Hormones Flashcards
(238 cards)
1
Q
What is the name for organs that secrete a hormone into the blood and release chemical messengers?
A
Endocrine glands.
2
Q
What are hormones actions on a whole body level?
A
Regulation and integration of ionic and fluid balance, energy balance, coping with environment, growth and development, reproduction.
3
Q
What are hormone actions on a cellular level?
A
Regulation of cell division, differentiation, death, motility, secretion, nutrient uptake.
4
Q
What are hormone actions on a molecular level?
A
Regulation of gene transcription, protein synthesis and degradation, enzyme activity, protein conformation, protein to protein interactions.
5
Q
What can be autocrine, paracrine or act on far off organs?
A
Hormones.
6
Q
What are steroid hormones?
A
Cholesterol derivatives e.g. testosterone, oestrogen, cortisol.
7
Q
What are peptide hormones?
A
Growth hormone, oxytocin, parathyroid hormone.
8
Q
What are amino acids derived hormones?
A
Thyroid hormones and catelcholamines.
9
Q
How can hormones travel?
A
Free in plasma or bound to a carrier protein.
10
Q
What other system is the endocrine system tightly integrated with?
A
The nervous system.
11
Q
How does the nervous system aid the endocrine system?
A
Hypothalamus receives sensory inputs, detects challenges in internal and external environments.
12
Q
What is the name given to the feedback loops linking the nervous system and endocrine system?
A
Negative feedback.
13
Q
What two hormones give positive feedback loops instead of negative?
A
Oxytocin and parturition.
14
Q
When is negative feedback seen?
A
When the output of a pathway inhibits inputs to the pathway.
15
Q
What endocrine organs does the pituitary gland control?
A
Adrenals, ovaries, testes, thyroids.
16
Q
What is the pituitary gland?
A
A small structure at the base of the brain that releases hormones that control the activity of the body’s other hormone glands.
17
Q
What is the optic chiasm?
A
Where optic nerves cross in the brain.
18
Q
What is the anatomical location of the pituitary gland?
A
Lies inferior to the hypothalamus with the optic chiasm between.
19
Q
What are the two sub sections of the posterior pituitary?
A
Infundibular stalk and pars nervosa.
20
Q
What are the three sub sections of the anterior pituitary?
A
Pars tuberalis, pars intermedia, pars distalis.
21
Q
What is the function of the anterior lobe - pars distalis - of the pituitary gland?
A
Portal blood vessels connect pituitary and hypothalamic capillary beds.
22
Q
What is the function of the posterior lobe - pars nervosa - of the pituitary gland?
A
Nerve fibres originate in the hypothalamus and transport hormones to posterior pituitary.
23
Q
What do the anterior lobe and posterior lobe have different of?
A
Different embryological origins.
24
Q
What two hormones does the posterior pituitary release?
A
Oxytocin and vasopressin (ADH).
25
What does oxytocin control?
Controls milk release from lactating breast, controls uterine contraction at onset of labour.
26
What does vasopressin do?
Acts on kidneys to reabsorb water.
27
In response to what, are hormones excreted from the posterior pituitary?
In response to nerve impulses.
28
What are the two nuclei in the posterior pituitary?
Paraventricular nucleus and supraoptic nucleus.
29
What characteristics do both nuclei in the posterior pituitary share?
Both produce both hormones, both produced from same pro-hormone.
30
What does interaction of oxytocin with its receptors do?
Raises the level of intracellular calcium in the myoepithelial cells of the mammary gland.
31
What do the myoepithelial cells do in response to oxytocin?
Contract, forcing milk into ducts.
32
What is the neuro-endocrine reflex in response to suckling?
Suckling - hypothalamus - posterior pituitary - oxytocin - milk squeezed out.
33
What does ADH do?
Regulates blood osmolarity and urine output.
34
What does increased plasma osmolarity (eg hemorrhage/dehydration) stimulate?
Osmoreceptors in hypothalamus.
35
How does ADH alter the permeability of the collecting duct?
ADH present = CD highly permeable to water, ADH not present = CD not permeable to water.
36
What concentration of urine do the varying conc of ADH produce?
ADH present = small volume of conc urine, ADH not present = large volume of dilute urine.
37
How does ADH make the collecting duct more permeable to water?
Integrates aquaporins in the membrane of the CD so more water can be transported out.
38
What is the anterior pituitary?
The regulator of the endocrine system.
39
How many different hormones does the anterior pituitary secrete?
Six.
40
What do most of the six hormones released by the anterior pituitary do?
Regulate the secretions of other endocrine organs.
41
What are the six hormones released by the anterior pituitary?
Growth hormone, prolactin, adenocorticotropic hormone (ACTH), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinising hormone (LH).
42
How can the one anterior pituitary gland produce so many hormones?
Has five different cell types - somatotrophs, lactotrophs, corticotrophs, gonadotrophs, thyrotrophs.
43
What do hormones from the hypothalamus control?
Release of anterior pituitary hormones.
44
What six hormones does the hypothalamus release to control the secretory activity of the anterior pituitary?
Corticotrophin releasing hormone (CRH), gonadotropin releasing hormone (GRH), thyrotropin releasing hormone (TRH), growth hormone releasing hormone (GHRH), dopamine (DA), somatostatin (SS).
45
Where is the growth hormone synthesised and stored?
In somatotrophs.
46
What are the growth hormone’s principle targets?
Bone and skeletal muscle.
47
What direct metabolic effects does GH have?
Anabolic, glucose sparing with an anti-insulin action, protects against hypoglycaemia, conserves glucose for CNS.
48
How does GH increase muscle mass in muscles?
Decreases glucose uptake, stimulates aa uptake/ protein synthesis, inhibits protein breakdown.
49
How does GH decrease fat deposits in adipose tissue?
Decreases glucose uptake, increases lipolysis.
50
How does GH stimulate IGF production in the liver?
Increases gluconeogensis, increases protein synthesis.
51
What is an example of an indirect effect of GH?
Stimulates insulin-like growth factor.
52
What are the GH actions va insulin-like growth factors?
GH - liver - IGF - skeletal growth/ soft tissue growth.
53
How does GH promote skeletal growth via IGF?
Cartilage formation, bone deposition, lengthening and thickening.
54
How does GH promote soft tissue growth via IGF?
Protein synthesis, cell proliferation.
55
When does bone response to GH cease?
When growth plates fuse.
56
What does the somatopause cause?
Decrease in lean body mass, decline in bone mineral density, increase in body fat.
57
What external conditions can cause somatostatin release?
Stress, exercise, fasting, sleep, hypoglycaemia, amino acids, sex hormones.
58
What are growth hormones disorders usually the result of?
Pituitary tumour secreting growth hormone.
59
What is GH excess - gigantism?
Refers to abnormally high linear growth due to XS action of IGF while epiphyseal growth plates open, normal proportions as soft tissue also affected.
60
What is GH XS - acromegaly?
Increased growth hormone later in life after fusion of epiphyses (growth plates).
61
What are symptoms of acromegaly?
Course facial features, enlarged hands and feet, protruding jaw, separation of teeth, enlarged tongue, thickened lips, deep voice, cardiomegaly, diabetes.
62
What is the usual cause of acromegaly?
Usually due to pituitary tumour.
63
What is GH insufficiency in children called?
Pituitary dwarfism.
64
What are characteristics of pituitary dwarfism?
Slow growth rate below 3rd ventile, normal proportions, poor muscle development, XS subcutaneous fat.
65
What does GH insufficiency in adults cause?
No major symptoms.
66
What components of the thyroid gland can be seen from a front view vs a back?
Front = right love, isthmus, left lobe, back = parathyroid glands.
67
Why is the thyroid gland termed a discrete organ?
Adheres to the trachea.
68
What is the primary structure of the thyroid gland?
Two large asymmetrical flat lobes connected by isthmus.
69
What regulates the thyroid gland?
Hypothalamus and pituitary.
70
How does the thyroid gland develop of gestation?
Fully developed at 12 weeks, responsive to TSH at 22w, can produce T3/T4 at 14w, hormones crucial for fetal growth.
71
Why does the thyroid gland have a rich blood supply?
Has left superior artery and vein, left inferior artery and vein and middle left thyroid vein.
72
What is the name for a functional unit of the thyroid gland and whats its size?
Follicle = 200-300um in diameter.
73
How many functional units are in each thyroid gland?
1000s.
74
What does each follicle consist of in the thyroid gland?
A layer of follicular cells (simple cuboidal epithelial) surrounding a colloid-filled cavity.
75
What are the two hormones excreted by the thyroid?
Triiodothyronine (T3) and thyroxine (T4).
76
How much of T4 and T3 does the thyroid secrete?
80-100ug of T4, 5mg of T3 per day.
77
Does T3 or T4 have greater biological activity?
T3 - about 10x much greater.
78
How many iodine atoms per molecule of T3 and T4 are there respectively?
Three and four.
79
What is the hormone class of thyroid hormones?
Amino acid derived, tyrosine, iodinated.
80
What is the reverse T3?
Biologically inactive.
81
What are the half life’s of T3, T4, rT3?
1-3days, 5-7days, 5hrs.
82
What percentage of T3 and T4 are present in free form?
<0.5%
83
What are T3 and T4 bound to in plasma?
Thyroxine-binding globulin and albumin.
84
What two principle raw materials does the synthesis of T3 and T4 require?
Tyrosines and iodine.
85
What are tyrosines provided by and secreted by for thyroid hormone synthesis?
Provided by thyroglobulin, secreted by follicular cells into lumen of follicle as colloid.
86
What is iodine and how is it used in thyroid hormone synthesis?
Iodine is essential requirement, is pumped into follicular cells against con gradient, dietary iodide is oxidised to iodine.
87
What does the iodine attached to tyrosine form before linking together to form T3 and T4?
DIT - diiodotyrosine and MIT - monoiodotyrosine.
88
What two major advantages does the thyroid gland have?
Capable of storing many weeks worth of thyroid hormone, if no iodine available, hormone secretion still maintained.
89
What percentage of thyroid hormone released is T4?
90%
90
Where does enzymatic conversion of T4 into T3 take place?
Peripheral tissue.
91
How can thyroid hormones influence gene expression?
Bind to intracellular receptors, complex with thyroid response elements (TRE) that bind DNA.
92
How can thyroid hormones stimulant transcription/translation of a number of proteins?
T3-THR complex binds to thyroid response elements within DNA.
93
What effects do transcribed proteins from thyroid hormones generally have?
Increased cellular metabolism, oxygen consumption, cellular glucose, circulation and respiration and promote nervous system and skeletal development.
94
What do thyroid hormones help maintain clinically?
Energy levels, weight, thermoregulation, heart rate, GI motility, mood.
95
What cardiovascular effects do thyroid hormones have?
Increased cardiac output, increased heart rate and contractility.
96
What is the importance of thyroid hormones increasing basal metabolic rate?
Temp regulation, adaptation to cold, O2 consumption, heat production, increases mobilisation and utilisation of glucose, fat, protein.
97
How do thyroid hormones have an effect on growth and maturation?
Bone growth, synergy with growth hormone, CNS development and function, thyroid hormone deficiencies result in mental impairment and short stature.
98
What other effects to thyroid hormones have?
Respiratory, skeletal muscle function, regulation of reproductive function, synergy with catecholamines.
99
How does a thyroid hormones lead to whole boy effects?
Hormones - cellular uptake - nuclear receptor - transcription of specific gens - cellular effect - whole body effect.
100
What aspects of thyroid function does TSH stimulate?
Every aspect including promoting release of thyroid hormones and increasing activity of iodide pump and iodination of tyrosine to increase production of thyroid hormones.
101
What is the name of the negative feedback loop relating to the pituitary and thyroid glands?
Hypothalmic-pituitary axis.
102
What is hypothyroid?
Underactive thyroid, metabolic rate decreased and weight gain.
103
What is hyperthyroid?
Overactive, metabolic rate increases and weight loss.
104
What are symptoms of hypothyroidism?
Dry cold skin, sensitivity to cold, weight gain despite loss of appetite, impaired memory, mental dullness, lethargy.
105
What is the clinical exam, diagnosis and treatment of hypothyroidism?
Reduced metabolic rate and cardiac output, low plasma levels of free T3/T4, thyroxine - TSH monitoring dose determination.
106
What can cause hypothyroidism?
Iodine deficiency (endemic goitre) or autoimmune disease (hashimoto’s thyroiditis) also - congenital, post radiation/surgery, medications, stress.
107
What is Endemic goitre?
Insufficient dietary iodine, insufficient T3/T4, abnormally high TSH, abnormal thyroid growth due to trophic effects on TSH.
108
What is Hashimoto’s disease?
Most common cause of hypothyroidism, autoimmune disease, leads to thyroid gland destruction.
109
How does Hashimoto’s disease cause hypothyroidism?
Antibodies against thyroglobulin or thyroid peroxidase, interferes with thyroid hormone synthesis, antibodies against TSH receptor, prevents stimulation of T3 and T4 release.
110
What is cretinism?
Congenital hypothyroidism, lack of essential hormones for brain development, intellectual disability, short body, thick tongue and neck, could be due to lack of gland or incorrect hormone synthesis.
111
What are symptoms of hyperthyroidism?
Loss of weight, XS sweating/intolerance to heat, palpitations and irregular heartbeat, anxiety and nervousness, exopthalamus.
112
What can be seen during a clinical exam for hyperthyroidism?
Raised metabolic rate and oxygen consumption, increased heart rate, hypertension.
113
What treatment can be used for hyperthyroidism?
Surgery to remove all or part of thyroid, ingestion of radioactive iodine that destroys most active cells, drugs that interfere with ability to make T3/T4.
114
What can cause hyperthyroidism?
Autoimmune diseases like Grave’s disease.
115
What happens in graves disease?
Abnormal antibodies that mimic TSH, activates TSH receptor inducing T3/T4 release.
116
How is Graves’ disease characterised?
Goitre, exopthalmos, lid retraction, muscle weakness, heart palpitations, irritability.
117
Where are the adrenal glands located?
As a pair above the kidneys.
118
What is each adrenal gland enclosed in?
A fibrous capsule surrounded by fat.
119
What is each adrenal gland equivalent to?
Two endocrine glands.
120
What are the two sub sections of the adrenal glands?
Inner adrenal medulla and outer adrenal cortex.
121
Despite each adrenal glands function being independent what do they share?
A common blood supply and play a role in response to stress.
122
How much do adrenal glands weigh?
6-10g
123
How do adrenal glands have a rich blood supply?
Adrenal arteries arise directly from the aorta - blood flows through cortex and drains into medulla.
124
What development of the adrenal gland happens at 7 weeks of life?
The primitive adrenal medullary tissue begins to invade the cortex.
125
How is the adrenal gland developed at birth?
The medullary cell mass if fully surrounded by the cortex.
126
What section of adrenal development isn’t complete until later in childhood?
Cortical differentiation into a zona glomerulosa, zona fasciculata and zona reticularis.
127
What is the adrenal medulla?
A modified part of the sympathetic nervous system, enlarged and specialised sympathetic ganglion.
128
What catecholamine hormones does the adrenal medulla secrete?
Adrenaline (epinephrine) and noradrenaline (norepinephrine).
129
Why is the adrenal medulla not a true endocrine gland?
Not under hormonal control.
130
What is the medulla composed of?
Chromaffin cells and specialised postganglionic neurons.
131
What are the preganglionic areas of the medulla?
Splanchnic nerve fibres.
132
What neurotransmitter is used in the medulla?
Acetylcholine.
133
When are the hormones released from the adrenal glands?
In response to acetylcholine being released from splanchnic nerve fibres.
134
What percentage of medulla secretions are each hormone?
80% = adrenaline, 20% = noradrenaline.
135
What does catecholamine release occur as part of?
A general sympathetic stimulation.
136
For what response are adrenaline and noradrenaline important for?
Fight or flight response.
137
What does the fight or flight response do?
Prepares body for acute stress.
138
What are some cardiovascular effects of adrenaline?
Increases heart rate, stoke volume, blood pressure, vasodilation of coronary and skeletal muscle vessels, vasoconstriction of blood vessels to non essential tissues, bronchodilation.
139
What are some metabolic effects of adrenaline?
Increases amount of energy for immediate use, liver converts glycogen to glucose, metabolic rate increases, blood flow changes, reducing digestive system activity and urine output.
140
What receptors does adrenaline interact with primarily?
Beta receptors - beta1, 2, 3.
141
What are the three morphologically distinct zones of the adrenal cortex?
Zona glomerulosa, fasciculata, reticularis.
142
What are each zones of the adrenal cortex responsible for?
Glom = mineralcorticoids (aldosterone - salt), fasc = glucocorticoids (cortisol - sugar), reti = gondocorticoids (androgens - sex)
143
What do steroid hormones initiate?
Transcription of mRNA: protein synthesis.
144
Where is enzyme expression variable?
Between the zones of the adrenal glands - glom lacks 17 hydroxylase whilst others lack 18.
145
What do high circulating testosterone levels lead to?
Masculinisation of fetal external genitalia to variable degrees.
146
What are androgens usually thought of as?
Male hormones - but female body produces small amounts too.
147
When are adrenal androgens released and why?
Insignificant amounts of testosterone, are T (and oestrogen) precursors.
148
What do the adrenal glands produce in response to low T?
Dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S) and androstenedione.
149
Where are the adrenal androgens converted to T?
Peripheral tissues.
150
What are DHEA and DHEA-S like compared to T?
Bind less efficiently to the androgen receptors (weak steroids).
151
What controls the adrenal androgens?
ACTH (anterior pituitary).
152
What effect do adrenal androgens have in males?
Contribution of T derived from glands pales to insignificance in comparison to normal output of T from testes.
153
What two roles may T/ adrenal androgens have in males despite not fully understood?
Male secondary characteristics, aggression in young boys.
154
Does over or under secretion of adrenal androgens have any noticeable consequences in males?
No, none known.
155
What effects do the adrenal glands have in females?
Ovaries make T but most converted to oestrogen immediately, adrenal glands therefore primary source of T.
156
What do adrenal androgens do in females?
Secrete half total and organic requirement, responsible for growth of pubic and axillary hair and sex drive, kick start puberty, maintain muscle and bone mass.
157
What can lead to XS production of adrenal androgen?
Overproduction of ACTH, adrenal tumor, Cushing’s syndrome.
158
What does XS production of adrenal androgen lead to?
Masculinisation of females, acne, hirsutism, irregular periods, breast shrinkage, PCOS.
159
How is XS androgen treated?
With anti androgen (cyproterone acetate and ethinylestradiol) to block androgen receptors.
160
What is DHEA-S the most abundant of?
Circulating hormones in young adults.
161
How is aldosterone essential to life?
Absence leads to circulatory failure and death within a few days if adrenal cortex is removed.
162
How is aldosterone secretion regulated?
By the plasma levels of sodium and potassium via the renin-angiotensin system.
163
What are the principle actions of aldosterone?
Control ECF volume, conserve body sodium, stimulate reabsorption of sodium in renal distal convoluted tubules in exchange for potassium.
164
How is aldosterone release controlled?
In response to renin-angiotensin system, decreased ECF volume and decreased renal blood flow, response to high plasma potassium.
165
What is a powerful stimulator of cortisol production and what does this include?
Stress - physical trauma, intense heat or cold, infection, mental or emotional trauma.
166
What does cortisol do?
Mediates body’s response to stress in response to endocrine signals, metabolic effects, increased plasma glucose and FFA conc, provide energy substrates to body tissues for response to stress.
167
How does cortisol increase catabolism?
Increases skeletal muscle protein catabolism, amino acids converted to glucose.
168
How does cortisol increase lipolysis?
Liberates free fatty acids and triglycerides from adipose tissue, used as energy source.
169
How does cortisol increase intake?
Stimulates appetite, weight gain.
170
Why can cortisol lead to enhanced obesity?
Causes fat stores and XS circulating fat to be relocated and deposited deep in abdomen.
171
Other than stress control and weight gain what other actions does cortisol take?
May contribute to emotional instability, anti-inflammatory, blocks processes which lead to inflammation, immunosuppressive, fall in antibody production and number of circulating lymphocytes, used clinically to treat following transplants.
172
What disease can lead to adrenal cortex hyper function?
Cushing’s disease.
173
What is Cushing's disease?
Overproduction of cortisol likely as a result of adrenal tumour or pituitary tumour.
174
What does Cushing's lead to?
Redistribution of body fat, muscle wastage, thin skin, bruising, changes in metabolism, hyperglyceamia, hypertension.
175
What is hypertension in Cushing's, what are treatments?
Cortisol in XS binds to aldosterone receptor, treatment = surgery radiation, medication.
176
What are two significant features of Cushing's?
Moon face and potbelly.
177
What are key characteristics of Conns disease - adrenal cortex hyperfunction?
Mineralocorticoid XS, rare, overproduction of aldosterone, retention of sodium, loss of potassium and alkalosis, hypertension through expansion of plasma volume.
178
What is Addison's diease?
Adrenal cortex hypofunction, rare, damage to glands/autoimmune, deficits in corticoids, weakness, weight loss, pigmentation and mucosal membranes.
179
How is XS melanin produced in Addison's disease?
XS ACTH act on melanocytes to produce melanin.
180
At what levels does calcium play a fundamental role?
Microscopic and macroscopic level.
181
What are some key processes that calcium is important in?
Component of bones and teeth (99% total), normal excitability of nerve and muscle cells, neurotransmitter and hormone release, muscle contraction, activation of enzymes, coagulation of blood, milk production.
182
How does calcium occur in nature?
Does not exist freely, mostly in soil systems as limestone, gypsum and fluorite.
183
How does calcium occur in the body?
Most abundant mineral, average adult body contains app 1kg, 0.1% in ECF, 1% in the cells, rest (.99%) in skeleton - hydroxyapatite.
184
How can bones serve as large reservoirs of calcium?
Release calcium when extracellular fluid concentration decreases and storing XS calcium.
185
What is the plasma calcium concentration?
2.2-2.6mM.
186
What are the three types of calcium in the body?
Protein-bound, ionised or free, complexed or chelated.
187
What is protein bound calcium?
Cannot diffuse through membranes and thus is not usable by tissues.
188
What is ionised or free calcium?
Physiologically active form.
189
What is complexed or chelated calcium?
Bound to phosphate, bicarbonate, sulfate, citrate and lactate.
190
What is hypocalcemia?
Too low levels of calcium that causes involuntary muscle contraction.
191
What is tetany caused by hypocalcemia?
Neuronal hyper-excitability.
192
How does hypocalcemia occur?
Low ionised calcium levels in the ECF increases the permeability of neuronal membranes to sodium ions, causes a progressive depolarisation which increases the possibility of APs.
193
What is hypercalcemia?
Too high levels of calcium leading to depression and kidney damage/stones, neurons less excitable.
194
What are three primary control points for calcium?
Absorption via intestines, excretion via kidney/urine, temporary storage via bones.
195
What form must calcium be in before it can be absorbed?
Soluble and ionised form.
196
What is regulation of calcium closely associated with?
Phosphate.
197
What three types of cells are important for bone formation and reabsorption?
Osteoblasts, osteoclasts, osteocytes.
198
What is the role of osteoblasts?
Synthesise and secrete collagen and promote deposition of calcium phosphate crystals, secrete factors that activate osteoclasts.
199
What is the role of osteoclasts?
Promote resorption of bone.
200
What is the role of osteocytes?
Essential role in exchange of calcium between ECF and bone.
201
What is known as hydroxyapatite?
Calcium phosphate - Ca10(PO4)6(OH)2
202
What is the acute control of calcium regulation?
Maintain constant free Ca2+ conc in plasma, rapid exchange between bone and ECF.
203
What is chronic control of calcium regulation?
Maintain total level in body long term, adjust GIT absorption and urinary excretion.
204
What is essential to be maintained in regards to calcium?
Intra and extracellular levels within narrow limits.
205
What is plasma Ca2+ conc determined by?
Net absorption of Ca2+ from GIT, net excretion of Ca2+ in urine, exchange of Ca2+ with bone.
206
What three hormones, in order of importance, control plasma Ca2+ conc?
Parathyroid hormone, 1,25-dihydroxycholecalciferol, calcitonin.
207
What is the role of the parathyroid hormone (PTH) gland?
Gland monitors conc of calcium in blood perfusing the glands.
208
What are the structural measurements on the PTH gland?
3-8mm in length, 2-5mm in width, total weight 1.6g.
209
What happens if the PTH gland is removed?
Fatal hypocalcemia.
210
What are key characteristics of the parathyroid hormones?
Peptide hormone, stored within chief cells, half life 5 mins.
211
How is the PTH secreted and released and whats its role?
Secreted continuously at low rate, released in response to low blood calcium, exerts effects on bone gut and kidneys.
212
What is the main target tissue of the PTH?
Kidney and bone.
213
How does PTH activate vitamin D?
Increased reabsorption of calcium from urine, fast acting decrease urinary calcium in mins, increased expression of enzyme 1alpha-hydroxylase.
214
What effect does the PTH have on bone?
Increased osteoclast activity indirectly causing increase in bone reabsorption.
215
Where is vitamin D2 from?
Plant sources.
216
Where is vitamin D3 from?
Obtained from diet, food supplements and synthesised in the skin in the presence of sunlight.
217
Are D2 and D3 active?
No, relatively inactive.
218
What are vitamin D2/D3 converted to?
1,25 dihydroxycholecalciferol AKA 1,25-dihydroxyvitaminD AKA 1,25-(OH)2D3 AKA calcitriol.
219
Why is vitamin D not a true vitamin?
People whose skin is exposed to sufficient sunlight do not need a dietary source.
220
What are the key roles of calcitriol?
Acts on cells on GIT to increase production of calcium transport proteins leading to increase in Ca uptake from GIT.
221
The calcitriol mechanism the only one to do what?
Increase calcium stores.
222
What is the action of calcitriol in bone?
Increasing rate of bone resorption, increases the secretion of osteoclast activating factors.
223
What is the action of calcitriol in the kidney?
Minor effect in decreasing urinary loss of calcium.
224
What inhibits PTH secretion and what inhibit PTH synthesis?
Hypercalcaemia and 1,25-dihydroxycholecalciferol respectively.
225
What is calcitonin used for?
To treat osteoporosis in postmenopausal women.
226
How does calcitonin work?
Secreted by C cells of thyroid gland, lowers level of free plasma calcium, inhibition of osteoclast activity (bone resorption reduced), increased excretion of calcium and phosphate by kidneys.
227
What are the major hormonal regulators of plasma calcium?
PTH, 1,25-(OH)2D3 and possibly calcitonin.
228
What other hormones are involved in regulation of plasma calcium?
Growth hormone, adrenal glucocorticoids and thyroid hormones, oestrogen and androgens.
229
What disorders cause hypercalcaemia and hypocalcaemia respectively?
Hyperparathyroidism and vitamin D deficiency.
230
What pathological causes of primary hyperparathyroidism/ hypercalcaemia is there?
Inappropriate secretion of PTH, elevated PTH and raised serum calcium, 85% caused by single parathyroid adenoma.
231
Where is hyperparathyroidism presented?
Bones, stones, abdominal groans and psychic moans.
232
Give a short summary and overview of processes that change in hyperparathyroidism?
Increased bone resorption, increased GIT absorption, decreased renal excretion.
233
What is rickets?
Skeletal deformities of weight bearing bones in children.
234
How does vitamin D deficiency (hypocalcemia) lead to rickets?
Bone remodeling impaired, failure of calcification.
235
What are causes of vitamin D deficiency?
Poor diet, malabsorption, decreased sunlight, liver or kidney disease.
236
Other than rickets what is another examples of a disease due to hypocalcemia?
Osteomalacia.
237
What does hypocalcemia lead to?
Increased excitability of nervous tissue, pins and needles, tetany, muscle cramps, convulsions.
238
What does vitamin D deficiency lead to?
Reduction in intestinal calcium absorption.
