endocrine physiology LOL Flashcards
To learn the very basics (265 cards)
1
Q
Lecture: introduction to the endocrine system 1 and 2
A
2
Q
Lecture: hypothalamus and the pituitary
A
3
Q
What is the endocrine system?
A
This is a collective term for the cells which produce chemical messenger substances that are
regarded as hormones.
4
Q
Classify hormones according to their chemistry and mechanisms of action upon target cells
A
5
Q
- Define the terms: troph; trophic hormone; hypophysiotropic hormone.
A
6
Q
List the neurohormones produced by the hypothalamus - including those secreted via
the neurohypophysis (posterior pituitary lobe).
A
7
Q
Describe diagrammatically the compartmentation and routes of communication within
the hypothalamus-pituitary gland complex.
A
8
Q
The feeding centre promotes feelings of hunger, whilst the satiety centre promotes feeling of fullness. These are hypothalamic centres.
What affect do they have on each other?
A
Satiety centre suppresses the feeding centre
but not vice verse obvs
9
Q
Is the satiety centre or the feeding centre sensitive to insulin
A
satiety.
10
Q
is the feeding centre and satiety centre just endocrine, or also neural?
A
neuroendocrine
neural and chemical
chemical being hormones AND from the food we eat
11
Q
What are the two theories of hunger
A
1) Glucostatic theory
2) Lipostatic theory
12
Q
whats glucostatic theory
A
hunger controlled by blood glucose levels- rise switches off feeding centre, switches on insulin/satiety centre
13
Q
what is lipostatic theory
A
hunger controlled by amount of fat stores- rise switches off feeding centre, switches on insulin/satiety centre
14
Q
What does leptin do
A
depresses feeding centre in hypothalamus
15
Q
Where is leptin released from
A
adipose tissue/ fat stores
16
Q
When does obesity result (endocrinally speaking)
A
when there is a disruption in the feeding and satiety pathways, i.e. satiety centre no longer switches off feeding centre
fact of interest: 2/3 of people in Scotland are considered overweight vs not
17
Q
what are the 3 categories of energy output (easy peasy)
A
cellular work
mechanical work
heat loss
18
Q
Metabolism how many of the biochemical reactions in the body
A
‘integration of all biochemical reactions in the body’.
19
Q
anabolic pathways are pathways that…
A
build up
think about anabolic steroids
20
Q
is cortisol an anabolic or catabolic steroid
A
catabolic (not building up muscle!)
21
Q
What happens in the absorptive state after eating (to ingested nutrients)
A
Ingested nutrients that are used to supply energy are stored, so any excess energy is stored in that absorptive state.
so glucose as glycogen in muscle
22
Q
is the absorptive state an anabolic or catabolic one
A
it’s anabolic- we’re BUILDING UP stores
23
Q
what’s happening in the post absorptive/fasting state
A
body starts to rely on stores/ nutrients in the plasma, built up in absorptive state (catabolic)
release glucose from glycogen, AND make new glucose from amino acids
24
Q
what does it mean, that the brain is the obligatory glucose user
A
brain can only use glucose
but other cells can use carbs, protein.
That’s why hypoglycaemia leads to coma and death.
25
when can the brain metabolize ketone bodies
starvation
26
Before excess glucose becomes fat, what does it become?
any excess glucose is broken into free fatty acids, then fat. Through glycogenesis.
27
what hormone initiates gluconeogenesis and glycogenolysis when glucose levels are low?
glucagon
28
what happens when glucagon stimulates the liver
new glucose is created from amino acids,and glycogen into glucose
29
Insulin is an anabolic hormone that does what (2)
stimulates process of glycogenesis to admit glycogen from glucose in the blood. i.e. stimulates formation of glycagon.
And stimulates uptake of glucose
30
What's happening to insulin in type 1 diabetes
No insulin is being made by the pancreas. Glucose builds up in the blood, can't be converted to glucagon or fat stores.
31
What's happening to insulin in type 2 diabetes
Body stops responding to insulin. Glucose builds up in the blood.
32
what part of the pancreas releases glucagon and insulin. Nb, insulin and glucagon exist IN BALANCE
islets of langerhans (islands of endocrine cells)
33
alpha, beta, delta cells of the pancreas produce what
alpha = glucagon
beta = insulin
delta = somatostatin
34
affect of insulin on fat synthesis
increases fat synthesis i.e. converting glucose into fat.
35
If levels of insulin rise, what will be happening to glucagon levels?
They decrease. Remember that it’s all a balance
36
What 4 actions increase when insulin levels rise? remember its an anabolic state
Glucose oxidation (being used)
Glycogen synthesis (stores built up)
Fat synthesis
Protein synthesis
It’s an anabolic state, (building) and blood glucose decreases.
37
What three actions increase when glucagon levels rise? (During the fasted state)
Glycogenolysis
Gluconeogenesis
Ketogenesis
38
What’s Glycogenolysis, which occurs in the fasting state?
Breakdown of glycogen
39
What’s Gluconeogenesis, which occurs in the fasting state?
Glucose formed from amino acids
40
What type of hormone is insulin?
Peptide hormone
41
How is insulin synthesised?
As a large preprohormone, preproinsulin, when is then converted into proinsulin. These are packaged as granules, and then cleaved again to give insulin.
42
Insulin is stored until what
The beta cell it’s in is activated and secretion occurs
43
Where in the beta cell is preproinsulin, converted to pro insulin?
In the endoplasmic reticulum
44
One Proinsulin, that packaged in granules, is later converted into insulin by being cleaved. How many copies of insulin does that produce?
Granules of proinsulin broken up to release active form of insulin. Multiple, not just one insulin molecule. And also c-peptide fragments that intersperse the copies of insulin.
45
By what method is insulin and c peptide releases into the plasma, following stimulates of the beta cells?
Exocytosis
46
Why is c peptide a useful indicator of pancreatic beta cell function, versus insulin?
Because c peptide resists degradation much more than insulin does, and c peptide can be independent of any exogenous insulin that your patient might be injecting
47
During what state is insulin released?
Absorptive state
48
When blood glucose levels rise, that triggers the release of insulin from the pancreas. What else triggersa release of insulin?
When amino acid levels go up
49
What is the only hormone that stimulates the uptake of glucose out of the blood?
Insulin
50
Excess glucose can be stored as glycogen in the liver and muscle tissue, but also as what in liver tissue and adipose tissue?
Triacylglycerols
51
Amino acids being consumed in our diet is being used how?
New protein, with any excess being converted to fat
We can also use amino acids as an energy source during starvation (breaking down muscle)
52
Why does using your amino acids/proteins in your diet, as energy during starvation, affect your immunity?
Your antibodies are proteins so if they’re gone, more vulnerable to infection
53
Mechanism by which insulin is released by the pancreas, depends on the activity of which channel?
The potassium ATP channel in the beta cells- so potassium ion channels that’s are sensitive to the levels of ATP that are in the cells (like, glucose).
54
Glucose enters the pancreatic beta cell through transporters known as what
GLUT transporters
55
How is potassium ATP channel involved in the exocytosis of insulin vesicles?
Glucose coming in, = increase in ATP. Which means said channels close, so k builds up. So that increases positive charge therefore cell is depolarised, therefore voltage gated Ca channels open and = exocytosis.
56
Insulin vesicle exits beta cell into circulation via what channel
Voltage dependant Ca2+ channels.
57
How does insulin lower BG?
Binds to tyrosine kinase receptors on the cell membrane of insulin dependant tissues, to increase glucose uptake of these tissues.
58
In muscle and adipose tissue, insulin stimulates mobilisation of which specific glucose transporter?
GLUT-4
59
When do GLUT-4 transporters move to the cell membrane from the cytoplasm?
In response to insulin binding to tyrosine kinase receptors on the surface of cells, so that glucose can be transported INTO the cell
Nb I feel like: insulin binds to cell, GLUT-4 transporters are triggered to move to membrane, meaning glucose can come into the cell.
60
True or false, there is an exocytosis of the GLUT4 transporters
Yes
61
Which cells can take up glucose independent of insulin and when?
Muscle cells
During exercise
62
How many tissue types require insulin to take up glucose?
Only adipose and muscle
But this makes up a large proportion of the body so like 65%
63
Muscle tissue mainly uses what instead of glucose
Free fatty acids, so don’t need insulin that way
64
Glut 1 transporters are found where? Are these insulin dependant?
Brain, kidney, red blood cells
## Footnote
whereas insulin dependant cells have GLUT 4. Like adipose and muscle cells.
65
Where are Glut 2 transporters? Are they insulin dependant/ found in cytoplasm?
Beta cells of the pancreas and in the liver
They are present in the cell membrane all the time therefore.
## Footnote
So: if they're insulin dependant, they're found in the cytoplasm > need insulin for the transporters to be exocytosed, if you get me. They are the GLUT 4.
Non insulin = GLUT 2- pancreas and liver
and GLUT 1- brain, kidney and red blood cells
66
Is the liver insulin dependant?
No you have glut-2 transporters found there. But insulin DOES enhance glucose uptake by hepatocytes
67
Why is glucose transport into hepatocytes affected by insulin status, if the liver isn’t insulin dependant (due to the presence of glut 2)?
Insulin stimulates hexokinase enzyme (after binding to tyrosine kinase receptor) which lowers the intracellular glucose concentration by converting glucose to glucose 6 phosphate
*therefore* maintaining concentration gradient.
68
What does the liver do to glucose when no insulin present?
Insulin was needed for the enzyme hexokinase to create concentration gradient.
If no gradient? Liver actually synthesises glucose via glycogenolysis- breaking down hepatic glycogen.
And gluconeogenesis from amino acids.
69
How does insulin increase glycogen synthesis in muscle and liver tissue?
In a roundabout way. By stimulating the enzyme glycogen synthase and inhibiting an enzyme that breaks down glycogen.
70
Three actions of insulin to liver
Stimulate uptake of glucose by helping create concentration gradient (converting glucose)
Increase glycogen synthesis by:
Switching on enzymes that synthesise glycogen, and switching off enzymes that would break down glycogen.
71
Does insulin inhibit or increase amino acid uptake and synthesis in muscle?
Increase by switching on and off relevant enzymes.
72
What affect of insulin onto enzymes of gluconeogenesis?
Inhibit
To stop the liver creating new glucose
73
Which three hormones are needed for growth?
Insulin and growth hormone
Because you need insulin to “permit” growth hormone
But also thyroid hormone
74
How does insulin have an affect on potassium entry into cells?
Stimulating sodium potassium ATPase
| We want k to build up incell, so that cell is depolarised.
## Footnote
That would make the exit Ca channels to open to release insulin
75
Any protein that is a target for the insulin receptor is known as what
Insulin receptor substrate
76
Half life of insulin
5 mins
77
Location of degradation of insulin
In liver (and kidneys) by enzyme insulinase
78
What 5 stimuli increase insulin release?
1) increased blood glucose
2) increased amino acids
3) glucagon
4) other hormones controlling GI secretion eg gastrin, secretin, CCK, GIP.
5) vagal nerve activity (helps control GI function, doesn’t it?!)
79
Gluconeogenesis is stimulated by what
Glucagon
80
Why is insulin released when stimulated by GI hormones, like gastrin, secretin and CCK?
In preparation for the increase in blood glucose that it knows is coming
81
What stimuli (3) inhibit insulin release?
Low blood glucose
Somatostatin
Stress e.g. hypoxia
82
Why is is good the the vagus nerve directly stimulates insulin release?
It means we get an insulin response faster than we would if we had to wait for glucose to be absorbed and get into the bloodstream
83
The amount of insulin that is released in response to intravenous glucose- more or less than oral administration of the same amount?
Less
Only blood response, not also vagal and incretin hormone response to the same amount
84
How does glucagon increase blood glucose in simpler terms? (3)
Releasing glucose from stores into the plasma by breaking it down (glycogenolysis)
The formation of new glucose from amino acids (glucaneogenesis)
Formation of new ketones (ketogenesis)
85
How is glucagon produced (considering it’s a peptide hormone like insulin)?
Starts off with preprohormone
That gets cleaved to a prohormone
That’s stored in vesicles until required for release from alpha cells, following stimulation
86
What is glucagon degraded by?
Liver
Also mainly acts on the liver
Half life of 5-10 mins
87
When is glucagon most active?
Post absorptive state
In between meals, FASTING state. (When you’re about to get hungry again)
88
Insulin receptors are tyrosine kinase receptors. What about glucagon receptors?
G-protein couples receptors that are linked to the adenylate cyclase/cAMP system.
89
Gluconeogenesis us s substrates from the breakdown of
Proteins
Amino acids
Lactate
Pyruvate
90
Triglyceride stores in adipose tissue can be broken down to release what
Glycerol and free fatty acids
91
If glucose is spare se what does the brain use
Ketones
Eg starvation or poorly controlled diabetes
92
Amino acids are also a potent stimulus for glucagon secretion. What would happen if they weren’t?
Hypoglycaemia
Because amino acids stimulate insulin release, which in the absence of glucagon uptake into cells, dramatically lowering BG.
93
Amino acids stimulate release of glucagon or insulin?
Trick question
Both
They’re in balance
94
Eat a meal high in protein. That triggers lots of insulin. What do we need therefore
Well the body will release glucagon as well, so it’s all okay, because glucagon will maintain BG
95
What does low insulin levels mean for adipose and muscle tissue?
They cannot readily access glucose because they’re insulin dependant tissues of the body
96
Affect of cortisol on glucagon release?
Stimulates it
97
What level does BG have to fall for glucagon release?
Below 5 millimolar
98
What affect does glucose have on glucagon release? And free fatty acids and ketones?
Well obvs inhibits
99
What affect does insulin have on glucagon release?
Inhibits
100
What affect does somatostatin have on glucagon release?
Inhibits
101
If we know vagus activity causes increase in insulin release, (and to a lesser extent glucagon).
On the other hand, what affect does sympathetic have on activity in islet cells/ release of glucagon?
We’re saying para increases insulin.
But Sympa increases glucagon and therefore inhibits insulin
102
Release of glucagon prevents
Hypoglycaemia
103
Growth hormone antagonises the action of what?
Insulin
104
Glucagon stimulates breakdown of glycogen in the liver, but not in the muscle. Which hormone does both?
Epinephrine
105
Which two hormones inhibit glucose uptake?
Growth hormone and cortisol
## Footnote
whenstressed, these AND epinephrine and glucagon rise
106
Why do you look diabetic in Cushing disease?
Because you have loads of cortisol, which inhibits glucose uptake/ makes tissues less sensitive to insulin, therefore elevation of blood glucose
107
Where are the two places somatostatin is released?
Delta cells of the pancreas
Released by the hypothalamus
108
Main action of pancreatic somatostatin?
Inhibit activity in the GI tract, released in response to nutrients coming.
Prevent exaggerated peaks
## Footnote
alsoinhibit glucagon and somatostatin
109
Why is synergetic somatostatin used in life threatening diarrhoea?
It slows the motility of the GI tract
110
Affect of somatostatin on insulin and glucagon?
Suppresses release- local affect on alpha and beta cells
111
Patients who have somatostatin secreting rumours often develop what kind of symptoms?
Diabetic like symptoms (loss of insulin release from beta cells)
112
The insulin independent mechanism of skeletal muscle that can take up glucose during exercise, increases the number of which transporters?
Nb exercise also increases insulin sensitivity
GLUT-4
113
Why is exercise strongly advised for individuals with type two diabetes?
Because exercise increases glucose uptake in an independent mechanism, and the effect has been found to persist for several hours after exercise.
114
In non active muscle, insulin must bind to its receptor why?
To stimulate the exocytosis of the GLUT 4 containing vesicles on the membrane
115
During starvation, the body can break down adipose tissue to release fatty acids to use as energy. Except for which organ?
The brain
116
In starvation, how does the body supply the brain with energy?
The liver will convert any excess free fatty acids to ketone bodies by beta oxidation, by the hormone glucagon
Meaning we don’t need to use protein
117
Which is the last store that is depleted in starvation?
Protein
118
Is the uptake of ketone bodies insulin dependant or independant?
Independant
Therefore for diabetes, not good. Because ketones are acidic. = ketoacidosis
119
What type of hormone is growth hormone
Peptide
120
What is growth hormone also known as
Somatotropin
121
Where is growth hormone released from
Anterior pituitary
122
Release of growth hormone is controlled via NEUROhormones, with the same or opposing action?
Opposing
123
Release of growth hormone is controlled via NEUROhormones, with the opposing action. Name these two:
Growth hormone inhibiting hormone aka somatostatin (think statin like stasis) GHIH
Growth hormone releasing hormone GHRH
124
Factors affecting what part of the body, determines the balance between GHRH : GHIH?
Hypothalamus
125
Permissive action from where is required before GH can stimulate growth?
Thyroid hormones and insulin
126
Why would children with poorly controlled diabetes have stunted growth, despite normal GH levels?
Because GH requires permissive action of thyroid hormones and *insulin* before it will stimulate growth
127
Why does GH secretion continue throughout adult life?
It continues to be essential in the maintenance and repair of tissue
128
What exact affect does GH have on cells?
Cell size (hypertrophy)
And
Cell division (hyperplasia)
129
What receptors does GH act on?
Tyrosine kinase receptors
130
What are the two main B-road actions of GH?
Growth of long bones- (indirect action mediated via IGF-I)
Regulation of metabolism (direct action)
131
I know that growth hormone has a direct affect on metabolism, but it only has an indirect affect on growth of long bones/ skeletal system. Through which hormone is that achieves?
Insulin-like growth factor (IGF-1) aka somatomedin C
As it *mediates* the action of growth hormone
132
Somatomedin (IGF-1) mediates the action of GH for long bones.
Name can be confused with:
Somatostatin -stasis- is the GH inhibiting hormone. GHIH. There is a constant balance between GHIH and what other hormone?
Growth hormone releasing hormone (GHRH).
Nb IGF acts on both bottom two hormones
133
IGF-1 aka somatomedin is secreted primarily by what, in response to what?
By the liver, in response to GH release.
134
Why is GH not secreted in urine? But rather has like 50% remain like a reservoir in the blood?
Because it is transported in the blood *bound* to carrier proteins. Means there is a reservoir to smooth out effects of the erratic pattern of secretion.
135
IGF exhibits negative feedback on GH by inhibiting what hormone, and stimulating what hormone?
Inhibits GHRH
Stimulates GHIH (somatostatin)
136
IGF is the ‘insulin like hormone’. It exhibits negative feedback on GH. Has it hyper or hypoglycaemic action on IGF-1?
Hypoglycaemic
137
Which dominates: the hypoglycaemic action of IGF-1, or the hyperglycaemic properties of GH?
The hyperglycaemic properties of GH
138
Affect of GH on insulin, and gluconeogenesis by the liver?
Increases gluconeogenesis
Reduces ability of insulin to stimulate glucose uptake by muscle and adipose tissue
Basically GH is releasing energy stores to support growth (has anti-insulin effect, like cortisol)
139
Why is GH said to be anti insulin
Basically GH is releasing energy stores to support growth (has anti-insulin effect, like cortisol)
140
What’s the difference in the action between cortisol and GH?
Unlike cortisol (and just like insulin) GH increases amino acid uptake and protein synthesis in almost all cells = anabolic effect.
141
Does cortisol stimulate protein anabolism or catabolism?
Catabolism
GH and insulin is anabolism of proteins.
| cause remember cortisol
142
Both insulin and GH cause increased amino acid uptake, and protein synthesis. What’s the difference between them?
Only GH causes increased glucose uptake.
143
What time of day is the most GH released?
Majority of GH released during first 2 hours of sleep (deep delta sleep)
144
How does amount of amino acids in the plasma, affect GHRH amounts?
Up = up
145
(Considering we have a growth spurt in puberty). What affect does oestrogen and testosterone have on GH release?
Stimulates GH release from the pituitary
146
What affect does stress and illness have on growth? (Two hormones)
Increases GHRH, but growth may be stunted due to catabolic action of cortisol
147
3 stimuli that increases GHIH (somatostatin secretion therefore down GH)?
Ageing
Glucose (more sugar = less growth!)
Cortisol
148
What’s the normal cause of hyper secretion?
Endocrine tumours
149
Difference in pathology between gigantism and acromegaly?
Hyper-secretion of GH in both. But in gigantism, due to a pituitary tumour BEFORE Epiphyseal plates of long bones close. = excessive growth.
Vs after
150
What are the two physiologically active forms of the thyroid hormone?
(They have long names, but like, just know them as:)
T3
T4
151
What are the two cells types in the thyroid gland?
C cells
Follicular cells
152
What do the c cells of the thyroid gland secrete?
Calcitonin, a calcium regulating hormone
153
What do the follicular cells of the thyroid gland do?
The cells support thyroid hormone synthesis and surround hollow follicles
154
Most of the thyroid gland is made up of which cell?
The follicular cells
155
The follicular cells of the thyroid form follicles- basically a hollow ball. What is that filled with?
Colloid
156
What’s colloid?
A sticky, glycoprotein substance, where we find thyroid hormones in precursor form
157
How many months supply of precursor thyroid hormones are stored in the follicles?
Like a few months
158
Follicular cells manufacture the *enzymes* that make thyroid hormones, as well as what?
Thyroglobulin, a large protein rich in tyrosine residues, that basically form the backbone of those thyroid hormones.
159
Involvement of follicular cells with iodine?
Concentrate iodine from plasma and transport it to the colloid to combine with tyrosine
160
What combines to form the thyroid hormones?
Thyroglobulin (produced by follicular cells, and rich in tyrosine residues)
Iodide from the plasma
161
Where is tyrosine and iodide derived from?
The diet
162
How does the iodide enter the follicular cells, through the action of which transporter? (Even against a concentration gradient!)
Sodium iodide transporter
163
How is iodide oxidised to iodine?
In the colloid, catalysed by the enzymes produced by the follicular cells, which are then exocytosed into the colloid.
164
1 iodine to tyrosine =
MIT
165
2 iodines plus tyrosine =
DIT
166
MIT and DIT can u servo conjugation reactions.
MIT + DIT =
DIT + DIT =
MIT + DIT = T3
DIT + DIT = T4
167
Name of enzyme that is found on the colloid side of the follicular cells
Thyroid peroxidase > oxidising iodide to iodine, adding iodines to tyrosine residues, and conjugating them to become T3 or T4
168
Why can’t we store thyroid hormones in their active form?
Because they’re lipophilic, so they’d just cross the cell membrane and get into the blood.
169
What stimulates T3&4 to go from colloid to follicular cell, and form vesicles?
Thyroid stimulating hormone
170
Where is thyroid stimulating hormone released from?
Anterior pituitary (specifically, the thyroglobulin)
171
What is the main carrier protein of T3&4 known as?
Thyroxine binding globulin
172
Do we have more T3 or T4 present in the plasma?
T4
173
Are thyroid hormones active when bound to thyroxine binding globulin?
Yes but not actually physiologically active, they can’t be used
174
Why is there more T4 than T3 in the plasma?
T4 has 6 x the longer half life (6 days)
175
As the physiologically active thyroid hormone in the plasma increases, what happens?
It switches off the hormones that stimulates the release- antagonists release of TSH from the anterior pituitary.
(So level of own hormone regulates itself, like GH)
176
Most TH circulating is T4. However, which is actually the most physiologically active?
DEFO T3
177
T4 is deiodinated to T3 by what
Deiodinase enzymes.
178
Where is T4 deiodinated? (To T3)
Half in the plasma, half inside target cells
179
Any cell that contains an intracellular receptor for thyroid hormone, also contains what enzymes?
Deiodinase enzymes that Deiodinase T4-T3
180
What thyroid hormone are you supplemented with, when you’ve had your thyroid gland removed?
T4
(Turns into T3 anyway, and has a longer glad life than T4)
181
Which hormone controls the release of thyroid hormone?
Thyrotropin releasing hormone from the hypothalamus
182
Exercise and pregnancy increase release of thyroid stimulating hormone. Why pregnancy?
Because thyroid hormones are critical for the growth of the fetus
183
Which two drug are inhibitory on release of thyroid hormones?
Glucocorticoids and somatostatin aka growth hormone inhibiting hormone. (Inhibitory on release of thyroid hormone).
184
Why is being cold the primary stimulus for the release of thyroid hormones?
Because thyroid hormones promote thermogenesis (by causing futile cycles of simultaneous catabolism and anabolism)
NB this is especially important in infants!
185
Lack of thyroid hormone means what?
Retarded growth
Because thyroid hormone stimulates receptor expression
186
What does maternal iodine deficiency result in?
Congenital hypothyroidism, which is crazy cuz it’s essential for brain development
187
In the womb, does the baby make its own or receive maternal thyroid hormones?
Maternal
188
Two main symptoms of hyperthyroidism?
Increased metabolic rate and heat production
189
The adrenal glands sit atop the kidneys. Are they retroperitoneal or intraperitoneal?
When considering the kidneys are retro …
190
What are the two parts of the adrenal glands?
Adrenal medulla and adrenal cortex
Medulla in the middle about 25%
191
What part of the adrenal gland is a modified sympathetic ganglion?
Adrenal medulla, making it a neuroendocrine gland
192
The adrenal medulla secretes from the post ganglionic cell. What does it secrete? (3)
Epinephrine aka adrenaline
And also
Norepinephrine
Dopamine
193
Is the adrenal cortex a neuroendocrine gland, or a true endocrine gland?
True endocrine gland
194
What 3 hormones does the adrenal cortex secrete?
Mineralocorticoid like ALDOSTERONE (involved in regulation of Na and K
Glucocorticoids e.g. cortisol
Sex steroids e.g. testosterone
195
What is cortisol mainly involved with?
Maintaining plasma glucose
196
Out of the three steroid hormones that the adrenal cortex secretes, which two are necessary for survival?
Aldosterone
Cortisol
So not sex hormones
197
Why do we consider the role of sex hormones secreted from the adrenal gland, as less important?
Because there is SO much more sex hormones secreted from gonads instead
198
Which is our areas hormone?
Cortisol
199
Which hormones secreted by the adrenal medulla, are associated with the stimulation of the sympathetic nervous system? (Fight and flight)
Epinephrine
Norepinephrine
200
Why would animals that have their adrenal glands removed, due within weeks?
Because aldosterone and cortisol together are essential for survival
201
The adrenal cortex, surrounding the medulla, is arranged in 3 concentric zones, why?
They’re producing different hormones
Aldosterone
Cortisol (glucocorticoid)
Sex hormones
202
So which part of the adrenal gland is secreting the ‘catecholamine neurohormone’?
Adrenal medulla
203
If all steroid hormones are made of cholesterol, and we have 3 different types made in the adrenal cortex, how are there different end products?
Different enzymes for different zones, so for the outermost zone, only enzymes like aldosterone synthase, that can make cholesterol into aldosterone, are there
204
21 hydroxylase is an enzyme required for the synthesis of which two steroid hormones from the adrenal cortex?
Aldosterone and cortisol
205
How are cortisol levels controlled?
A negative feedback loop within the hypothalamic-pituitary-adrenal pathway
206
Why does a deficit in 21-hydroxylase cause adrenal hyperplasia?
Increased ACTH secretion responsible.
Because there body is over stimulated to try and fix the break in the negative feedback system (so this happens, despite no cortisol or aldosterone being made)
207
What does ACTH do?
Stimulates release of the steroid hormones from the adrenal cortex
208
ACTH stimulates release of the steroid hormones from the adrenal cortex. What about the adrenal medulla?
No, that’s controlled by the sympathetic nervous system
209
Cortisol is a glucocorticoid hormone that influences what
Glucose metabolism
210
95% of plasma cortisol is bound to what?
A carrier protein, cortisol binding globulin (CBG)
211
How many cells of the body have cytoplasmic glucocorticoid receptors?
All nucleated cells
212
What happens after the hormone receptor complex migrates to the nucleus? (Eg cortisol)
Binding to DNA, to alter gene expression transcription and translation
213
Why do the effects of cortisol persist for a relatively long time?
Because we’ve either increased protein synthesis or we’ve switched off protein synthesis- so basically a change in protein synthesis that persists for a relatively long period of time, days or weeks.
214
How long is the response to peptide hormones usually?
Usually only present for only minutes usually
215
Which type of hormone from the adrenal gland is well known for their anti inflammatory effect?
Glucocorticoids
216
Which type of hormone from the adrenal gland is well known for their use in suppressing the immune system?
Glucocorticoids
217
How often is cortisol released throughout the day?
Plasma levels of cortisol show a very characteristic pattern- following by a preceding pattern of ACTH release
So there is a peak in the morning
218
Effect of cortisol on blood pressure?
Increases blood pressure
219
Is cortisol hyper or hypoglycaemic?
Hyper
220
Cortisol has what action on glucagon?
It had a permissive action on glucagon, helping to protect the brain from hypoglycaemia
221
How to describe the action of cortisol on insulin?
Opposing
222
What affect does cortisol have on muscle protein?
Stimulates breakdown of muscle protein to provide gluconeogenic substrates for the liver
223
Cortisol stimulates formation of gluconeogenic enzymes from where, leading to what?
Enhancing gluconeogeneis and glucose production.
Enzymes from the liver.
224
What’s lipolysis?
Breakdown of triacyglycerols into glycerol and free fatty acids
225
Cortisol has what affect on adipose tissue?
Stimulates lipolysis, which creates an alternative fuel supply that allows blood glucose levels to be protected
226
What affect does cortisol have on insulin sensitivity?
Decreases insulin sensitivity
Cortisol is acting to oppose glucose, and increase glucose levels
227
Negative affect on bones of cortisol?
Decreases calcium absorption from the gut, and increases bone resorption- so basically stimulates breaking down of bone which leads to osteoporosis
228
Too much cortisol has what affect on mood
Increases depression and causes impaired cognitive function- hyper cortisolaemia
229
What are the three side effects of high levels of cortisol?
Osteoporosis
Depressive mood
Hypertension
230
Low levels of cortisol are association with hyper or hypotension?
Hypotension
231
Affect of cortisol on the immune system?
Suppression
232
Why would you give cortisol following an organ transplantation?
Because it suppresses the immune system.
It reduces circulating lymphocyte count
Reduces antibody formation
Inhibits inflammatory response.
233
Why do you end up with a loss of percutaneous fat when taking glucocorticoid therapy like cortisol?
as a result of stimulating lipolysis in our fat
(Gives skin a thin appearance, and more fragile)
234
Why get muscle wasting with glucocorticoid therapy such as you take when you have asthma, Uc, rheumatoid arthritis.
Protein catabolism
235
Care must be required when withdrawing glucocorticoid treatment why??
Due to the enhanced negative feedback effects of exogenous cortisol: can lead to atrophy of the adrenal gland
236
Affect of aldosterone on sodium and potassium? (2)
Increases reabsorption of sodium
Promotes excretion of potassium
237
Loss of aldosterone leads to life threatening hypo or hypertension
Well obviously hypotension
It increases blood volume by increasing Na+ amount in the plasma, and therefore increases blood pressure.
238
Why does a pheochromocytoma (a neuroendocrine tumour of the adrenal medulla) result in increased BP?
Results in hyper stimulation of adrenaline acetylcholine and norepinephrine etc.
therefore increase in cardiac output, therefore increase in blood pressure.
239
What happens when there is a problem with the hypothalamus? What affect on CRH, ACTH, and cortisol?
Hypersecretion of all three hormones
240
What are the three classifications of the endocrine hormones?
Peptide/protein hormones- composed of chains of amino acids (most common)
Amine hormones (just a few amino acids) like tyrosine
Steroid hormones - derived from cholesterol
241
What is the inactive fragment cleaved from insulin pro hormone?
C peptide
242
Steroid hormones are most commonly bound to what
Albumin
243
What two organs are the principal organisers of the endocrine system?
Hypothalamus and pituitary
244
What are the two parts of the pituitary gland?
Anterior (front 2/3)
Posterior (back 1/3)
245
Difference in the two parts of the pituitary gland?
Front 2/3 is true endocrine tissue
Back 1/3 posterior is neuroendocrine
246
Which are the two hormones of the posterior pituitary gland? (made in hypothalamus remember)
vasopressin and oxytocin
247
All hormones that are released by the hypothalamus and the posterior pituitary are what type of hormone?
Neurohormone
248
What’s the differences between tropic and non tropic hypothalamic neurohormones?
Non-tropic hormones are hormones that directly stimulate target cells to induce effects.
Whereas
Tropic hormones act on another endocrine gland
249
How does the hypothalamus and the pituitary work together?
The hypothalamus synthesis hormones
These hormones are transported to the nerve terminal in posterior pituitary, ready for release
The posterior pituitary release
250
Affect of growth hormone onto insulin?
Growth hormone inhibits insulin
251
Is this hyper or hypo:
FT3/FT4 high
TSH low
Hyperthyroidism aka thyrotoxicosis
252
Is this hyper or hypo?
FT3/FT4 low
TSH high
Hypothyroidism
253
Why might a virus trigger diabetes mellitus?
Viral mimicry, so the virus surface mimics that of pancreatic beta cells
254
2/3 of islet cells in the pancreas is what type of cell
beta cells
255
Why does central adiposity cause diabetes mellitus?
Because there is an increase in free fatty acids, (that enter the blood due to leukocytes being stressed) and with more fatty acids in the blood, insulin receptor sensitivity decreases. Therefore glucose remains in the blood.
256
Why might genetic errors lead to type 2 dm?
if *lots* of gene variants code for low insulin production.
Therefore any extra weight as environmental trigger, body can't keep up with demands of glucose.
257
Commonest cause of death in diabetes mellitus?
myocardial infarction
258
Diabetes mellitus accelerates atherosclerosis. How much more likely is stroke, and heart disease?
stroke = 3 times more likely
heart disease = 20 times more likely
259
Why does diabetes cause atherosclerosis?
Glucose stops LDL from binding to its receptor in the liver, so LDL rises, therefore hyperlipidaemia, therefore deposits around the body.
260
What's 'glycosylation' in diabetes?
when glucose gets added to proteins in the blood (bc of a rise). This is initially reversible.
261
Example of proteins that glucose gets added to?
collagen (gets stuck in basal lamina of small vessels)
262
Glucose can't bind to albumin unless
It's also glycosylated to other proteins, leading to hypalbuminaemia
263
Why hypoalbuminaemia in diabetes?
Because basically: albumin binds to glucose, which has bonded to proteins (that allows it), because there is excess glucose and the body is like, 'I don't know what to do with this'.
264
Why peripheral nerve damage in diabetes?
Because of the arterioles supplying the nerves- the arterioles suffer from build ups of collagen that is glycosylated.
NB its the vessels getting damaged!
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