Endocrine Flashcards
1
Q
what 3 kinds of chemical messengers are used for signalling?
A
paracrine- hormones sent to neighboring target cells, NT and hormones (endocrine)
2
Q
what are the major functions of the endocrine system?
A
-Metabolism
-Growth and development
-Reproduction
-Stress response
-Water and electrolyte balance
3
Q
what is the difference between primary and secondary endocrine organs?
A
primary- make and secrete hormones
secondary- involved in a variety of biological processes in addition to hormone secretion
4
Q
what factors regulate hormone secretion?
A
NT, other hormones, metabolites and ions
5
Q
is diabetes an endocrine disorder?
A
yes
6
Q
what are the 2 classes of hormones?
A
Hydrophobic and Hydrophilic
7
Q
what kinds of hormones are hydrophobic? what are characteristics of hydrophobic hormones?
A
steroids and thyroid hormones
-poor solubility
-travel in blood bound to carrier proteins
-can cross the lipid bi-layer
-receptor found inside the cytosol or nucleus
8
Q
what kinds of hormones are hydrophilic? what are characteristics of hydrophilic hormones?
A
peptides and catecholamines
-water soluble
-travel freely in the blood
-cannot cross the lipid bilayer
-receptor found ON membrane
9
Q
how are signals sent for hydrophobic hormones?
A
hydrophobic hormones bind to a receptor to create a complex that is able to diffuse across the membrane
https://youtu.be/RnERznH4Gz8?si=uZ6sSIdhNiVImRuB
10
Q
A
5, 2, 1, 4, 3
11
Q
how are signals sent for hydrophilic hormones?
A
messenger binds to receptor outside of the cell which activates G-coupled receptor
-receptor converts GDP to GTP and cAMP is made
-Protein kinase A is then activated and cellular proteins are phosphorylated
https://youtu.be/RnERznH4Gz8?si=uZ6sSIdhNiVImRuB
12
Q
A
2, 1 ,6, 5, 4, 3
13
Q
how does caffeine affect hydrophilic messenger activity?
A
Inhibits phosphodiesterase’s which typically turn off cAMP signal. Inhibition of cAMP will leave signal on for longer which decreases adrenaline effects-
inhibits supressing effects
https://youtu.be/jOfquPE1cnU?si=fd7CY6xebkoWJfGU&t=200
14
Q
where is the pituitary located in relation to the hypothalamus?
A
the pituitary lies outside of the brain and is conncted under the hypothalamus
15
Q
what are the paraventricular nuclei?
A
located in the hypothalamus and extending to the posterior pituitary; they make and secrete ADH and oxytocin
16
Q
what are the nuceli sending axons to median eminence?
A
neurons that origin in the hypothalamus and feed into the median emimence
17
Q
what kind of blood circulation is there in the anterior and posterior pituitary?
A
portal circulation- blood goes against conventional flow of blood
18
Q
is the anterior pituitary located in front or behind the posterior pituitary?
A
in front
19
Q
what is the main function of the posterior pituitary?
A
make and secrete ADH and oxytocin
20
Q
what is the major role of ADH (vasopressin)?
A
conservation of body water and blood volume
-increases water reabsorption in the kidneys
-increases blood pressure through vasoconstriction
21
Q
explain step-wise how ADH affects the kidneys?
A
- ADH Release: Stimulated by high blood osmolarity or low blood volume.
- Receptor Binding: ADH binds to vasopressin receptors (V2) in renal collecting ducts.
- Second Messenger Activation: ADH activates adenylate cyclase, forming cAMP.
- Aquaporin Insertion: cAMP triggers insertion of aquaporin-2 channels.
- Water Reabsorption: Aquaporin channels allow water reabsorption.
- Urine Concentration: Increases water reabsorption, leading to concentrated urine.
22
Q
what detects osomolarity in order to regulate ADH release?
A
-reduced stretch of walls due to high osmolarity (low blood volume)
23
Q
fill in this chart
A
24
Q
what system do hormones travel through to get to the capillaries?
A
the portal system
25
what kinds of hormones regulate the release of hormones produced in the anterior pituitary?
hypothalimic hormones
26
explain the general negative feedback system for hormones
there are 2 feedback systems to ensure proper regulation
1) increases in hormone 3 will supress releasing hormone from hypothalamus
2) increases in hormone 3 will inhibit stimulating hormone from the anterior pituitary
27
explain the feedback system for cortisol release
1) increased cortisol levels will work on the hypothalamus to inhibit release of corticotropin releasing hormone (CRH)
2) increased levels of cortisol will work on the anterior pituitary to inhibit release of adrenocorticotropic hormone (ACTH)
28
what hormones are released from the hypothalamus?
1) GHRH- growth hormone releasing hormone
2) GnRH- gonadotropin-releasing hormone
3) SST- somatostatin
4) TRH- thyrotrophin-releasing hormone
5) DA- Dopamine
6) CRH- corticotropin-releasing hormone
29
what hormones are released by the anterior pituitary?
growth hormone, thyroid stimulating hormone, prolactin, ACTH, FSH and LH
30
what affect does GHRH have on growth hormone?
increases GH release
31
what affect does SST have on growth hormone?
inhibits it
32
what affect does TRH have on TSH?
increases it
33
what affect does DA have on prolactin?
inhibits it
34
what affect does CRH have on ACTH?
increases it
35
what affect does ACTH secretion have?
cortisol release
36
what affect does prolactin secretion have?
breast development and milk production
37
what affect does TSH secretion have?
secretes thyroxine and triiodothyonine hormones (T4/T3)
38
what does growth hormone stimulate the release of? what affect does this have on metabolism?
secretion of IGF-1, protein synthesis and carb/lipid metabolism
39
what affect does FSH and LH secretion have?
improvement in reproductive development/ maturation
40
Around what age ie brain growth rapid?
4-8 years old
41
what ages are most common for growth spirts in humans?
postnatal growth spirt and puberty growth spirt
42
what is the epiphyseal plate?
site of bone growth
-cartilage between epiphysis and diaphysis
43
where are taget cells for GH and IGF-1 located?
in the epiphyseal plate
44
what are osteoblasts?
site of bone production
-provides collagen and proteoglycans
45
what are osteoclasts?
cells responsible for resorption or breakdown of the bone
-secretes acid to breakdown minerals
46
what are osteocytes?
osteoblasts that have become mineralized
-bone maintainers
47
what happens to bones without minerals?
they become very flexible and have little structure
48
what hapoens to bones that don't have collagen?
They have no flexibility and may easily break
49
how does bone growth occur?
chondrocytes (bone cells) grow in size and become trapped by osteoblasts in order to be calcified and die
50
what are the steps in bone growth? what causes growth plate closure?
51
explain the steps in bone reparation?
1) blood escapes from bone making a hematoma
2) Tissue repair begins with fibrocartilaginous callus (compact bone)
3) osteobalsts produce spongy bone and to convert fibrocartilage to a bony callus, joining broken bones
4) osteoblasts build new compact bone and osteoclasts absorb spongy bone
52
what factors influence growth?
53
explain the GH feeback system
increased GH stimulates increased IGF-1 which:
1) ihibits GH at the anterior pituitary
2) inhibits GHRH at the hypothalamus
3) stimulates the release of SST (GH inhibitor)
54
what factors stimulate GH?
-sleep
-exercise
-stress
-low blood glucose
55
how does GH/ IGF-1 affect growth?
increased cell size- hypertrophy
increased cell number- hyperplasia
56
how does GH/ IGF-1 affect metabolic actions?
57
what is acromegaly?
excessive GH when growth plates are not open or responsive to it; past adolescence- GH gets triggered in other places high in cartilage (face)
58
what is gigantism?
excessive GH while growth plates are open and responsive to it
59
what are the effects of growth hormone-secreting hormone?
60
what important functions does Ca+ have?
-bone / teeth health
-muscle contraction
-heart contractions
-vesicle release
-blood clotting
61
where is the storage site for Ca+?
The bones
62
how do osteoblasts work with Ca+?
responsible for bone deposition and addition of Ca+ to the bone
63
how do osteoclasts work with Ca+?
responsible for bone resorption and release of Ca+ from the bone into the blood
64
what 3 hormones control plasma Ca+ levels?
1) parathyroid hormone (PTH)
2) Calcitriol (1,25-dihydroxycholecalciferol)
3) calcitonin
65
what are the three main target sites for hormones that control plasma Ca+ levels?
1) bones
2) kidneys
3) digestive tract
66
what stimulates PTH release?
low plasma [Ca+]
67
what does PTH release do to the bones?
stimulates bone resorption
68
what affect does PTH have on the kidneys?
-increases Ca+ reabsorption
-decreases phosphate reabsorption
-stimulates sythesis of calcitriol---> increases Ca+ absorption in the digestive tract
69
what is the overall effect of PTH?
increases plasma [Ca+ ]
70
what is hyperparathyroidism?
excess secretion of PTH = high blood [Ca+] levels
-tumours/hyperfunction of the parathyroid glands
-Vit D3 deficiency or chronic kidney disease
71
what is hypoparathyroidism?
inadequate secretion of PTH = low blood Ca+
-trauma to parathyroid glands
autoimmune damage to parathyroid glands
-congenital malformation
-PTH resistance if low blood [Ca+] but high [PTH}
72
what are symptoms of Hyperparathyroidism?
73
what are symptoms of Hypoparathyroidism?
74
what organs does calcitriol act on? what does it do?
digestive tract- absorption
kidneys- increase calcium reabsorption
75
what is the overall effect of calcitriol on the body?
increase plasma [Ca+]
76
how is calcitriol synthesized?
1) Vit D (7-dehydrocholesterol) is absobed by the skin and [Vit D] increase
2) in the liver, vit D is converted into 25-OH D3 by 25-hydroxylase which incerases the [ ] in blood
3) in the kidneys PTH stimulates the conversion of 25-OH D3 into Calcitriol by 1-hydroxylase
4) calcitriol levels increase which causes and increase in Ca+ absorption
77
what does Vit D defieciency cause?
rickets
-softening of bones due to mineral deficiency
-increases cancer risks and autoimmune diseases
78
where is calcitonin secreted from?
C cells in the thyroid gland
79
what kind of hormone is calcitonin?
peptide hormone
80
what triggers the release of calcitonin?
high plasma [Ca2+]
81
what is the difference between calitriol and calcitonin?
-calcitriol increases the [Ca2+] in plasma
-calcitonin is released in response to high levels of [Ca2+] in order to decrease plasma [Ca2+]
82
what actions does calcitonin have on the body?
1) reduces activity of osteoclasts - inhibit bone reabsorption
2) inhibits Ca+ reabsorption by the kidneys
3) protects the skeleton from Ca+ loss during pregnancy and lactation
83
what is the overall effect of calcitonin release?
decreased plasma [Ca+]
84
what is osteoporosis?
"porous bone"
-decreased bone mass leading to bone fragility and. increased fracture risk
85
what are risk factors of osteoporosis?
86
what can prevent osteoporosis?
87
what are treatments for osteoporosis?
88
how is TH regulated?
stimulation - cold
inhibition - stress and warmth
89
what is the function of the colloid in the thyroid?
contains thyroglubulin protein which is a precursor for thyroid hormones
-also contains enzymes and iodine
90
what happens to the number of colloid follciles if the thyroid is inactive?
they increase in number
91
how are thyroid hormones synthesized?
1) Iodide Uptake: Active transport of iodide into thyroid follicular cells.
2) Thyroglobulin Synthesis: Production and secretion of thyroglobulin into the follicular lumen.
3) Iodide Oxidation:Conversion of iodide to iodine within the follicular lumen.
4)Iodination of Tyrosine: Attachment of iodine to tyrosine residues on thyroglobulin.
5)Coupling of Iodotyrosine: Formation of T4 and T3 by coupling iodotyrosine residues.
6)Endocytosis of Thyroglobulin: Internalization of thyroglobulin-T4/T3 complexes into follicular cells.
7)Lysosomal Proteolysis: Breakdown of thyroglobulin, releasing T4 and T3.
8)Release of T4 and T3: Diffusion of T4 and T3 into bloodstream for transport
92
what are the 3 thyroid hormones?
T4, T3 and RT3
93
which thyroid hormone is the most abundant?
T4
94
which thyroid hormone is the most active?
T3
95
what actions do T3/T4 have?
-regulation of BMR
-normal growth
-brain function and development
-promotion of energy mobilization when in excess
-inrease of beta adrenergic receptors
95
what is RT3?
Reverse thyroid hormone
-an inactive form of T3
96
what is hyperthyroidism?
excess thryoid hormone
97
what causes hyperthyroidism?
-tumours
-thyroid stimulating immunoglobulins
98
what are symptoms of hyperthyroidism?
goiter (can occur withy hyper/hypothyroidism), proptosis, nervousness, insomnia, increased HR, eye disease, weight loss and anxiety
99
what is graves disease?
an autoimmune disease where the body has antibodies against the TSH receptor
100
what is the most common disease associated with with hyperthyroidism?
grave's disease
101
what is hypothyroidism?
thyroid hormone deficiency
102
what are causes of hypothyroidism?
-lack of iodine in diet
-under active thyroid
103
what are symptoms of hypothyroidism?
*opposite of hyperthyroidism
-lethargy
-fatigue
-cold-intolerance
-weakness
-hair loss
-weight gain
104
what is cretinism?
dwarfism and an under-development of the brain resulting from hypothyroidism
105
what is myxedema?
hypothyroisim disease where the body retains excess water causes pufiness in the face
106
how does an iodine deficeincy affect T4 and T3?
it leaves the thyroid gland unable to produce T4/T3
107
what causes a goiter?
-iodine deficiency results in a lack of negative feedback; causing an excess TSH secretion
-excess TSH stimulates growth of the thyroid gland (enhances follicular cell division)
108
what is the precursor for adrenal cortex hormones?
cholesterol
109
what does dehydroepiandrosterone differentiate into?
androstenedione
110
what does progesterone differentiate into?
corticosterone ---> aldosterone
111
what is the precursor to cortisol?
17-Hydroxyprogesterone
112
what is an example of a mineralocorticoid?
aldosterone
113
what is an example of a glucocorticoid?
cortisol
114
what types of hormones are sex hormones?
androgens
115
what part of the adrenal cortex is aldosterone secreted from?
zona glomerulosa
116
what part of the adrenal cortex is cortisol secreted from?
zonae fasciculata and reticularis
117
what part of the adrenal cortex are sex hormones secreted from?
zonae fasciculata and reticularis
118
what does aldosterone do? what organ does it target?
targets the kidneys to increase Na+ reabsorption
-water is also reabsorbed
-Increases K+ secretion
overall: increases blood volume and plasma osmolarity and lowers blood [K+]
119
what is the mechanism of aldosterone secretion?
-aldosterone diffuses towards target call
-receptor-ligand complex causes transcription events
-creates and inserts channels on the apical membrane of the target cell
-increases synthesis and insertion of K+ cells which leads to increased Na+ absorption
-K+ circulation increases
-Na+ is retained and K+ is excreted
120
what stimulates aldosterone secretion?
-high plasma [K+]
-angiotensin II
121
what is excess aldosterine production called?
hyperaldosteronemia
122
how is cortsol regulated? explain the feedback
123
what is the action of glucocorticoids (cortisol) ?
-promote energy mobilization
-required for GH secretion
-maintain vessel responsiveness to catecholamines
-adaptive response to stress
-clinical use (inhibit inflammation and allergic response)
124
what are metabolic effects of cortisol?
gluconeogenisis, protein catabolism and lipolysis
124
what occurs from hyper secretion of glucocorticoids?
125
what is Cushing's syndrome?
excess cortisol secretion leading to many symptoms:
-buffalo hump
-hypertension
-thin skin, arms and legs
-red cheeks
-increased visceral fat storage
126
what is Addison's disease?
low levels of cortisol leading to adrenal insufficiency
-excess Na+ loss and K+ retention
-poor stress tolerance
-hypotension
-hypoglycemia
-weakness, lethargy, loss of appetite
127
what hormones are categorized as catecholamines?
epinephrine and norepinephrine
128
what are the precursors of NE and EN?
tyrosine ---> L-dopa ---> dopamine ---> NE ---> EN
129
what are CV actions of epinephrine?
-increases HR
-increases force of contraction
-increases cardiac output
130
what are the actions of epinephrine?
131
what is the absorptive state?
timeframe 3-4 hours after a meal
-nutrient in the bloodstream are plentiful
-glucose is primary fuel
132
what is the postabsorptive state?
timeframe between meals (fasting state)
-energy stores must be mobilized
-fatty acids are the primary fuel
133
How are carbs dealt with in the absorptive state?
Glucose = primary fuel
-glycogen synthesis and storage
-conversion of excess glucose to triglycerides and storage in fat
134
what is glycogenesis?
synthesis and storage of glycogen
135
How are carbs dealt with in the post-absorptive state?
glycogen breakdown and glucose synthesis
136
what is glycogenolysis?
glycogen breakdown
137
what is gluconeogenesis?
glucose synthesis
138
how are proteins dealt with in the absorptive state?
-protein synthesis
-conversion of excess amino acids to triglycerides and storage as fat
139
how are proteins dealt with in the post-absorptive state?
-protein breakdown
-AA used for gluconeogenisis by liver
140
how are lipids dealt with in the absorptive state?
-triglyceride synthesis and storage (lipogenesis)
141
how are lipids dealt with in the post-absorptive state?
-triglyceride breakdown
-FA primary fuel
-glycerol conversion to glucose
-FA conversion to ketones
142
what is lipogenesis?
triglyceride synthesis and storage
143
what is lipolysis?
triglyceride breakdown
144
summary of transition between apsorptive and post-absorptive:
145
what cells secrete insulin?
beta cells
146
what cells secrete glucagon?
alpha cells
147
what kind of hormone is insulin?
peptide hormone
148
when is secretion of insulin increased? what does is it stimulated by?
during the absorptive state
stimulated by:
-glucose in plasma
-AA in plasma
-Increased PS activity
-incretins (GLP-1, GIP)
149
what occurs to insulin during the post absorptive state? what hormones cause this?
it decreases
inhibited by:
-epinephrine
-somatostatin
150
what does insulin promote?
-the synthesis of energy storage molecules (anabolism)
-glucose uptake by cells
151
explain how blood glucose levels are regulated by insulin
152
explain the steps in insulin signalling
Insulin binds to receptor
-glucose receptors are added to membrane
-glucose uptake increases
153
what are targets of insulin action?
muscle, adipocytes and the liver
154
what effect does increases in plasma insulin have on muscles?
increases glucose uptake and utilization
-glycogen synthesis
-AA uptake
-protein synthesis
155
what effect does increases in plasma insulin have on adipocytes?
increases glucose uptake and utilization
-triglyceride synthesis
156
what effect does increases in plasma insulin have on the liver?
decreases gluconeogenisis
-glycogen synthesis
-triglyceride synthesis
-no ketone synthesis
157
what effect does decreases in plasma insulin have on muscles?
decreased glucose uptake / utilization
-glycogen catabolism
-protein catabolism
-AA release
-FA uptake and utilization
158
what effect does decreases in plasma insulin have on adipocytes?
decreased glucose uptake/utilization
-triglyceride catabolism and release of glycerol / FA
159
what effect does decreases in plasma insulin have on the liver?
increased glucose release due to removal of inhibitory effects on glycogen catabolism and gluconeogenisis
-increased ketone synthesis / release
160
how does glucagon regulate glucose levels?
as plasma glucose levels decrease, plasma glucagon increases which stimulates glycogenolysis, gluconeogenesis and ketone synthesis
161
what stimulates glucagon release?
-decreased plasma glucose
-increased AA in plasma
-increased sympathetic activity
-epinephrine
162
what are inhibitors of glucagon release?
-somatostatin
-insulin
-increased glucose in plasma
163
what actions does glucagon release to the liver cause?
increased:
-glycogenolysis
-gluconeogenesis
-ketone synthesis
-protein breakdown
decreased:
-glycogen synthesis
-protein synthesis
164
what actions does glucagon release to the adipose tissue cause?
-increased lipolysis
-decreased triglyceride synthesis
165
does GLUT2 in the liver cells respond to insulin?
no, glucose uptake in the liver cells is not insulin dependent
166
what is the biochemical response to insulin on muscle cells?
increased:
-GLUT 4 translocation
-enzymes for glycogen synthesis
-AA uptake
-protien synthesis
decreased:
-enzymes for glycogenolysis
167
what is the biochemical response to insulin on adipocytes?
increased:
-GLUT 4 translocation
-Lipoprotein lipase
-enzymes for FA synthesis
-enzymes for triglyceride synthesis
168
what is the biochemical response to insulin on liver cells?
*glucose uptake not insulin dependent
increased:
-enzymes to keep glucose in cells
-enzymes for glycogen synthesis
-enzymes to make pyruvate
-enzymes for lipogenesis
decreased:
-enzymes for gluconeogenesis
-enzymes for gluconeogenesis
169
what is diabetic ketoacidosis?
condition where ketones are acidic, causes blood pH to lower
-results from insulin deficiency
170
what are characteristics of diebetic ketoacidosis?
-urinary excretion of glucose and ketones
-osmotic diuresis
-plasma acidosis
171
what is diabetes mellitus?
high blood glucose levels and relative insulin deficiency
172
what is type 1 diabetes?
insulin secretion is reduced or absent
-treated by insulin injections or pump because if taken orally the stomach would digest it
173
what is type 2 diabetes?
-cell responsiveness to insulin is reduced
-treated by diet/medication
174
how is food intake regulated?
leptin - supresses hunger
ghrelin- stimulates hunger
175
how does leptin work to control energy stores?
food intake > energy expenditure ---> increased fat deposition resulting in leptin secretion ----> works on the hypothalamus to decrease food intake and incerase metabolim
-negative feedback
176
what is hypoglycaemia?
most serious acute complications in intensively treated diabtes
-a condition in which your blood sugar level is lower than the standard range
177
what is the sympathetic response to low plasma glucose?
adrenal medulla releases epinephrine to work on skeletal muscle, liver and adipose tissue
-glycogenolysis, gluconeogenesis and lipolysis are stimulated to increase plasma glucose
178
what are long term complications of diabetes mellitus?
