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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
Where is it stored
Stored in vesicles as proinsulin in RER | Cleave to insulin and C peptide when needed
26
What causes release of insulin
``` 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
What happens when insulin becomes low
ATP levels low as no glucose kATP channels open and K leaks out Hyperpolarises cell Ca channels close
28
What stimulates insulin release
``` Increased BG = main stimulus Increased AA Glucagon (insulin needed to take up glucose produced) Other GI secretion hormones Vagal nerve ```
29
What GI hormones
``` Gastric Secretin - acid in duodenum CCK - fat in duodenum GLP-1 Prevents glucose surge ```
30
Why does oral glucose cause larger increase in insulin than IV
Stimulates GI hormones and vagal nerve GLP-1 in small intestine Incretin effect
31
What stimuli inhibit release
Low BG Somatostatin (GHIH) Sympathetic A2 Stress e.g. hypoxia
32
What happens if no insulin
Cell's unable to take up glucose as believe there is none Leads to increased production of glucose by liver Further increases BG
33
How does insulin promote glucose uptake and glycogen synthesis
Binds to receptors on insulin sensitive tissue - liver, muscle + adipose Stimulates mobilisation of GLUT 4 transporters so glucose transported into cells
34
What is only insulin dependent tissue
Muscle | Adipose
35
What happens if you remove insulin
Can get hyperkalaemia as K not taken up into cell
36
What is glucose in other tissue dependent on
Brain / kidney / RBC = Glut 1+3 | B cells / liver = glut 2
37
How does glucose enter if not by insulin
Travels down conc gradient
38
What happen in the liver
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
What is glucagon and where is it produced
Peptide hormone Alpha cells of pancreas Acts mainly on liver and degraded there
40
What are glucagon receptors on tissue
G-protein coupled receptor | Linked to AC / cAMP
41
What happens when receptors phosphorylated by glucagon
Increased glycogenolysis in liver Increased gluconeogensis of AA and glycerol (from lipolysis) Ketogenesis from FFA Lipolysis
42
What does glucagon not act on
Muscle
43
What hormones form glucose counter regulatory control
Epinephrine (Adrenaline) Cortisol - glucose needed in stress GH
44
What does epinephrine cause
Muscle glycogenolysis Liver glycogenolysis and gluconeogensis Lipolysis
45
What does cortisol do
Liver gluconeogensis Lipolysis Protein catabolism so AA can be used Inhibits uptake of glucose
46
What does GH do
Liver gluconeogensis Lipolysis Inhibits uptake
47
What must the body always ensure
Enough glucose for brain as other tissues can use FFA
48
What promotes release of glucagon
``` Low blood glucose High AA Sympathetic Cortisol Stress ```
49
Why does high AA stimulate insulin and glucagon
Prevents hypoglycaemia following insulin release in response to AA
50
What stimuli inhibit release of glucagon
Glucose FFA / ketones Insulin Somatostatin
51
What is somatostatin
Peptide hormone produced by D cells of pancreas and hypothalamus Inhibits glucagon and insulin
52
What is it stimulated by
High blood glucose | High AA
53
What is the role of somatostatin
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
What do patients with pancreatic SS secreting tumours develop
Sx of DM
55
What can synthetic SS be used to treat
Life threatening diarrhoea due to tumours as slows absorption
56
How does ANS parasympathetic (vagus) nerve affect diabetic hormones
Increases insulin Increases glucagon to lesser extent Associated with anticipatory phase of digestion
57
What does sympathetic nerve do
Inhibits insulin Promotes glucose mobilisation Increases glucagon and epinephrine Fight or flight
58
What happens during exercise
Increase entry into skeletal muscle (even if no insulin) Increased insulin sensitivity increased insulin independent glut 3 transporter
59
What happens during starvation
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
What happens if underlying pathology not starvation
Metabolic acidosis = DKA | If extreme hyperglycaemia as no insulin so cells believe there is no glucose
61
What slows absorption of glucose
Fat so if hypo don't give fatty food

Endocrine (17 decks)

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