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Phase 1 revision > SUGER- ENDOCRINE (see reproduction for first two lectures) > Flashcards

SUGER- ENDOCRINE (see reproduction for first two lectures) Flashcards

1
Q

What is the pituitary gland also called?

A

hypophysis

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2
Q

Where does the pituitary sit?

A

Lies in a pocket of the sphenoid bone at the base of the brain called the sella turcica, just below the hypothalamus and optic chiasm.

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3
Q

What is the infundibulum?

What does it contain?

A

The pituitary gland is connected to the hypothalamus by the infundibulum or pituitary stalk, containing axons from neurones in the hypothalamus as well as
small blood vessels.

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4
Q

What are the two adjacent lobes of the pituitary called?

A

1) Anterior pituitary gland/adenohypophysis

2) Posterior pituitary gland/ neurohypophysis

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5
Q

What is the hypothalamus made up of?

A

Supraoptic nuclei, paraventricular nuclei and neurosecretory neurones.

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6
Q

What do the neurosecretory neurones do?

A

They release, releasing hormones in the pituitary portal system to the anterior pituitary gland.

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7
Q

Describe the embryology of the pituitary gland

A

1) The two glands (anterior & posterior) develop from different tissues BEFORE joining together
2) A protrusion of ORAL ECTODERM called RATHKE’S POUCH grows upwards to from the anterior pituitary (adenohypophysis)
3) The posterior pituitary (neurohypophysis) is NEURAL ECTODERM in origin and is rather a neural extension of the neural components of the hypothalamus - protruding from the developing brain ventrally.
4) The two tissues grow tightly apposed, despite being different in origin.

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8
Q

What type of hormones are TSH, FSH and LH?

A

Glycoproteins. They all have the same alpha subunit but different beta subunit.

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9
Q

What type of hormones are ACTH, GH and prolactin?

A

Polypeptides

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10
Q

Describe the hypothalamus. What are the functions?

A

• Collection of brain ‘nuclei’
• Connections to almost all other areas of the brain
• Important for homeostasis + primitive functions – appetite, thirst, sleep, temperature regulation
• Control of autonomic function via brainstem
autonomic centres
• Control of endocrine function via pituitary gland

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11
Q

Describe the hypothalamus- anterior pituitary hormone regulation system.

A

1) Stimulated to release hypophysiotropic hormones by other areas of the CNS e.g. receptors that detect the outside environment.
2) Secretes hypophysiotropic hormones which reach the anterior pituitary via the Hypothalamo-Hypophyseal portal vessels/veins and further stimulate the anterior
pituitary to release 6 hormones.
3) The generation of action potentials in these neurones causes them to secret hormones via EXOCYTOSIS (like how other neurones release neurotransmitters).
4) The hypophysiotropic hormones bind to specific receptors from which they can stimulate or inhibit the secretion of the different anterior pituitary hormones.

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12
Q

Name the hypophysiotropic hormones and the hormones they stimulate

A

1) Corticotropin-releasing hormone (CRH) - stimulates the release of adrenocorticotropic hormone (ACTH)
2) Growth hormone-releasing hormone (GHRH)&raquo_space;»> (GH)
3) Thyrotropin-releasing hormone (TRH)&raquo_space;»»»(TSH)
4) Gonadotropin-releasing hormone (GnRH)&raquo_space;>lutenizing hormone (LH) & follicle stimulating hormone (FSH)
5) Dopamine (DA) - INHIBITS the release of prolactin

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13
Q

What effect does somatostatin have on growth hormone?

A

Somatostatin inhibits release of GHRH so inhibits release of GH. This inhibits growth and protein synthesis.

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14
Q

What effect does dopamine have on prolactin?

A

Dopamine inhibits prolactin. This inhibits growth and milk production.
This is relevant in prolactinomas, dopamine is given to supress the tumours.

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15
Q

What are the neural connections between the hypothalamus and anterior pituitary gland?

A

There are no neural connections between the hypothalamus and anterior pituitary gland

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16
Q

What is the arterial blood supply of the anterior pituitary gland like?

A

It has no arterial blood supply, but receives blood through a portal venous circulation from the hypothalamus - known as the hypothalamo-hypophyseal portal vessels/veins.

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17
Q

What is the purpose of the hypothalamo-hypophyseal portal vessels/veins?

A

1) Offer a local route for blood to be delivered directly from the hypothalamus to the cells of the anterior pituitary
2) This provides a mechanism for hormones of the
hypothalamus to directly alter the activity of the cells of the anterior pituitary gland, bypassing the general circulation and thus efficiently regulating
hormone release from that gland

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18
Q

How many different types of hormone producing cells does the anterior pituitary gland have?

A

5

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19
Q

How many hormones does the anterior pituitary gland make?

A

6

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20
Q

What are hypophysiotropic hormones?

A

The hypothalamic hormones that regulate anterior pituitary gland function are collectively.

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21
Q

What is the three-hormone sequence?

A

1) A hypophysiotropic hormone controls
the secretion

2) Of an anterior pituitary gland hormone which controls the secretion
3) Of a hormone from some other endocrine gland - this last hormone than acts on its target cells

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22
Q

What are the benefits of the three-hormone sequence?

A

1) It permits a variety of hormonal feedback, the most important of which being NEGATIVE FEEDBACK.
2) Allow the amplification of a response of a small number of hypothalamic neurones into a large peripheral hormonal signal.

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23
Q

Anterior Pituitary hormones:

1) WHERE ARE THEY FOUND?
2) HISTOLOGICALLY WHAT TYPE OF CELL?

A

1) Follicle-stimulating hormone (FSH) - produced in gonadotrophs
(basophilic cells - purple/dark blue)

2) Lutenizing hormone (LH) - produced in gonadotrophs (basophilic cells - purple/dark blue)

3) Adrenocorticotropic hormone (ACTH- also known as corticotropin) - produced in corticotrophs
(basophilic cells - purple/dark blue)

4) Thyroid-stimulating hormone (TSH - also known as thyrotropin) - produced in thyrotrophs
(basophilic cells - purple/dark blue)

5) Prolactin - produced in lactotrophs
(acidophilic cells - dark pink/red)

6) Growth hormone (GH - also known as somatotropin) - produced in somatotrophs
(acidophilic cells - dark pink/red)

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24
Q

Name the 6 peptide hormones secreted by the anterior pituitary.
PG FLAT

A

P: Prolactin
G: GH

F: FSH
L: LH
A: ACTH
T: TSH

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25
FSH and LH
- Target the gonads - Stimulate germ cell development (in females = ovum, in males = sperm) - Stimulate the release of hormones (in females = estradiol & progesterone, in males = testosterone)
26
GH
Stimulates growth & protein synthesis
27
ACTH
Stimulates the adrenal cortex to secrete CORTISOL
28
TSH
Stimulates thyroid to secrete T3 & T4 resulting in an increase in metabolism
29
Prolactin
Stimulates the breasts to produce milk & helps with breast development
30
What is the purpose of negative feedback in the anterior pituitary?
Negative feedback is effective in dampening hormonal responses thereby limiting the extremes of hormone secretory rates.
31
Use corticol concentration in a stressful as an example to Long Loop Negative feedback
1)A stressful stimulus elicits increased secretion of CRH and in turn ACTH and then cortisol 2) This results in an elevation in plasma cortisol concentration that feeds back to inhibit the CRH- secreting neurones of the hypothalamus AS WELL AS the ACTH-secreting cells of the anterior pituitary 3) This means that cortisol does not increase as much as it would have done without negative feedback - this is important due to the damaging effects of excess cortisol on immune function & metabolic reactions
32
What is a long-loop negative feedback?
The way in which the hormone secreted by a third endocrine gland in a sequence exerts a negative feedback effect over the anterior pituitary and/or the hypothalamus.
33
Why is there no LONG LOOP NEGATIVE FEEDBACK in the case of prolactin?
This anterior pituitary hormone does not have major control over another endocrine gland - meaning that is dos not participate in the three hormone sequence.
34
Why is there still NEGATIVE FEEDBACK in the case of prolactin?
Since prolactin does act on the hypothalamus to STIMULATE the secretion of dopamine which then in turn INHIBITS the secretion of prolactin.
35
What is a SHORT LOOP NEGATIVE FEEDBACK?
The influence of an anterior pituitary gland hormone on the hypothalamus.
36
What are the main effects of an ANTERIOR PITUITARY GLAND TUMOUR?
1) Pressure on local structure: - Mainly the OPTIC NERVES resulting in bitemporal hemianopia. 2) Pressure on normal pituitary - Resulting in the excess or inadequate release of pituitary hormones - hypo/hyper-pituitarism
37
Describe the embryology of the pancreas
- At junction of foregut and midgut 2 PANCREATIC BUDS (dorsal & ventral) are generated and eventually fuse to form the pancreas - Exocrine function begins after birth - i.e. secretion of bile salts, amylase & trypsin - Endocrine (hormone) functions from 10-15 weeks
38
What is the exocrine function of pancreas?
Secrete products into a duct (pancreatic duct) from where the secretion then enters the small intestine in the case of the pancreas.
39
Brief overview of the anatomy of the pancreas
- Retroperitoneal - Lies posterior to the greater curvature of the stomach - 12-15cm long, head lies near the C-portion of the duodenum - Main pancreatic duct joins with the bililary system where the bile secretions come from
40
What effect can large gallstones have on the pancreas?
block secretions due to the joining of the main pancreatic and bile duct
41
What are ACINAR CELLS? | What proportion are they in the pancreas?
98-99% of the cells are small clusters of glandular epithelial cells - called ACINI.
42
What is the function of Acinar cells?
- Exocrine function is performed by acinar cells - They manufacture & secrete fluid and digestive enzymes (lipase, trypsin etc.) in form of pancreatic juice - Which is released into the gut via the pancreatic ducts which enters the small intestine at the duodenal papilla (2nd part of duodenum) through the ampulla of vata
43
What is the Islet of Langerhans? | What proportion are they in the pancreas?
- endocrine activity performed by these cells - Manufacture and release several peptide hormones into portal vein - 1-2% of the cell are ISLET OF LANGERHANS CELLS
44
Cells of the Islets of Langerhan and the hormones they secrete
- Delta cells : secrete somatostatin - Alpha cells: secrete glucagon - Beta cells: secrete insulin
45
What is paracrine cross-talk?
The beta and alpha cells lie within close proximity. These cells all lie within the islets & are close to allow for cell-to-cell communication. i.e local insulin release inhibits glucagon
46
Insulin - How many amino acids? - Effects? - Structure?
* 51 amino acid Polypeptide * Reduces glucose output by the liver * Increases the storage of glucose, fatty acids & amino acids * Stops the breakdown of fat & muscle * Insulin has two cysteine bridges
47
Glucagon - How many amino acids? - Effects?
* 29 amino acid peptide | * Mobilises glucose, fatty acids & amino acids from stores
48
What type of actions do insulin and glucagon have?
RECIPROCAL ACTIONS---> | Stimulates the breakdown of fat & muscle
49
What is the effect of insulin on carbohydrate metabolism?
1) Suppresses hepatic (liver) glucose output • Decreases glycogenolysis & gluconeogenesis 2) Increases glucose uptake into insulin sensitive tissues; •Muscle - glycogen & protein synthesis • Fat - fatty acid synthesis 3) Suppresses: • Lipolysis • Breakdown of muscle (decreased ketogenesis)
50
What is the effect of glucagon on carbohydrate metabolism?
1) Increases hepatic glucose output • Increases glycogenolysis & gluconeogenesis 2) Reduces peripheral glucose uptake 3) Stimulates peripheral release of gluconeogenic precursors (glycerol &amino acids) 4) Stimulates: • Lipolysis • Muscle glycogenolysis & breakdown (increased ketogenesis)
51
Pro-insulin
Proinsulin is the precursor of insulin. It contains then Alpha & Beta chains (disulphide bridges link A & B chains) of insulin joined together by a C PEPTIDE.
52
What happens when pro-insulin turned into insulin? | What can you look for in the blood when insulin released?
The pro insulin is cleaved from it's C peptide and then used to make insulin which is the packaged into insulin secretory granules. When there is insulin release there will also be a high level of C peptide in the blood from the cleavage of the pro insulin from it.
53
How can you tell that someone has overdosed on insulin?
Synthetic insulin does not have C peptide, so if you have high insulin but low C peptide, you know it's because of synthetic insulin.
54
Insulin secretion by BETA CELLS in the pancreas | 10 steps!!
1) They have special glucose transporters on their cell surface membrane called GLUT2 glucose transporters. 2) When glucose levels are high this enable the GLUT2 receptor to activate allowing glucose INTO the beta cell 3) Once inside the beta cell the enzyme hexokinase (from glycolysis) breaks down the glucose into glucose-6-phosphate 4) This process uses up an ATP molecule and releases ADP 5) The ADP released in the cell then gets converted back to ATP 6) The ATP then binds to a K+ ATP channel on the cell membrane of the beta cell and closes the channel 7) K+ ions are unable to leave the cell resulting in the DEPOLARISATION of the beta cell membrane 8) This causes the opening of voltage-gated Ca2+ channels meaning Ca2+ ions are able to diffuse into the cells via diffusion 9) The Ca2+ ions bind to the insulin secretory granules (containing insulin) resulting in the granule moving to the cell membrane and fusing with it to release its contents via exocytosis 10) Resulting in INSULIN SECRETION
55
GLUT2 receptor is a low affinity receptor, what does this mean?
Meaning that it only binds when there is a high concentration of glucose.
56
BIPHASIC INSULIN RELEASE
B-cells can sense the rising glucose levels and aim to metabolise it by releasing insulin. First phase response is the RAPID RELEASE of stored insulin. Second phase response is SLOWER due to the release of newly synthesised hormone. SEE CURVE
57
Insulin action in Muscle and Fat cells. How they cause more glucose uptake?
1) Insulin secreted into the blood will then bind to insulin receptors located on the cell membranes of muscle & fat cells 2) This triggers an intracellular signalling cascade resulting in the mobilisation of intracellular GLUT4 vesicles to the cell membrane 3) The GLUT4 vesicles become integrated/fused into the cell membrane 4) The increased number of plasma membrane glucose transporters results in a greater rate of glucose diffusion into the cells by facilitated diffusion 5) Thereby decreasing blood glucose levels
58
If blood glucose is HIGH what will the liver do? | Short term and Long term action?
SHORT TERM - convert glucose to glycogen) in a process called glycogenesis LONG TERM - make triglyceride (lipogenesis)
59
If blood glucose is LOW what will the liver do? | Short term and Long term action?
SHORT TERM - (convert glycogen to glucose) in a process called glycogenolysis LONG TERM - make glucose (gluconeogenesis) from amino acids/lactate
60
Where are some locations of glucose sensors?
Primary glucose sensors are in the pancreatic Islets of Langerhans. Glucose sensors are also located in the medulla, hypothalamus & carotid bodies. Inputs from eyes, nose, taste buds & gut all involved in regulating food.
61
Incretins
Secreted by endothelial cells in the GI tract in response to eating - amplifies the insulin response to glucose.
62
Major incretins
- Glucagon-like peptide 1 (GLP-1) | - Glucose-dependent insulinotropic peptide (GIP)
63
Postprandial (after eating a big meal) what is enhanced by incretins?
1) Rising plasma glucose stimulates pancreatic B-cells to secrete insulin 2) Plasma glucose inhibits GLUCAGON secretion by pancreatic A-cells 3) Slower gastric emptying means that you don't feel the need to snack so glucose input reduced.
64
What is the function of Dipeptidyl peptidase IV?
It cleaves the GLP1 of two AA and stops it from working. Prevents HYPOGLYCAEMIA!
65
Describe the regulation of carbohydrate metabolism in a FASTING STATE
1) ALL glucose comes from the liver: gluconeogenesis/ glycogenolysis 2) Glucose delivered to insulin independent tissues such as the brain & red blood cells 3) Insulin levels are very low in the fasting state so muscles use free-fatty acids for fuel
66
Describe the regulation of carbohydrate metabolism in a POST PRANDIAL STATE
* After feeding there is a physiological need to dispose of the nutrient load * The rising glucose levels (occur 5-10 mins after eating) stimulates a 5-10 fold increases in insulin secretion and suppresses glucagon * 40% of ingested glucose goes to the liver * 60% to the periphery, mostly muscle * The ingested glucose helps to replenish GLYCOGEN STORES in both liver & muscle * The excess glucose is converted into fats * High insulin levels suppress lipolysis resoling in the levels of non-esterified fatty acids to fall
67
Hypoglycemia what happens?
Stimulates the release of glucagon • Glucagon acts on the liver to: - Convert glycogen into glucose - Form glucose from lactic acid and amino acids • Glucose released from the liver raises blood glucose levels back to normal
68
Hyperglycemia what happens?
Hyperglycaemia stimulates the release of insulin • Insulin acts on various cells to: - Accelerate the facility diffusion of glucose INTO cells - Speed up the conversion of glucose into glycogen - Increase the uptake of amino acids and increase protein synthesis - Speed up the synthesis of fatty acids - Slow glycogenolysis (breakdown of glycogen to glucose) - Slow gluconeogenesis (formation of new glucose) •The action of insulin result in the fall in glucose levels
69
Diabetes Mellitus
A disorder of carbohydrate metabolism characterised by hyperglycaemia.
70
How do Sulphonylureas work?
Increase insulin secretion by closing the potassium channels.
71
What is the Pathogenesis of Diabetic ketoacidosis?
1) Absence of insulin secretion 2) No hepatic or muscle/fat insulin effect 3) ketone production and unrestrained glucose means that more glucose enters blood 4) So you get hyperglycemia and raised plasma ketones

Phase 1 revision (5 decks)

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