Endocrinology - introduction to diabetes mellitus Flashcards

(30 cards)

1
Q

In what tissues is GLUT4 common?

A

Muscles and fat

(myocytes and adipocytes)

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2
Q

What are characteristics of GLUT4 receptor?

A

insulin depdenet

7-fold increase glucose uptake

lies in vesicles

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3
Q

Effect of insulin on muscle cell?

A

increase GUT4 expression on CM

increased protien synthesis (helped by other hormones)

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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)

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5
Q

what effect does insulin have on liver (glucogenesis)?

A
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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

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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

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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

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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

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10
Q

What happens to glycerol released into blood?

A

Take into liver + fed stored at triglycerides

when fasting glucogensis to produce glucose

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11
Q

What is unique about brains usage of fuels?

A

doesn’t use fatty acid

MOST preferred glucose

if needed use ketone bodies

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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

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13
Q

What hepatic glycogenolysis?

A

when fed state GLU4 uptake of glucose stored as glycogen

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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

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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

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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
pathophysiology of T2 diabities?
insulin resistance residues in liver, muscle and adipose tissues effects metabolism of glucose, fatty acid **enough insulin prevent ketogenesis and proteolysis**
26
What is insulin resistance mechanism?
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
effects of insulin resistance
hypertension increased weight high glucoses low LDL, high TG inflammatory resp adipocytokines decrease energy expenditure
28
symptoms of T2 diabites
hyperglycaemia overweight dyslipidaemia less osmotic symptoms - urine later inulsin deficnicu eye disease renal failure nerve disease stroke
29
Dietary reccomend and education?
total calories reduce fat reduce refined carbs increase complex carb decrease sodium increase soluble fibre DAFNE - type 1 DESMON - type 2
30
mangement of diabites mellitus?