endocrinology Flashcards

1
Q

What is a hormone ?

A

a chemical signal synthesised by specialised target cells and secreted into the blood to act on target cells

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2
Q

What are hormones secreted by ?

A

endocrine glands

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3
Q

What are peptide hormones ?

A
they are trascribed from DNA 
translated form mRNA on ribosomes 
modfied by the golgi 
packaged into secretory vesicles 
hydrophillic
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4
Q

What are steroid hormones ?

A

hydrophobic
they are synthesised from cholesterol
released by diffusion as they are lipophilic
eg. testosterone

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5
Q

What are biogenic amines ?

A

derived from tyrosine

they can be lipophilic or hydrophilic so can be released by diffusion or exocytosis

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6
Q

What are neurohormones ?

A

they are released from neuroendocrine cells directly into the blood

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7
Q

Why do hydrophilic peptide hormones travel freely ?

A

blood is an aqueous solution

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8
Q

How are hydrophobic steroid and thyroid hormones transported ?

A

need transport proteins

these can be specific or non specific

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9
Q

How is the steroid hormone cortisol transported ?

A

80% - transcortin - specific carrier
15%- albumin - non-specific
5% - free

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10
Q

What is free hormone ?

A

only free hormone is biologically active
binding to a carrier protein lengthens half life as free hormone is usually degraded by the liver
carrier proteins prevent liver degradation

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11
Q

What is the mechanism of hydrophilic hormones such as peptide hormone and biogenic amines ?

A

they cant pass the lipid bilayer
bind to receptors on the plasma membrane
activate a number of intracellular pathways

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12
Q

What is the mechanism of action of hydrophobic hormones ?

A

enter the cell s they can cross the lipid bilayer
bind to intracellular receptors in the nucleus
bind to receptors on DNA
hormone-receptor complex acts as a TF
this can alter protein levels

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13
Q

What is an example of a steroid hormone that binds to DNA and becomes a TF ?

A

cortisol

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14
Q

What are the intracellular pathways activated by hydrophilic hormones ?

A

cyclic AMP pathway
phosphoinositide pathway
tyrosine kinase pathway

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15
Q

What activates the cyclic AMP pathway ?

A

ADH and LH

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16
Q

What activates the phosphoinositide pathway ?

A

adrenaline and ADH

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17
Q

What activates the tyrosine kinase pathway ?

A

insulin - binds to a receptor tyrosine kinase that results in a phosphorylation cascade

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18
Q

What are the 2 types of endocrine control ?

A

homeostatic or adaptive

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19
Q

What is homeostatic endocrine control ?

A

the balance of bodily functions

eg. ADH water balance

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20
Q

What is adaptive endocrine control ?

A

adapting to specific changes in the environment

eg.insulin is released in response to high blood glucose

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21
Q

What are the 2 types of endocrine responses ?

A

simple - involving one endocrine gland

comp;ex - involving 2 or more endocrine glands

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22
Q

What is an example of a direct endocrine reflex arc ?

A

the release of insulin from the pancreas in response to high blood glucose
insulin is not released when the blood glucose level returns back to normal

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23
Q

What is an example of complex control ?

A

hypothalamus - pituitary - thyroid gland axis

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24
Q

How are complex responses controlled ?

A

with feedback loops

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25
What is a negative feedback loop ?
the hormone output reverses a particular stimulus | eg. insulin
26
What is a positive feedback loop ?
the hormone output reinforces and encourages the stimulus | eg. oxytocin in uterine contraction
27
What is the hypothalamus ?
a link between neural and endocrine systems | it is a collection of neuronal cells in the brain that receives input from the body
28
Which stimuli is the hypothalamus sensitive to ?
``` blood-bourne olfactory hear info stomach reproductive tract long term stress infection ```
29
What does the hypothalamus control ?
pituitary gland
30
What connects the pituitary gland and the hypothalamus ?
the pituitary gland is at the bottom of the brain and is connected to the hypothalamus by the pituitary stalk
31
What are the 2 separate parts of the pituitary gland ?
anterior pituitary posterior pituitary they are independent of each other due to their different connections to the hypothalamus
32
How is the anterior pituitary connected to the hypothalamus ?
by the portal vessels the hypothalamus releases neurohormones into the portal vessels which travel to stimulate the release or inhibition of anterior pituitary hormones from families of endocrine cells
33
How is the posterior pituitary connected to the hypothalamus ?
by neurosecretory neurones | the axons of these neurones synapse at blood vessels after travelling down the pituitary stalk
34
Where are posterior pituitary hormones synthesised ?
hypothalamus
35
Where are posterior pituitary hormones stored and released ?
posterior pituitary
36
What are magnocellular neurones ?
they span down the pituitary stalk and make Oxytocin and ADH
37
How are oxytocin and ADH released into the blood ?
an action potential travels down the magnocellular neurone | triggers exocytosis of a post.pituitary hormone into the blood
38
What is oxytocin secreted from ?
paraventricular nuclei
39
What is ADH secreted from ?
supraoptic nuclei
40
What does oxytocin do ?
it circulates in the blood and acts on the mammary glands and the uterus in the mammary gland it stimulates milk ejection in the uterus it stimulates contraction
41
What is mammary gland ejection known as ?
let down reflex
42
What is uterine contraction known as ?
ferguson reflex
43
what stimuli is ADH released under ?
low blood pressure high blood osmolarity low blood volume
44
What are the target cells for ADH ?
cells in the collecting duct of the kidney | smooth muscle around blood vessels
45
What secretes the anterior pituitary hormones ?
families of endocrine cells
46
What controls the release of hormones from the families of endocrine cells ?
neurohormones released from the hypothalamus into the portal vessels
47
What do the gonadotropins do ?
they trigger responses in the gonads gametogenesis - FSH steroidogenesis - LH they are released by the family of endocrine cells known as the gonadotrophs
48
What does growth hormone do ?
trigger metabolism in organs and tissues - eg carb metabolism or lipid synthesis they are released from the somatotrophs
49
What does TSH ?
triggers the release of the iodothyronines from the thyroid gland released from the thyrotrophs
50
What does prolactin do ?
triggers milk synthesis in mammary glands and sodium reabsorption in the kidney released from the lactotrophs
51
What does ACTH ?
triggers aldosterone and cortisol release from the adrenal cortex released from the corticotrophs
52
What is a tropic hormone ?
a hormone whos target is an endocrine cell
53
What are the tropic anterior pituitary hormones ?
ACTH TSH gonadotropins
54
What is a trophic hormone ?
stimulates cell growth | eg. GH and prolactin
55
How is secretion of the anterior pituitary hormones controlled ?
neurosecretory hormones that are released from the hypothalamus they can be release stimulating or release inhibiting
56
What are the release stimulating hormones ?
Corticotropin releasing hormone GH-releasing hormone Gonadotropin releasing hormone TSH releasing hormone
57
What are the release inhibiting hormones ?
GH-inhibiting hormone | dopamine/PIH - inhibits prolactin from the lactotrophs
58
What are the possible types of endocrine pathologies ?
hormone excess hormone deficiency abnormal responsiveness of target tissue to the hormone
59
What is hyperthyroidism ?
excess thyroid hormone release | symptoms are bulging neck and eyes
60
What is primary hypersecretion due to the thyroid ?
adenoma in the thyroid gland releases excess thyroxine excess thyroxine works via the direct/indirect pathways to inhibit TSH and TRH graves disease symptoms present thyroxine levels are high TSH/TRH are low
61
What is secondary hypersecretion due to a problem with the pituitary ?
a tumour in the anterior pituitary means excess TSH is released. thyroxine will act via the indirect/direct pathways to inhibit TSH and TRH TSH cannot be inhibited as the negative feedback loop is overidden by the increased activity of the anterior pituitary TRH is inhibited normally by thyroxine excess thyroxine is produced leading to symptoms of excess thyroxine is high TSH is high TRH is low
62
What is secondary hypersecretion due to a problem with the hypothalamus
an adenoma in the hypothalamus can mean that excess TRH is released this leads to excess TSH and thyroxine thyroxine will try to act via the indirect/direct negative feedback loops to try to inhibit further release but it is overidden by the increased hypothalamic drive so that all hormones are at high levels in the blood symptoms of excess
63
What is graves disease ?
an autoimmune disease where the body produces antibodies against the thyroid gland these antibodies stimulate receptors on thyroid cells to produce thyroxine thyroid gland enlarges usually due to primary hypersecretion
64
Treatment option for graves disease ?
anti-thyroid drugs such as thioamides - reduce thyroid gland function Radioactive iodine - accumulates in the thyroid gland - radioactivity destroys thyroid gland thyroidectomy
65
Which crystals provide the structural integrity of enamel and bone ?
calcium hydroxyapatite (99%)
66
What is calcium needed for ?
trigger neurotransmitter release blood coagulation muscle contraction
67
What happens to the nervous system if the extracellular calcium levels fall below normal ?
nervous system becomes more excitable because of the increased permeability of neuronal membranes to sodium ions this leads to hyperexcitability - tetanic contractions - hypocalcaemic tetany - indicated by trousseas sign
68
What are the 2 types of calcium in the ECF ?
filterable - free and anion bound - 60% | non fliterable - protein bound -40%
69
What proteins is calcium bound to ?
albumins and globulins
70
What is the osmolarity of calcium in the plasma ?
2.5 mM
71
of the intake of calcium how much is absorbed by te GI tract ?
35%
72
How much calcium is excreted in the urine ?
20% - this is only 2% of the filterbale calcium
73
What is on the surface of the axial skeleton ?
rapidly exchangeable pool of calcium
74
When calcium moves from the ECF into the bone to form crystals what is this called ?
bone formation
75
What is bone resorption ?
when calcium moves out of the bone into the ECF fluid
76
What is the paracellular pathway ?
calcium ions move between the cells works by passive simple diffusion occurs in the ileum if there is no conc gradient there is no uptake and calcium transport is stopped
77
What is the transcellular pathway ?
calcium moves through the cells in the cell it binds to CBP which prevent any unregulated triggering calcium leaves the cell by being pumped out by ATPases
78
What is advantageous about the transcellular pathway ?
small amounts can be transported into the blood aganst the conc gradient
79
Where does the transcellular pathway take place ?
duodenum and the jejunum
80
What is the rate limiting step in the transcellular pathway ?
the pump is the rate limiting step as it can become saturated and lower the rate of calcium transport
81
What happens during filtration at the nephron ?
the filterable calcium (free and anion bound) is remived from the blood
82
How is calcium reabsorped in the kidney ?
60% in the transcellular pathway via the proximal tubule 30% by the paracellular pathway in the loop of henle 9% in the distal tubule via the transcellular pathway
83
What is bone remodelling ?
the continuous process by which bone is reabsorbed and formed
84
During growth what happens to bone?
the rate of bone formation exceeds the rate of bone resorption
85
What happens once adult bone mass has been achieved ?
equal rates of formation and resorption | then resorption exceeds formation and bine mass slowly deccreases
86
Where does bone resorption and formation happen ?
in the trabecular bone
87
80% of the bone is which type of bone ?
compact bone
88
What feature of trabecular bone means it is good for calcium exchange ?
greater surface area
89
What are the primary cell types involved in formation and resorption ?
osteoclasts osteoblasts osteocytes
90
What are osteoblasts ?
differentiated bone forming cells | they secrete osteoid
91
What is osteoid ?
organic bone matrix made of collagen secreted by osteoblasts calcium phosphate precipitates on it prior to full mineralisation
92
What are osteocytes ?
mature bone cells enclosed in the bone amtrix connected to the suraf ecells and each other by canalliculi - allow for ion and nutrient exchange
93
What are osteoclasts ?
large multi nucleated cells derived from monocytes they resorb bone by having hydrolytic enzymes that release calcium into the ECF
94
How does PTH work ?
by stimulating bone resorption via the hydrolytic enzymes in osteoclasts
95
Where is parathyroid hormone synthesised and secreted ?
the chief cells of the parathyroid glands
96
How is PTH initially translated ?
as a pre hormone that is biologically inactive the prosequences are cleaved off to yield a biologically active peptide of 84 amino acids this is exocytosed into the blood
97
What is the job of PTH ?
increase plasma calcium as it is a hypercalcaemic hormone | the stimulus for this is a decrease in plasma calcium
98
What does PTH do to bone ?
it increases osteoclast number increases osteoclast activity decrease collagen synthesis - less osteoid formation so less bone formation therefore net transfer to the plasma
99
What does PTH do to the kidney ?
stimulates calcium reabsorption in the distal tubule via the transcellular pathway decreases urinary calcium also stimulates the activity of 1-alpaha hydroxylase in the kidney
100
What does 1-alpha hydoroxylase do ?
catalyses the formation of 1,25 DHCC
101
What does PTH do in the GI tract ?
it has no direct effect it works indirectly to stimulate 1- alpha hydroxylase
102
What is the natural form of 1,25 DHCC ?
vitamin D3
103
What is the structure of 1,25 DHCC ?
it is a highly aromatic structure
104
What are the 2 sources of vitamin D3 ?
diet and skin
105
How is vitamin D3 made in the skin ?
cholesterol is converted to 7-dehydrocholesterol and then with UV light it is made into vitamin D3
106
Is vitamin D3 active or inactive ?
it is inactive it must be converted to 1,25 DHCC
107
How is vitamin D3 converted to 1,25 DHCC to be active?
vitamin d3 enters hepatic circulation enzyme places a hydroxyl group on C25 this enters renal circulation and 1- alpha hydroxylase puts a hydroxyl group on carbon 1
108
How is 1,25 DHCC activity stimulated ?
by PTH
109
What does PTH do to 1-alpha-hydroxylase ?
PTH also stimulates 1-alpha hydroxylase to produce 1,25 DHCC
110
What type of hormone is 1,25 DHCC ?
it is a hypercalcaemic hormone
111
How does 1,25 DHCC regulate the transcellular pathway ?
it induces the production of CBPs
112
What do the CBPs do ?
they buffer high intracellular calcium concentrations that arise during initial absorption - this allow calcium to be uptaken against a high concentration
113
How does 1.25 DHCC act as a steroid hormone ?
it alters the amount of CBp by promoting its synthesis at the gene expression level
114
What effec does 1,25 DHCC have in the kidney ?
it increases the absorption in the distal tubule but this is minor
115
What is the effect of 1,25 DHCC in the bone ?
it promotes the actions of PTH - bone resorption
116
Why is regulation of the hypercalcaemic hormones needed ?
because they stimulate each other and this can lead to hypercalcaemia
117
How is the level of PTH regulated ?
1,25 DHCC inhibits PTH gene expression in a form of feedback control
118
What does calcitonin do ?
it decreases calcium concentrations it is a hypocalcaemic hormone
119
What is the main target for calcitonin ?
it targets the osteoclasts by inhibiting their motility and cell shape which inactivates them less bone resorption
120
What effect does calcitonin have on the intestine ?
no effect on the intestine
121
What effect does calcitonin have on the kidney ?
decreases tubular reabsorption of calcium - but this is weak
122
Why does calcitonin only have a small effect on calcium conc ?
excess calcitonin does not result in hypocalcaemia removal of the parafollicular cells does not cause hypercalcaemia suggests that 1,25 DHCC and PTH dominate
123
What is osteoporosis ?
``` reduced bone density and mass loss of organic matrix equilibrium is disrupted resorption > formation trabecular bone is reduced ```
124
What is oestrogen ?
a potent stimulator of bone formation
125
What is treatment for metabolic bone diseases ?
increased calcium oestrogen replacement / androgens anti resorptive drugs
126
What is osteomalacia / rickets ?
inadequate mineralosation of bone matrix bones lack mineral phase and structural strength caused by vit.D deficiency
127
What is vitamin D dependent rickets type 2?
inability to convert vitamin D3 into 1,25 DHCC due to a mutation in the 1,25 DHCC receptor impaired intestinal calcium absorption
128
What are the potential causes of hypercalcaemia ?
primary hyperparathyroidism Adenoma in parathryroid gland hyperplastic parathyroid tissue excessive production of 1,25 DHCC
129
What are the symptoms of hypercalcaemia ?
neuromuscular supression - neuronal cells less permeable to sodium kidney stones and blocked arteries
130
What are the treatment options for hypercalcaemia ?
anti resorptive agents salmon calcitonin surgery
131
other cause sog hypercalcaemia ?
malignant cells - destruction of bone - release calcium vit . D dependent hypercalcaemia - too much 1,25 DHCC made from too much vitamin D acromegaly - stimulation of 1-alpha - hydroxylase by GH - excess 1,25 DHCC
132
What are the causes of hypocalcaemia ?
PTH deficient hypoparathyroidism PTH ineffective hypoparathyroidism - biologically inactive PTH PTH resistant hypoparathyroidism - pseudoparathyroidism - cells not responsive to PTH
133
What is secondary hyperparathyroidism ?
malabsorption of vitamin D in GI tract cant convert vitamin D to 1,25 DHCC in kidney decreases plasma calcium PTH stimulkated tries to return calcium level to normal via the osteoclasts expense of significant calcium from the bone
134
What does the pancreas consist of ?
islets and exocrine cells
135
What is a festure of islets ?
they are highly vascularised which allows hormones to be moved around the body easily
136
What proportion of cells in the pancreas are exocrine ?
98%
137
What types of hormone secreting cells are there in an islet ?
D cells aloha cells beta cells
138
What do alpha cells release ?
glucagon - hyperglycaemic hormone
139
What do beta cells release ?
secrete insulin - hypoglycaemic hormone
140
What do D cells release ?
somatostatin
141
What does somatostatin do ?
regulates glucagon/insulin secretion by inhibiting their secretion
142
What is somatostatin ?
a GIH | hypothalamic neurohormone
143
What type of hormones are glucagon , insulin and somatostatin ?
peptide hormones
144
How are the 3 hormones released form the endocrine secreting cells ?
exocytosis into the blood
145
Which pathway does insulin trigger ?
tyrosine kinase signal transduction pathway
146
Which pathway does glucagon trigger ?
cAMP signal transduction pathway
147
What stimuli lead to increased insulin secretion ?
raised blood glucose amino acids - trigger insuin so they can be taken up digestive hormones
148
How can insulin be secreted by neuronal stimulation ?
alpha receptors stimulate insulin secretion in sympathetic pathways
149
How can insulin be secreted in parasympathetic pathways ?
at cholinergic synapses
150
What stimuli decreases insulin secretion ?
low blood glucose | somatostatin
151
How is insulin secretion decreased ?
insulin secretion can be decreased by beta receptors in reactions to stress , hypoxia and hypothermia
152
Describe the direct endocrine reflex arc of insulin release post a glucose meal ?
insulin secreted post meal target cells take up glucose insulin levels fall as high blood glucose is no longer a stimulus
153
What happens to glucagon levels post a carb meal ?
they decrease | as blood glucose is being returned to normal
154
What is a glucose tolerance curve ?
it shows the appearance and disappearance of glucose post meal this can be used to diagnose diabetes
155
What happens to glucose in anabolic reactions ?
insulin triggered - glucose taken up by muscle glucose is taken up by the liver - without the need for insulin (dont use GLUT4 which is insulin dependent ) Adipose tissue and the liver take up glucose to make triglycerides
156
What happens to glucose in catabolic reactions ?
glucagon is released in the fasting state glycogen in the muscle broken down to glucose 6 phosphate in the muscle glycogen is fully broken down to release glucose
157
Can adipose tissue convert triglycerides to glucose ?
no
158
What happens to amino acids in the muscle ?
they go to the liver and take part in gluconeogenesis to make glucose
159
What happens to excess fatty acids in the liver ?
made into ketone bodies
160
What happens when a protein rich meal is taken ?
increase in glucagon and insulin
161
What do amino acids trigger ?
insukin release so they can be taken up
162
What happens when the insulin is release and what stops this ?
insulin fully removes any glucose from the blood this means that subjects can become hypoglycaemic to stop this glucagon levels are also raised - raise blood glucose
163
What is diabetes mellitus ?
a family of metabolic diseases | can involve an inadequate production of insulin or an abnormal responsiveness by target tissue to insulin
164
What are the symptoms of DM ?
chronic hyperglycaemia nocturia - to remove excess glucose weight loss - individuals enter the fasting state despite high blood glucose blurred vision - glucose precipitates in the eye excessive thirst - glucose is osmotically active in the blood - increases blood osmolarity
165
What is type 1 diabetes ?
insulin dependent autoimmune disorder means that beta cells are destroyed - no insulin production enter a fasted state
166
What happens during type 1 diabetes ?
muscles break down proteins adipose tissue breaks down triglycerides liver also synthesises glucose in gluconeogenesis ketogenesis - leads to ketoacidosis leads to hyperglycaemia
167
What is type 2 diabetes ?
insulin resistant diabetes abnormal target cells responsiveness eventually become insulin dependent
168
why is the hyperglycaemia not as severe in type 2 ?
their is functioning insulin metabolism not normal delayed respkjksne to ingested glucose
169
What is the treatment in type 2 ?
exercise | drugs to prevent hyperglycaemia - bignanides - metmorfin - inhibit gluconeogenesis
170
What does the adrenal gland consist of ?
adrenal medulla | adrenal cortex
171
What does the adrenal medulla secrete ?
catecholamines eg. noradrenaline
172
What are the zones i the adrenal cortex ?
Zona reticularis zona fasiculata zona glomerulosa
173
What does zona reticularis secrete ?
glucocorticoids and sex hormones
174
What does zona fasiculata secrete ?
glucocoritcoids eg . cortisol
175
What does zona glomerulosa secrete ?
mineralcorticoids eg aldesterone
176
What are the corticosteroids ?
mineralcorticoids and glucocorticoids
177
What are the glucocorticoids ?
steroid hormones secreted from the adrenal coretx - eg.cortisol
178
What are the mineralcorticoids ?
class of steroid hormones secreted from the adrenal cortex - have a highly aromatic structure
179
What is an example of a mineralcorticoid ?
aldesterone
180
What is an example of a glucocorticoid ?
cortisol
181
How do the mineralcorticoids work ?
they stimulate sodium absorption in the kimndey and this follows with water absoprtion whicb allows an increase in blood pressure and blood volume .
182
What is aldesterone secretion controlled by ?
renin-angiotensin pathway
183
What does the renin- angiotensin pathway control ?
blood pressure
184
Desribe the renin angiotensin pathway ?
decrease in blood pressure and volume detected by the juxtaglomerular cells in the kidney the kidney releases renin the liver releases angiotensinogen angiotensinogen is converted to angiotensin 1 by renin this enters the pulmonary circulation ACE converts angiotensin I to angiotensin II angiotensin II causes vasoconstriction of the arterioles angiotensin II travels to the adrenal cortex this stimulates aldesterone secretion in the kidneys this causes increased sodium absorption and increased water absorption leads to increased blood pressure and volume
185
What is ADH stimulated by ?
angiotensinogen II
186
What does ADH target ?
collecting duct in the kidney | smooth muscle around vessels - allows the increase in blood pressure
187
What does angiotensin II in the plasma stimulate ?
arterioles - vasoconstriction cardiovascular centre in the medulla oblangata - cardiovascular response hypothalamus - ADH and thirst Adrenal cortex - aldosterone
188
How is blood pressure calculated ?
BP= CO X PR
189
How does angiotensin II increase the blood pressure ?
it increases Bp as angiotensin increases BP through PR rising due to vasoconstriction
190
Describe the hypothalamic - pituitary - adrenal cortex for cortisol ?
CRH ACTH Adrenal cortex - releases cortisol
191
How is cortisol continuously secreted ?
over a diurnal rhythm
192
What does cortisol secretion increase with ?
``` stress anxiety emotion trauma oxygen deprivation ```
193
Why do animals die of their adrenal glands are removed ?.
they are exposed to significant environmental stress
194
What are the actions of cortisol ?
immune system - function suppressed (thymus and lymphatic tissue reduced in effectiveness) liver -gluconeogenesis Muscle - protein catabolism and the amino acids can be used for gluconeogenesis Adipose tissue - lipolysis - triglycerides can be used as an alternative to glucose
195
What is addisons disease ?
disorder of the adrenal glands reduced cortisol and aldesterone production cant cope with stress or dehydration
196
What effect does cortisol have on glucagon ?
a permissive effect in the absence of cortisol glucagon is unable to respond effectively to hypoglycaemia cortisol must be present to ensure full responsiveness to glucagon
197
Why is cortisol useful as a therapuetic drug ?
immunosuppressant | this can be used in allergic reactions and prevention of transplant rejection
198
What is the problem with exogenous cortisol ?
the body cannot distinguish between exogenous and indogenous cortisol exogenous cortisol can activate direct/indirect pathways of negative feedback this stops the bodily production of cortisol shut down of hypothalamic - pituitary axis if exogenous cortisol is to be stoppped - must be gradual to relieve inhibition of the hypothalamic - pituitary- adrenal axis body can produce exogenous cortisol
199
What is cushings syndrome ?
hypercortisolism excess lipolysis - redistribution of fat hyperglycaemia - excess gluconeogenesis susceptibility to infection - immunosupressant muscle thinning - protein breakdown
200
What are the causes of hypercortisolism ?
latrogenic - cortisol therapy adrenal tumour - adenoma pituitary tumour