Endocrinology - introduction to diabetes mellitus Flashcards

1
Q

In what tissues is GLUT4 common?

A

Muscles and fat

(myocytes and adipocytes)

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

What are characteristics of GLUT4 receptor?

A

insulin depdenet

7-fold increase glucose uptake

lies in vesicles

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

Effect of insulin on muscle cell?

A

increase GUT4 expression on CM

increased protien synthesis (helped by other hormones)

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

What effect can cortisol have on muscle cells?

A

proteolysis

and transportation glucogenic amino acids in blood to liver

(as starving state so low glucose so body uses alternative energy sources)

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

what effect does insulin have on liver (glucogenesis)?

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

What are 3 fuel sources of body? How long does each last?

A

short term - carbs stored in liver and muscles i.e glucagon

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

What is lipoprotein lipase function (enzyme)?

A

breaks down trigglycerides in blood so able to leave circulation (it’s too big)

moves into adipose tissue

breaks it down into glycine and non esteric fatty acids

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

What happens to glycerol and NEFA in adipose tissue?

A

If insulin present converted to trigylceride (stored) + stimulated uptake of glucose via GLUT4

When cortisol/GH present break down triglycerides that are stored to glycerol and NEFA that are released into blood to liver

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

What is the hepatic portal circulation?

What is it’s function?

A

takes nutrients straight to liver for processing

and insulin release quickly to rest of body

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

What happens to glycerol released into blood?

A

Take into liver + fed stored at triglycerides

when fasting glucogensis to produce glucose

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

What is unique about brains usage of fuels?

A

doesn’t use fatty acid

MOST preferred glucose

if needed use ketone bodies

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

How are ketone bodies produced in fasting state?

A

NEFA (from breakdown of triglyercides in adipose tissue) coverted to ketone bodies in liver

ketone bodies another alternative body fuel

problem: WHEN both GLUCOSE and KETONE BODIES in blood

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

What hepatic glycogenolysis?

A

when fed state GLU4 uptake of glucose stored as glycogen

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

Where else in the body is glycogen stored?

A

muscles

released back to glucose when needed i.e fasting

Can also use NEFA as energy source

NOT able to release glucose into circulation

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

overall what happens in fasted state?

A

low insulin

high glucagon

normal/lower side glucose

high NEFA levels

up intially but used up so after a while low amino acid levels

breakdown protiens and lipids

increase hepatic glucose

muscle use lipids as energy source

brain use glucose then ketone bodies

if prolonged ketone production

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

What are diagnosis of diabetes mellitus

A

Fasting glucose > 7.0mmol/L

Random glucose >11.1mmol/L

Oral Glucose Tolerance Test

Fasting glucose

75g glucose load

2-hour glucose

HbA1c >48mmol/mol

Diagnosis requires 2 positive tests or 1 positive + osmotic symptoms

17
Q

What physiology of Type 1 diabities (genetic)?

A

autoimmune - death B cells

no insulin produced

18
Q

How does it affect metabolism?

A

a lot of urine produced. As a lot of glucose in urine, osmotic diarhosis.

production a lot ketone bodies (ketoacidosis)

19
Q

Symptoms of T1 diabities?

A

weigh loss

hypergycaemia

glycosuria- polyuria, nocturia, polydipsia

ketones in blood and urine

20
Q

Diagnosis test for T1 diabities rather than T2?

A

Antibodies - GAD, IA2

C-peptide - low c peptide

presence of Ketones

21
Q

What are complications insulin?

A

Can cause hypoglycaemia which is has horrible side effects

22
Q

Body’s reponse to hypoglycaemia?

A

Increase cortisol, GH, glucagon, catecholamines that have a ‘fed state’ respsonse

incarease lipolysis

increase hepatic glucose

increase glucogenolysis

increase gluconeogenesis

23
Q

effect on awarness of hypoglycaemia?

A

reduced ability reconginse HYPO

due to loss of counterreg reponse - as body so use to having it

reccurent HYPO - body use to having this exprience, higher thershold

24
Q

Symptoms of hypoglycaemia

A

autonomic - sweating, pallor, palpatations, shaking

neuroglycopenic - slurred speech, poor vision, confusion , seizures, loss of consciousness

severe - need 3rd party assistance

25
Q

pathophysiology of T2 diabities?

A

insulin resistance residues in liver, muscle and adipose tissues

effects metabolism of glucose, fatty acid

enough insulin prevent ketogenesis and proteolysis

26
Q

What is insulin resistance mechanism?

A

When binds activates P13K - Akt (metabolism) and MARK pathway ( growth)

effects on P13K - Akt pathway but body produced more insulin for effect

MORE STIMULATION FOR metabolic actions

27
Q

effects of insulin resistance

A

hypertension

increased weight

high glucoses

low LDL, high TG

inflammatory resp

adipocytokines

decrease energy expenditure

28
Q

symptoms of T2 diabites

A

hyperglycaemia

overweight

dyslipidaemia

less osmotic symptoms - urine

later inulsin deficnicu

eye disease

renal failure

nerve disease

stroke

29
Q

Dietary reccomend and education?

A

total calories

reduce fat

reduce refined carbs

increase complex carb

decrease sodium

increase soluble fibre

DAFNE - type 1

DESMON - type 2

30
Q

mangement of diabites mellitus?

A