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Endocrine > Background to DM > Flashcards

Background to DM Flashcards

1
Q

What centres in hypothalamus determining energy intake

A

Feeding centre

Satiety centre

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2
Q

What does feeding centre do and how

A

Promotes hunger
Leptin = peptide hormone released by fat in adipose tissue
Decreases feeding activity

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3
Q

What does satiety centre do and what are theories behind

A

Promote feeling of full
Glucostatic - as BG increases, drive to eat decreases
Lipostatic - as fat increases, drive to eat decreases

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4
Q

What determines cellular output

A

Cellular work / metabolism
Mechanical work / movement
Heat loss = 50%

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5
Q

What is anabolism

A

Synthesis of larger molecules for stage

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6
Q

What state are you in after eating

A 
Anabolic state (Absorption) 
Nutrients supply energy which is stored
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7
Q

What hormone dominates anabolic state

A

Insulin

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8
Q

What is catabolism

A

Breakdown of large molecules to release energy

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9
Q

What state are you in between meals

A 
Catabolic (post-absorptive) 
Rely on stores to provide energy
Glycogenolysis from glycogen
Gloconeogenesis from AA / FA
Ketogenesis
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10
Q

What hormone dominates catabolic state

A

Glucagon

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11
Q

What catabolic steroids are prescribed in. medicine

A

Glucocorticoid

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12
Q

What do most cells use for energy

A

FA
CHO
Protein - AA

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13
Q

What does brain use

A

Can ONLY use glucose

Uses ketones in extreme starvation

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14
Q

What happens in absorptive state

A

Glucose, AA and FA enter blood from GI tract

Glucose and AA stimulate insulin

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15
Q

What is the only hormone to lower BG

A

Insulin

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16
Q

What is main energy source in body

A

Glucose

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17
Q

What is excess glucose stored as and where

A

Glycogen in liver and muscle by glycogenesis

Stores are limited so if excess then glucose converted to fat

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18
Q

How is fat / FFA stored

A

TAG in adipose tissue by lipogenesis

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19
Q

What is lipolysis

A

Breakdown of TAG to release FFA and glycerol
FFA used as energy
Glyceral goes to liver and converted to glucose

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20
Q

What happens if excess FFA breakdown

A

Converted to ketone

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21
Q

What are AA used for

A

To make new proteins

Can be used to make glucose in extreme starvation

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22
Q

What do 4 islet cells (A,B,delta,F) of pancreas produce

A 
A = glucagon 
B = insulin
Delta = somatostatin (GHIH) 
F = pancreatic polypeptide
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23
Q

What does insulin promote

A 
Lipogenesis
Glycogenesis
Protein synthesis 
Inhibits lipolysis and glucogenesis
Reduces muscle protein loss
Increases cellular uptake of K 
Permissive to GH
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24
Q

What is insulin

A

Peptide hormone stimulating uptake of glucose in liver, skeletal muscle and fat tissue

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25
Q

Where is it stored

A

Stored in vesicles as proinsulin in RER

Cleave to insulin and C peptide when needed

26
Q

What causes release of insulin

A 
B cells of pancreas activated when high BG
Glucose enters through GLUT 
Provides energy so ATP created
Causes Katp channel to close 
Intracellular K rises
Cell depolarises
Voltage gated Ca channels open
Triggers insulin exocytosis
27
Q

What happens when insulin becomes low

A

ATP levels low as no glucose
kATP channels open and K leaks out
Hyperpolarises cell
Ca channels close

28
Q

What stimulates insulin release

A 
Increased BG = main stimulus
Increased AA
Glucagon (insulin needed to take up glucose produced)
Other GI secretion hormones
Vagal nerve
29
Q

What GI hormones

A 
Gastric
Secretin - acid in duodenum
CCK - fat in duodenum 
GLP-1 
Prevents glucose surge
30
Q

Why does oral glucose cause larger increase in insulin than IV

A

Stimulates GI hormones and vagal nerve
GLP-1 in small intestine
Incretin effect

31
Q

What stimuli inhibit release

A

Low BG
Somatostatin (GHIH)
Sympathetic A2
Stress e.g. hypoxia

32
Q

What happens if no insulin

A

Cell’s unable to take up glucose as believe there is none
Leads to increased production of glucose by liver
Further increases BG

33
Q

How does insulin promote glucose uptake and glycogen synthesis

A

Binds to receptors on insulin sensitive tissue - liver, muscle + adipose
Stimulates mobilisation of GLUT 4 transporters so glucose transported into cells

34
Q

What is only insulin dependent tissue

A

Muscle

Adipose

35
Q

What happens if you remove insulin

A

Can get hyperkalaemia as K not taken up into cell

36
Q

What is glucose in other tissue dependent on

A

Brain / kidney / RBC = Glut 1+3

B cells / liver = glut 2

37
Q

How does glucose enter if not by insulin

A

Travels down conc gradient

38
Q

What happen in the liver

A

Not insulin dependent but helps
Insulin activates hexokinase lowering glucose conc as converts to glucose 6 phosphate
If fasted liver synthesis glucose via glycogenolysis and gluconeogenesis increasing conc and glucose moves out

39
Q

What is glucagon and where is it produced

A

Peptide hormone
Alpha cells of pancreas
Acts mainly on liver and degraded there

40
Q

What are glucagon receptors on tissue

A

G-protein coupled receptor

Linked to AC / cAMP

41
Q

What happens when receptors phosphorylated by glucagon

A

Increased glycogenolysis in liver
Increased gluconeogensis of AA and glycerol (from lipolysis)
Ketogenesis from FFA
Lipolysis

42
Q

What does glucagon not act on

A

Muscle

43
Q

What hormones form glucose counter regulatory control

A

Epinephrine (Adrenaline)
Cortisol - glucose needed in stress
GH

44
Q

What does epinephrine cause

A

Muscle glycogenolysis
Liver glycogenolysis and gluconeogensis
Lipolysis

45
Q

What does cortisol do

A

Liver gluconeogensis
Lipolysis
Protein catabolism so AA can be used
Inhibits uptake of glucose

46
Q

What does GH do

A

Liver gluconeogensis
Lipolysis
Inhibits uptake

47
Q

What must the body always ensure

A

Enough glucose for brain as other tissues can use FFA

48
Q

What promotes release of glucagon

A 
Low blood glucose
High AA
Sympathetic
Cortisol
Stress
49
Q

Why does high AA stimulate insulin and glucagon

A

Prevents hypoglycaemia following insulin release in response to AA

50
Q

What stimuli inhibit release of glucagon

A

Glucose
FFA / ketones
Insulin
Somatostatin

51
Q

What is somatostatin

A

Peptide hormone produced by D cells of pancreas and hypothalamus
Inhibits glucagon and insulin

52
Q

What is it stimulated by

A

High blood glucose

High AA

53
Q

What is the role of somatostatin

A

Inhibits activity of GI
Slows absorption to prevent exaggerated peaks
Inhibits secretion of GH
Suppress insulin and glucagon in paracrine fashion
NOT counter regulatory

54
Q

What do patients with pancreatic SS secreting tumours develop

A

Sx of DM

55
Q

What can synthetic SS be used to treat

A

Life threatening diarrhoea due to tumours as slows absorption

56
Q

How does ANS parasympathetic (vagus) nerve affect diabetic hormones

A

Increases insulin
Increases glucagon to lesser extent
Associated with anticipatory phase of digestion

57
Q

What does sympathetic nerve do

A

Inhibits insulin
Promotes glucose mobilisation
Increases glucagon and epinephrine
Fight or flight

58
Q

What happens during exercise

A

Increase entry into skeletal muscle (even if no insulin)
Increased insulin sensitivity
increased insulin independent glut 3 transporter

59
Q

What happens during starvation

A

Body relies on glucose stores
Adipose borken into FFA which can be used by most cells
Converts FFA to ketone body so brain can use
Spares protein

60
Q

What happens if underlying pathology not starvation

A

Metabolic acidosis = DKA

If extreme hyperglycaemia as no insulin so cells believe there is no glucose

61
Q

What slows absorption of glucose

A

Fat so if hypo don’t give fatty food

Endocrine (17 decks)

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