DM?

A

o Orlistat - pancreactic lipase inhibitor

o Metformin - insulin sensitiser

o Sulphonylureas - makes existing pancreas secrete more insulin

o Alpha glucosidase inhibitors - delays glucose absorption

o Thiazolidinediones - acts on adipocytes and insulin sensitiser peripherally in fat and muscles

29
Q

Metformin?

A

Biguanide class - oral anti-hyperglycaemic drug
- insulin sensitiser

o Used in OBESE T2DM patient where diet alone has NOT succeeded

o Reduces insulin resistance

  • reduces HGO
  • increases peripheral glucose disposal

GI SEs
Do NOT use if severe liver/cardiac failure or mild renal failure

30
Q

Insulin sensitisers?

A

LOWER your blood sugar by increasing the muscle, fat and liver’s sensitivity to insulin

31
Q

Sulphonylurea?

A

E.g. Glibenclamide

Act on beta-cells
o BLOCK ATP-sensitive K+ channel
o Causes influx of Ca2+
o Increases insulin secretion

o Used in LEAN patients w. T2DM

SEs include

  • weight gain
  • HYPOglycaemia
32
Q

Acarbose?

A

Alpha glucosidase inhibitor!

o Prolongs absorption of oligosaccharides
- allows insulin secretion to cope following defective first phase insulin

As effective as metformin
BUT
SE include flatulence

33
Q

Thiazolindeinediones?

A

e.g. Pioglitazone

Peroxisome proliferator-activated receptor agonist (PPAR-g agonist)

o Insulin sensitiser (mainly peripheral)
o Adipocytes rearranges so weight gain is peripheral and NOT central
o Improvement in glycaemia & dyslipidaemia

SE include hepatitis & HF

34
Q

GLP-1?

A

Glucagon like peptide-1

Secreted from L-cells in response to nutrients in the gut (incretin effect)
 o stimulates insulin
 o supresses glucagon
 o increases satiety
 o restored B-cell glucose sensitivity

Has a SHORT half-life
o broken down by DPPG-4

35
Q

Drugs associated with GLP-1?

A 
GLP-1 agonist e.g. Exenatide, Liraglutide
 o injectable
 o long acting GLP-1 agonist
 o Decrease [glucagon]
 o Decrease [glucose]
 o WEIGHT LOSS!
Gliptins - DPPG-4 inhibitor
 o Increase half-life of exogenous GLP-1
 o Increase [GLP-1]
 o Decrease [glucagon]
 o Decrease [glucose]
 o NEUTRAL effect on weight!
36
Q

Empaglifozin?

A

Na+-glucose transporter INHIBITOR

o increases glycosuria
o HbA1C lower

Note - beta-cell function continues to DECLINE despite efforts to improve symptoms w. drugs

37
Q

What other aspects of T2DM can be controlled w. drugs other than hyperglycaemia?

A
  1. BP (90% have this problem)
2. Dyslipidaemia
 o high cholesterol
 o high TGs
 o LOW HDLs
Can lead to MACROvascular problems!
38
Q

Gestational diabetes & impaired glucose tolerance?

A

HIGH risk at developing diabetes in later life!

39
Q

Why is screening difficult in T2DM?

A

Does NOT present until complications arise!

40
Q

What was found to be the best cure/symptom reliever for T2DM incidence?

A

Intensive lifestyle!
inc. good diet & exercise

Better than drugs like metformin

41
Q

Diabetes comparison - T1 vs. T2?

Prevalence
Typical age
Onset
Habitus
FHx
Geography
Weight loss
Ketosis prone
Serum insulin
HLA association
Islet B-cells
Islet cells Abs
A

ONENOTE!!

Year 2 - Endocrinology (19 decks)

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