Brainscape's Knowledge GenomeTM

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


See full index

Year 2 Diabetes & Endocrinology (JK) > The endocrine pancreas 1+2 > Flashcards

The endocrine pancreas 1+2 Flashcards

1
Q

Body energy = energy intake - ?

A

energy output

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

the 2 hypothalamic centres which determine energy intake

A

feeding centre

satiety centre

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

Feeding centre

A

promotes feeling of hunger and drive to eat

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

satiety centre

A

promotes feeling of fullness by suppressing the feeding centre

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

What 3 things control activity in the 2 hypothalamic centres which determine energy intake?

A

neural signals
chemical signals
presence of chemicals in the plasma

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

What is the glucostatic theory?

A

food intake is determined by blood glucose

as BG increases, drive to eat decreases, inhibit feeding centre and stimulate satiety centre

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

What is the lipostatic theory?

A

food intake is determined by fat stores

as they increase, drive to eat decreases, inhibit feeding centre and stimulate satiety centre

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

What hormone is linked to the lipostatic theory and what is its function?

A

Leptin

peptide hormone which is released by fat stores which depresses feeding activity

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

What will occur if these 2 hypothalamic centres are disrupted? What are other common causes of this?

A

obesity

more often due to just eating too much and not exercising enough

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

What are the 3 types of energy output

A

cellular work
mechanical work
heat loss

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

What is the only part of our energy output which we can regulate?

A

mechanical work - large scale eg muscle

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

Define metabolism

A

integration of all biochemical reactions in the body

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

The 3 parts of metabolism are

A

extracting energy from food
using that energy
storing energy

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

Is catabolism or anabolism linked to storage?

A

anabolism

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

What is the absorptive state?

A

after eating - ingested nutrients supply energy needs and excess is stored

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

Is the absorptive state anabolic or catabolic phase?

A

anabolic

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

What is the post-absorptive state?

A

between meals/overnight pool of nutrients in plasma decreases - fasted state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Is the post-absorptive state anabolic or catabolic phase?

A

catabolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What organ is named as the main obligatory glucose utiliser?

A

brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What other energy source can the brain use and when?

A

ketone bodies

starvation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens if in the post-absorptive state, Bg is not maintained?

A

hypoglycaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is BG maintained in the post - absorptive state?

A

gluconeogenesis and glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is gluconeogenesis?

A

make new glucose from amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is glycogenolysis?

A

making glucose from glycogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Normal [BG]?
5mM
26
Hypoglycaemia [BG]?
< 3mM
27
What 2 hormones tightly regulate [BG]?
insulin and glucagon
28
Where are the 2 endocrine hormones produced in the pancreas and what % of the pancreas is endocrine?
islets of Langerhans | 1%
29
What is the blood supply to the islets of Langerhans?
copious
30
4 types of islets of Langerhans and what they produce
``` alpha = glucagon beta = insulin delta = somatostatin F = pancreatic polypeptide ```
31
What Is insulin?
A peptide hormone secreted by pancreatic beta cells which stimulates glucose uptake by cells
32
What are the different molecules names in the formation of insulin?
preproinsulin proinsulin insulin and c peptide
33
How is insulin stored?
in a vesicle as insulin and c peptide until activated
34
What is the major stimulus for insulin secretion?
[BG] increase
35
What is the only hormone which can lower [BG]?
insulin
36
What state (absorptive or post-absorptive) does insulin dominate?
absorptive
37
Why do most cells use glucose as energy source during the absorptive state?
Easy to metabolise
38
How is excess glucose stored? (2 ways)
glycogen in liver and muscle | TAG in adipose tissue and liver
39
What happens to excess amino acids?
converted to fat
40
What happens to excess fatty acids?
TAG in liver and adipose tissue
41
What specific ion channels do beta cells have and what are they sensitive to?
K+ | [ATP]
42
How do K+ ion channels in beta cells work to release insulin ultimately?
``` glucose enters through GLUT after a meal metabolism and [ATP] increases K-ATP closes and cell depolarises voltage dependent calcium channels open calcium causes exocytosis of insulin ```
43
What receptors does insulin bind to and on what kind of tissues?
tyrosine kinase | insulin sensitive --> muscle and fat
44
Insulin stimulates the mobilisation of what kind of transporters?
GLUT-4
45
Where do GLUT-4 transporters live?
cytoplasm of unactivated muscle and adipose tissue
46
GLUT-1 transports...
basal glucose uptake into many tissues eg brain, RBC, kidney
47
Where are GLUT-2 transporters found?
b cells of pancreas and liver
48
What are the 3 GLUT non insulin dependent receptors?
1.2.3
49
Is the liver insulin sensitive?
no
50
What GLUT receptors does the liver use?
GLUT 2
51
How does insulin effect glucose transport into the liver?
glucose enters down concentration gradient | glucose transport into hepatocytes is enhanced by insulin status
52
Why does insulin have an effect on glucose transport into liver?
hexokinase enzyme lowers [glucose] in the cell and forms a concentration gradient in favour of glucose entering into the hepatocytes
53
List some other anabolic functions of insulin
``` glycogen synthesis in muscle and liver amino acid uptake into muscle protein synthesis TAG synthesis in adipocytes and liver inhibits gluconeogenic enzymes ```
54
List 2 other actions of insulin which are due to activation of multiple transducer pathways
permissive effect on HGH | promotes K+ entry into cells
55
Insulin half-life and what is it degraded by?
5 mins | liver and kidneys
56
What happens to insulin bound receptors when insulin action is complete?
endocytosed | destroyed by insulin protease
57
Stimuli which increase insulin release
``` increase [BG] glucagon vagal nerve activity increased amino acids in plasma incretin hormones eg CCK ```
58
Stimuli which inhibit insulin release
decreased [BG] somatostatin stress eg infection sympathetic alpha 2 effects
59
Why does glucagon increase insulin release?
insulin required to take up glucose created via gluconeogenesis stimulated by glucagon
60
Why does vagal activity increase insulin release and discuss iv vs oral glucose
parasympathetic - GI hormones incretin hormones increase insulin oral glucose better due to direct effect + incretin hormones and vagal stimulation of B cells
61
What is glucagon?
peptide hormone produced by alpha cells of the pancreatic islets and is a glucose mobilising hormone
62
What organ does glucagon primarily act upon?
liver
63
Half life of glucagon and what is it degraded by?
5-10 mins | liver
64
What 4 hormones make up the glucose counter regulatory system?
glucagon HGH cortisol epinephrine
65
When is glucagon most active?
post-absorptive state
66
Receptors for glucagon?
GPCR to adenylate cyclase/cAMP
67
When glucagon receptors are activated what happens?
phosphorylate specific liver enzymes
68
3 consequences of phosphorylation of specific liver enzymes
increased gluconeogenesis increased glucogenolysis formation of ketones from FA
69
What is the net result of glucagon action on the liver enzymes?
increased [BG]
70
What is the pattern of glucagon secretion and when does this increase?
constant | when [BG] < 5.6mM
71
Why do amino acids also stimulate glucagon aswell as insulin release?
adaption for high protein meal | prevent hypoglycaemia
72
How is glucose spared for the brain in the post absorptive state?
lower insulin muscle and fat cannot readily access glucose glucose sparing for brain
73
Stimuli that promote glucagon release
``` low [BG] amino acids in plasma sympathetic innervation and epinephrine, B2 effect cortisol stress ```
74
Stimuli that inhibit glucagon release
insulin glucose somatostatin FFA and ketones
75
Parasympathetic effect on islet cells
increase insulin, to a less degree glucagon | vagus - anticipatory phase of digestion
76
Sympathetic effect on islet cells
increase glucose mobilisation | increase glucagon and epinephrine and inhibit insulin
77
What is somatostatin?
peptide hormone produced by D cells in pancreas and hypothalamus , also known as GHIH.
78
How does somatostatin act?
slow down absorption in Gi tract to prevent surges | prevents glucagon and insulin
79
How can somatostatin be used clinically (GI)
diarrhoea and tumours who have symptoms of diabetes
80
What does exercise do to glucose uptake?
increase in muscle without insulin being present by increasing insulin sensitivity of muscle
81
What happens with GLUT-4 receptors and what are long term effects of exercise?
increase in number and migrate to cell surface without insulin effect persists and long term effects if regular exercise
82
How are ketone bodies formed?
in starvation FFA are formed from adipose tissue and make ketone bodies by conversion in the liver
83
What 2 parts of the body are ketone bodies used by?
brain and muscle
84
Benefit of ketone bodies
spares the protein which would be broken down in starvation
85
What is diabetes mellitus?
loss of control of blood glucose levels
86
What is type 1/IDDM diabetes?
autoimmune destruction of the pancreatic b cells | destroys ability to produce insulin and compromises ability to absorb glucose
87
Treatment of type 1 diabetes
need insulin injections every day
88
What is ketoacidosis?
similar to starvation - lack of access to nutrients | lack of insulin depresses ketone body uptake
89
Harm of ketoacidosis
build up in blood - acidic | life threatening and death
90
2 ways ketones are detectable
urine | acetone breath
91
What is type 2 diabetes?
insulin resistance of peripheral tissues and fat and muscle no longer respond to normal insulin levels
92
2 reasons why fat and muscle no longer respond to insulin
reduced number of receptors | abnormal response of insulin receptors
93
What happens to b cells in type 2 diabetes?
nothing - still intact | may even be hyperinsulinaemia
94
What is type 2 diabetes associated with?
obesity, diet, exercise
95
Usual age for type 2 diabetes
>40 but decreasing
96
Treatment of type 2 diabetes
diet and exercise oral hypoglycaemic drugs eg metformin sulphonylureas
97
Why can type 2 diabetes treatments not be used in type 1?
requires functioning b cells
98
Diagnostic criteria for diabetes
hyperglycaemia
99
What test is done to diagnose diabetes?
glucose tolerance test
100
Why is [BG] increased in type 1 and type 2 diabetes?
type 1 - inadequate insulin release | type 2 - inadequate tissue response
101
Briefly describe how a glucose tolerance test would be done
patient ingests glucose after fasting [BG] should return to fasting in an hour if not returned by 2 hours is diabetic
102
How to convert to mM from mg/dl?
divide by 18
103
Why are there risks associated with hyperglycaemia?
glucose is a highly reactive molecule
104
4 hyperglycaemia complications
retinopathy neuropathy nephropathy CVD
105
Who is especially at risk of diabetic hypoglycaemia?
type 1 on exogenous insulin
106
How is hypoglycaemia staged?
changes in [BG]

Year 2 Diabetes & Endocrinology (JK) (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions