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ENDO-SOM Flashcards

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1
Q

what are hormones?

A
  • chemical messengers that have an effect on target organs

- only specific target cells with specific receptor will respond to hormone

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2
Q

what are the 4 classifications of hormones?

A
  • steroid hormones (lipid-derived hormones)
  • amino acid derived hormones
  • peptide hormones
  • Eicosanoids (chemical messengers derived from fatty acid
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3
Q

what is autocrine signalling?

A

when a cell sends signals to itself

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4
Q

what is endocrine signalling?

A

signalling using the circulatory system to transport ligands

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5
Q

what is paracrine signalling?

A

neighbouring cells signal to each other

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6
Q

what are examples of steroid hormones hormones?

A

mineralcorticoids
glucocorticoids
sex hormones-androgens

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7
Q

what are steroid (lipid derived) hormones derived from?

A

cholesterol—>pregnenolone…

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8
Q

where are amino acid derived hormones generally derived from?

A

tyrosine

tryptophan

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9
Q

what are examples of amino acid derived hormones?

A
  • thyroid hormones-T3/T4

- catecholamines

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10
Q

what are peptide hormones formed from?

A

amino acid chains

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11
Q

what type of hormones are the most common?

A

peptide

eg oxytocin/ TSH/ prolactin/ insulin

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12
Q

why can’t peptide hormones pass through phospholipid bilayer?

A

not lipid-soluble

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13
Q

what are chemical messengers derived from fatty acids important in?

A

inflammation , blood pressure , clotting

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14
Q

what is a receptor?

A

protein molecule usually embedded within plasma membrane surface of cells
-receives chemical signals from outside of cell

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15
Q

what are the different types of receptors?

A
  • intracellular (eg steroid hormone receptors)

- cell surface

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16
Q

what do cell surface receptors do?

A

perform signal transduction-converting extracelular signal to intracellular signal

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17
Q

what are the types of cell-surface receptors?

A
  • G protein-linked receptors
  • enzymes-linked receptor
  • ion channel-linked receptors
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18
Q

how does binding to G protein-linked receptors work?

A
  • ligand binds to receptor
  • activates G protein
  • G protein interacts with either iron channel or enzyme in mem
  • each receptor has own specific extracellular domain and G-protein binding site
  • GDP—–>GTP once bound to G protein receptor
  • GTP binds to adenyl cyclase-activates it
  • catalyses conversion of ATP to cAMP
  • cAMP activates PKAs
  • GTP is hydrolysed to GDP + pi
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19
Q

how do enzyme-linked receptors work?

A

-cell surface receptors with intracellular domains are associated with enzymes
-have large extracellular and intracellular domains
-when ligand binds to extracellular domain-signal is transferred-activates enzyme component of the receptor which leads to a response
Eg-tyrosine kinase-insulin binds to

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20
Q

how do ion channel-linked receptors work?

A
  • Ligand binds to receptor
  • conformational change in protein structure-allows ions eg Na+, Ca2+, Mg2+ and H+ to pass through
  • change activity of ion-binding enzymes and voltage-sensitive channels-to produce response
  • eg neurons with ACh and serotonin
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21
Q

what is receptor down-regulation?

A

-receptors exposed to excessive ligands results in ligand-induced desensitisation or internalisation of that receptor

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22
Q

what is receptor up-regulation?

A

-super sensitised cells after repeated exposure to drug or prolonged absence of ligand

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23
Q

are receptor agonists up-regulation or down-regulation of their respective recpetors?

A

down-regulation of their respective receptors

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24
Q

are receptor antagonists up-regulation or down-regulation of their respective receptors?

A

up-regulation

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25
what is the blood vessel network called that connects the pituitary gland to the hypothalamus?
hypothalamohypophyseal-portal system
26
what are the 5 subtypes on anterior pituitary cells and what do they secrete?
- somatotroph- GH secreting - corticotroph- ACTH secreting - thyrotroph- TSH secreting - gonadotroph- LH/ FSH secreting - lactotroph- prolactin secreting
27
where is the anterior pituitary derived from in embryology?
from the ectoderm of Rathke's pouch
28
where is the posterior pituitary derived from in embryology?
from the downward extension of neural ectoderm forming the floor of diencephalon
29
what are the types of hypothalamic signals to the pituitary?
- stimulatory | - inhibitory
30
what are the main functions of growth hormone in children?
-linear growth
31
what are the main functions of GH in adults?
- protein synthesis - carbohydrate metabolism - lipolysis - calcium homeostasis
32
what is IGF-1?
insulin-like growth factor 1
33
what is the role of IGF-1?
-produced in the liver in response to GH stimulation, mediates most GF effects
34
what can be used to help diagnose GH abnormalities?
plasma levels of IGF-1
35
what are the 3 parts of the adrenal cortex?
- zona glomerulosa (outermost) - zona fasciculata (middle) - zona reticularis (inner)
36
what hormones are secreted by the zona glomerulosa and what does it help to regulate?
-secretes mineralcorticoids important in fluid homeostasis. EG. aldosterone-regulates absorption/uptake of K+ and Na+ levels in the kidney
37
what hormones are secreted by the zona fasciculata? Give an example of a specific hormone and what it does.
-secretes glucocorticoids -important for carbohydrate, protein and lipid metabolism EG.cortisol which raises blood glucose and cellular synthesis of glycogen
38
what is the secretion of cortisol controlled by?
Its secretion is controlled by a hormone from the pituitary - ACTH.
39
what is secreted by the zona reticularis?
secretes androgens | (and small amounts of glucocorticoids)
40
what are glucocorticoids?
class of steroid hormone-widely used for inflammatory and autoimmune diseases e.g. cortisol
41
what are mineralcorticoids?
Mineralocorticoids are a class of steroid hormones that regulate salt and water balances e.g. Aldosterone
42
describe the CRH-ACTH-cortisol axis. | hypo-pit-adrenal axis
- hypothalamus releases CRH (corticotropin-releasing hormone) - stimulates anterior pituitary gland to release ATCH (adrenocorticotropic hormone) - stimulates adrenal cortex (z.f.) to release cortisol
43
what are the main functions of cortisol?
- increase glucose production (increase gluconeogeneis/ hepatic glycogen synthesis/ inhibits peripheral glucose uptake) - inhibits protein synthesis - increases protein breakdown - stimulates lipolysis - increases appetite - increases sodium retention and potassium loss-inflammatory response - make vessels vasoconstrict-raise BP - suppress immune response - forms essential part of the body’s response to stress-fight or flight
44
describe the negative feedback loops in the CRH-ACTH-cortisol axis.
- cortisol can reduce its own secretion via feedback to the anterior pituitary to reduce ACTH and the hypothalamus to limit the secretion of CRH - ACTH also provides negative feedback limiting its secretion via CRH
45
describe the TRH-TSH-thyroid axis. | hypo-pit-thyroid axis
- hypothalamus releases TRH (thyrotropin-releasing hormone) - stimulates anterior pituitary to release TSH (thyroid-stimulating hormone) - stimulates thyroid to release T3/ T4-which produce effect on target tissues/organs
46
describe the negative feedback loops in TRH-TSH-thyroid axis.
Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland
47
outline the main functions of thyroid hormones (T3/4).
- CARDIOVASCULAR: increase heart rate and cardiac output - BONE: increased bone turnover and resorption - GI: increased gut motility - LIPIDS: increased lipolysis - SYMPATHETIC NERVOUS SYSTEM: increased catecholamine sensitivity
48
which hormones are released from the posterior pituitary?
- oxytocin | - ADH (vasopressin)
49
what are the roles of vasopressin (ADH)?
- increase in reabsorption of water - increases blood vol - increases blood pressure
50
what are the roles of oxytocin?
- roles in female reproduction. -released in large amounts during labor, and after stimulation of the nipples - a facilitator for childbirth and breastfeeding.
51
what are the limits in which normal blood glucose is regulated within?
4.0-7.0 mmol/L
52
what are the 2 main pancreatic endocrine hormones involved in regulating blood glucose?
- glucagon | - insulin
53
what are the 4 main glucose receptors and where are they situated?
- GLUT1-brain/ RBCs/ placenta - GLUT2-liver/kidneys/ intestine - GLUT3-brain - GLUT4-muscle/ adipose tissue
54
how is glucose uptake from gut and glomerular filtrate in kidney achieved?
by Na+ dependent glucose transporters not GLUT 1-Na+ gradient from lumen to the cell is needed for glucose uptake 2-transport is saturable -if glucose in lumen rises above certain level not all glucose is absorbed-causes glucosuria in diabetes (glucose in urine)
55
what are the 2 minor pancreatic endocrine hormones?
- somatostatin-inhibits secretion of pancreatic hormone-including insulin and glucagon - pancreatic polypeptide-secreted by PP cells decreases food intake and increases energy expenditure
56
what are the pancreatic endocrine cells called?
Islets of Langerhans
57
which cells make up the Islets of Langerhans and what do they secrete?
- alpha cells-secrete glucagon | - beta cells-secrete insulin
58
what stimulates insulin release?
- high blood glucose - parasympathetic system - Gastric inhibitory polypeptide GIP and GLP-1 (2 primary incretin hormones) secreted from the intestine upon ingestion of glucose to stimulate insulin secretion
59
how many amino acids make up insulin?
51
60
state the steps outlining how beta cells work to release insulin.
1-K channels open at rest- K+ ions diffuse out of cell creating PD across cell (inside more -ive than outside) 2-when glucose conc high-enters beta cells through GLUT2 transporter 3-glycolysis occurs in b-cell-generating ATP 4-causes K+ channel to close-PD across cell becomes +ive 5-chanmge in PD causes Ca2+ V.G. channel to open 6-Ca2+ enters cell 7-causes vesicles containing insulin to fuse with p. membrane and release 8-increase in GLP1 stimulates the release of insulin
61
what are the actions of insulin?
- increases glucose uptake into fat and muscle - stimulates glycogen synthesis - stimulates storage of triglyceride in adipose tissue - increases protein synthesis - decreases hepatic gluconeogenesis
62
what is the role of GLUT4 in glucose uptake?
-insulin binds to receptor and initiates recruitment of GLUT4 to cell surface-integrated into cell mem allow glucose to be transported into cell
63
what are the effects of feeding on the liver?
- rise in nutrients - increased in glycogen synthesis - reduced gluconeogenesis-(reduced glucose/ ketones/ amino acids in blood) - increased protein synthesis
64
what are the effects of feeding on fat?
- increased lipogenesis | - decreased lipolysis- (reduced fatty acids in blood)
65
what are the effects of feeding on muscle?
- increased glycogen synthesis - reduced gluconeogenesis - increased protein synthesis - switch to carbohydrate oxidation
66
what is the effect of glucagon on blood glucose levels?
-raises blood glucose level
67
what is the main target organ of glucagon?
liver
68
how does glucagon raise blood glucose levels?
- stimulates glycogen breakdown and inhibits glycogen synthesis - inhibits FA synth by diminishing production of pyruvate - stimulates gluconeogenesis in liver and blocks glycolysis
69
what state is the body in to stimulate glucagon?
fasting
70
what effect does fasting state have on liver?
- reduced glycogen synth - reduced protein synth (low glucose/ high ketone/ low AA in blood) - increased gluconeogenesis
71
what effect does fasting state have on fat?
- reduced lipogenesis (increased FA in blood) | - increases lipolysis
72
what effect does fasting state have on muscle?
- reduced glycogen synth - increased gluconeogenesis - reduced protein synth - switch to lipid oxidation -fat burning
73
how many amino acids make up glucagon?
29
74
whats the half-life of insulin?
5 mins
75
whats the half-life of glucagon?
4-6mins
76
what stimulates glucagon release?
low blood glucose
77
what inhibits insulin release?
sympathetic activity
78
name the different types of diabetes?
- TYPE 1 - TYPE 2 - TYPE 3c - LADA - MODY - SCONDARY DIABETES
79
what is type 3c diabetes secondary to?
pancreatic disease
80
what is LADA diabetes?
late inset autoimmune disease leading to diabetes
81
what is MODY diabetes?
maturity onset diabetes of the young-rare inherited form of type 2
82
what is secondary diabetes?
Secondary diabetes is diabetes that results as a consequence of another medical condition. eg from crushing's syndrome/ haemochromatosis
83
what is the ration of people in the UK who suffer from type 1 diabetes?
1:3000
84
what is hyperglycaemia?
blood sugar exceeds normal limits
85
what is hypoglycaemia?
blood sugar below normal limits
86
what caused type 1 diabetes?
-autoimmune disease causing islet cell destruction
87
how does type 1 diabetes affect how insulin works?
- complete insulin deficiency - uncontrolled gluconeogenesis - failure of glucose uptake into muscles and fats
88
what does type 1 diabetes lead to if untreated?
- development of hyperglycaemia - ketoacidosis- ketone build up - eventual coma and death
89
what can occur is there is insulin excess?
hypoglycaemia - can occur in diabetes treatment - serious as brain starved of glucose
90
what are the risk factors for type 2 diabetes?
- older age (as generally late onset 40+) - obesity - inactivity - family history - ethnicity
91
what is type 2 diabetes caused by?
- insulin resistance | - insulin deficiency
92
how does insulin resistance cause type 2 diabetes?
- peripheral tissues not responsive to insulin - higher levels of insulin required to keep blood glucose in normal range - genetic component - exacerbated by obesity and lack of physical activity
93
how does progressive insulin deficiency cause type 2 diabetes?
- pancreas does not make enough insulin - amyloid and fat deposits - defective incretin response
94
what effect does type 2 diabetes have on fat cells?
- reduced insulin response - high cholesterol - high blood pressure - inflamed arteries - increased blood clotting
95
how can type 2 diabetes lead to hyperglycaemia?
- pancreatic beta-cells initially compensate for insulin resistance by increasing production-maintaining normal blood glucose levels - in. most patients b-cell function worsens-leading to hyperglycaemia
96
where is the thyroid gland located?
-thyroid gland located immediately below the larynx and anterior to upper part of trachea
97
what is the name of the narrow band that connects the 2 lobes of the thyroid gland?
isthmus-which overlies 2nd to 4th tracheal cartilage
98
what are the functional units of the thyroid gland?
follicles
99
which cells are interspersed between follicles in the thyroid gland and what do they secrete?
C cells | -secrete calcitonin for calcium homeostasis
100
what do thyroid gland follicles consist of?
- layer of epithelium | - central cavities containing colloid-constiuents=large glycoproteins/ thyroglobulin
101
what are follicular cells of the thyroid gland dependent on?
TSH
102
which molecules are essential for synthesis of thyroid hormones?
- iodine | - tyrosine
103
what is tyrosine synthesised from?
thyroglobulin
104
outline the steps in thyroid hormone synthesis.
1-IODINE TRAPPING- iodine is actively transported and iodide into cytosol of follicular cells in response to TSH 2-SYNTHESIS OF THYROGLOBULIN (TGB)- TGB produced in RER and golgi packaged in secretory vesicles-released into follicle lumen by exo -occurs at same time as iodine trapping 3-OXIDATION OF IODINE -I- is oxidised to iodine-when it passed through membrane into follicle lumen 4-IODINATION OF TYROSINE -iodine reacts with tyrosine aas of TGB -binding of single I forms monoiodtyrosine -binding of 2-diiodotyrosine -region of TGB with attached I atom=colloid 5-COUPLING OF T1 and T2 2x T2= T4 T1 + T2= T3 5-PINOCYTES AND DIGESTION OF COLLOID -parts of colloid re enter follicular cells via pinocytosis and merge w lysosomes -TGB broken down by digestive enzymes, T3/ T4 cleaved off
105
what % of hormones released from the thyroid appear as T4 and what happens to the majority of T4 hormones?
90% | -mostly converted to from T4 to T3 (from monoiodoination of T4)
106
where does the conversion of T4 to T3 occur?
liver | kidneys
107
describe the secretion of thyroid hormones
- T3 and T4 are lipid soluble (even though aa derivatives) so diffuse out of follicular cell into interstitial fluid via plasma membrane then into blood - T3 and T4 bind to thyroxine binding protein in the blood to be transported to target cells
108
what are some physiological roles of thyroid hormones?
- increase ATP production-Na+/ K+ ATPase synthesis, ^ mitochondria/ ^ respiration enzymes - increase heart rate, BP, and force of heart beat-up-reg B-andrenergic receptors-increase catecholamine binding - BMR can increase by 60-100% - increase production of GH and IGFs-results in increase of formation of ossification centres in bone
109
what is the sympathomimetic effect of thyroid hormones?
thyroid hormone increase target cell responsiveness to catecholamines-SNS/ ADRENAL
110
what is a sympathomimetic effect?
any action like one produced by the sympathetic nervous system
111
describe the mechanism of thyroid hormone release
- TSH binds to TSH receptor on cell surface | - activates secondary messenger-cAMP from ATP
112
which hormone do thyroid hormones stimulate?
-growth hormone-important i promoting growth and development of brain during fetal and postnatal life
113
what are the symptoms of hypothyroidism?
- weakness - cold intolerant - mental slowness - dry skin - depression - muscle cramps - infertility - Mild weight gain - hoarseness - constipation
114
what are the signs of hypothyroidism?
- bradycardia - dry skin - relayed relaxation - hypertension - slow speech - slow movements - non-pitting edema
115
what are some of the causes of hypothyroidsim?
- autoimmune (Hashimoto’s) thyroiditis - atrophic - iodine 131 treatment - pituitary disease
116
what are some of the causes of hypothyroidism?
- autoimmune (Hashimoto’s) thyroiditis - atrophic - iodine 131 treatment - pituitary disease
117
how could you assess hypothyroidism in a labortory evaluation?
- -increased TSH-most sensitive test-primary hypo | - -anti-thyroid peroxidase TPO and anti-thyroglobulin Tg antibodies-suggest Hashimoto’s thyroiditis
118
what can be used as a therapy for hypothyroidism?
T4 | -can alleviate symptoms
119
what is T4?
Thyroxine
120
what is T3?
triiodothyronine
121
what is primary hypothyroidism caused by?
low levels of blood thyroid hormone due to destruction of the thyroid gland.
122
what is secondary hypothyroidism?
-failure of the pituitary gland to secrete thyroid stimulating hormone (TSH). --This is usually caused by a tumor in the region of the pituitary.
123
what specific roles is T3 involved in?
- maintain muscle control - brain function - development - heart functions - digestive functions
124
what specific roles is T4 involved in?
- metabolism - mood - body temperature
125
what shape is used to describe the suprarenal glands?
pyramidal
126
how much do the suprarenal glands weigh?
5g
127
why are the adrenal glands yellow on colour?
high lipid content
128
which artery supplies the suprarenal glands?
superior suprarenal artery
129
which vein drains the adrenal glands?
suprarenal veins
130
what percentage of the adrenal cortex does the zona glomerulosa make up?
15%
131
what percentage of the adrenal cortex does the zona fasciculata make up?
80%
132
what percentage of the adrenal cortex does the zona reticularis make up?
5%
133
what is the role of aldosterone?
regulates blood pressure- stimulates the conservation of sodium and eliminate potassium, enhancing the absorption of water by kidneys and other glands
134
how is aldosterone production regulated?
renin-angiotensin system
135
describe the renin-angiotensin system in aldosterone production
- change in blood pressure (low-renal perfusion) -detected by baroreceptors (or low Na+ detected by macula densa cells) stimulates the release of renin to be released from the kidney - renin acts on angiotensin to form angiotensin I - angiotensin-converting enzyme is released from lungs - ACE acts on angiotensin I to from angiotensin II - angiotensin II acts on adrenal glands to stimulate release of aldosterone from zona g. of adrenal cortex
136
how is aldosterone synthesised?
in zona glomerulosa - Angiotensin II binds to GPCR - ATP--->cAMP - activates protein kinase C - PKC and calcium stimulate the conversion of cholesterol to aldosterone in the mitochondria
137
what are examples of diseases of the adrenal cortex due to hormonal overproduction?
- Conn's syndrome | - Cushing's syndrome
138
what causes Conn's syndrome?
- excess of mineralcorticoid-aldosterone | - controls sodium and potassium in the blood
139
what causes Cushing's syndrome?
-glucocorticoid excess-excess cortisol
140
what are the clinical features of Cushing's syndrome?
- irritability - moon faced - interscapular fat - hypertension - diabetes - osteoporosis - bruising - muscle weakening - striae (stretch marks)
141
how would you confirm diagnosis of Cushing's syndrome?
-24 hour urine free cortisol -salivary cortisol -midnight cortisol Overnight dexamethasone suppression test -serum ACTH -CRH/ high dose dexameth suppression test -pituitary MRI scan -inferior petrosal sinus sampling -CT scan adrenals
142
what does high levels of aldosterone (Conn's) cause?
- hypertension - hypokalaemia - metabolic alkalosis
143
how would you confirm Conn's syndrome?
- high aldosterone to renin ratio - use CT/MRI SCAN - adrenal vein sampling-allows differentiation between unilateral and bilateral aldosterone production - surgical Rx-adrenalectomy - medical rX-aldosterone antagonists-spironolactone, amiloride, triamterene
144
how is cortisol synthesised?
- in zona f. - ACTH binds to GPCR receptor - ATP--->cAMP - activates protein kinase A - stimulates the conversion of cholesterol to cortisol in mitochondria
145
when are cortisol levels highest?
morning
146
what are the actions of cortisol in gluconeogenesis?
- hepatic glycogen synthesis | - inhibit peripheral glucose uptake
147
what are the actions of cortisol in lipolysis?
- Increased appetite | - Fat deposition
148
what are the actions of cortisol in protein catabolism?
Decreased protein synthesis
149
what are the actions of cortisol affecting sodium retention?
- Potassium loss | - Anti-inflammatory
150
what are the causes of primary adrenal insufficiency of cortisol?
- autoimmune adrenalitis - infections - neoplastic infiltration and metastasis - infiltration - thrombosis - adrenal haemorrhage
151
what are the causes of secondary adrenal insufficiency of cortisol?
- pituitary diseases | - drugs-long term steroids
152
what are the clinical features of Addison's disease?
- weight loss - skin pigmentation-^ACTH--> ^melanin - dizziness and postural hypotension-low aldosterone-->low blood vol (due to low reabsorption by kidneys)-also dehydration - hypoglycaemia-low cortisol=reduced gluconeogenesis-causes fatigue
153
what is the name of primary adrenal insufficiency of cortisol?
Addison's disease | and insufficient aldosterone
154
what is the name of secondary adrenal insufficiency of cortisol?
Hypopituitarism
155
what could be used to diagnose adrenal insufficiency?
- hyponatraemia and hyperkalaemia - inappropriately low cortisol for the level of stress - short synacthen - anti-adrenal antibodies - Endocrine tests for thyroid/ pit - imaging CT-abdomen/ MRI-pituitary
156
how would you initially treat adrenal insufficiency?
IM/ IV hydrocortisone
157
how would you later treat adrenal insufficiency?
oral hydrocortisone and fludrocortisone
158
what are examples of 2 adrenal androgens?
- --->dehydroepiandrosterone (DHEA) | - ----->androstenedione
159
where are adrenal androgens secreted from?
zona reticularis
160
what is the secretion of androgens controlled by?
ACTH
161
what are androgens?
hormones that contribute to growth and reproduction in both men and women
162
what may excess adrenal androgens lead to in pre pubertal boys?
precocious development of secondary sexual characteristics
163
what may excess adrenal androgens lead to in female foetus?
pseudo hermaphroditism
164
which class of hormones are secreted from the adrenal medulla?
catecholamines
165
which hormones are examples of catecholamines?
- adrenaline | - noradrenaline
166
how is adrenaline synthesised?
1-catecholamines formed by hydroxylation and decarboxylation of tyrosine 2-tyrosine transported into catecholamine-secreting neurons and adrenal medullary cells 3-converted in to DOPA and Dopamine in cytoplasm 4-catecholamines are released from autonomic neurons and adrenal medullary cells by exocytosis
167
outline the actions of catecholamines
- prepare body for sympathetic fight-or-flight response - breakdown of glycogen to glucose-glycogenolysis - breakdown of fats---->fatty acids - increase rate and force of cardiac muscle contraction - enables body to deal with physical and psychological stress
168
what is pheochromocytoma?
adrenal medullary catecholamine secreting tumour | example of adrenal medullary hormone hypersecretion disorders
169
what is the clinical representation of pheochromocytoma?
- hypertension - palpitations - sweating - heat intolerance - pallor - flushing - pyrexia - headache
170
how would pheochromocytoma be diagnosed?
-high 24hr catecholamine excretion -high plasma meta and noretanephrines -MRI/ CT MIBG scan
171
how could you manage and then treat pheochromocytoma?
manage: alpha and beta blockers treatment: surgery
172
how much is the total body calcium?
approx 1000g
173
what percentage of calcium is stored in bones as hydroapatite?
99%
174
where is 1% located of calcium located?
- blood - extracellular fluid - soft tissues
175
what are the functions of calcium in the body?
- cell division - plasma membrane integrity - protein secretion - neural excitability - cell adhesion - glycogen metabolism - muscle contraction-includes cardiac - neuronal excitability - blood coagulation
176
what is the daily calcium requirements for children?
350-550 mg/day
177
what is the daily calcium requirement for teens?
800-1000 mg/day
178
what is the daily calcium requirements for adults?
700 mg/day
179
what is the normal range of Ca levels in serum?
2.18 to 2.62 mmol/L
180
what happens if blood calcium levels drop?
1-release of PTH from chief cells of the parathyroid | 2-causes effects on bone/ kidneys/ intestines increasing blood calcium levels
181
what are the effects of PTH on bone?
- inhibits osteoblasts - stimulates osteoclasts - bone is broken down-releasing calcium ions into bloodstream
182
what are the effects of PTH on the kidneys?
- PTH stimulates kidney tubule cells to recover waste calcium from the urine - PTH stimulates kidney tubule cells to release calcitriol
183
what are the effects of calcitriol on the intestines?
-stimulates intestines to absorb calcium from digesting blood
184
what happens if blood calcium levels are high?
-high conc of calcium stimulate parafollicular cells in the thyroid to release calcitonin
185
what are the effects of calcitonin on bone (target organ)?
- stimulates osteoblasts - inhibits osteoclasts - calcium is removed from blood and used to build bone - lowering blood calcium
186
what are 80% of phosphates stored as in the bones and where is the rest stored?
- stored as hydroxyapatite in bones | - in soft tissues both as inorganic and organic molecules
187
what do phosphates in bones help with?
-skeletal integrity
188
what are the roles of phosphate in the body?
- bone and teeth formation - DNA synthesis - ATP synthesis - cell membrane constituent-phospholipids
189
what is the daily requirement of phosphates?
550mg
190
what is the range of blood phosphate levels?
0.8-1.5 mmol/L
191
what is the systematic regulation of phosphates maintained by and where?
maintained by: - PTH feedback - vitamin D - intestines - kidney - bones
192
name 2 disorders of phosphate homeostasis?
- hypophosphataemia | - hyperphosphataemia
193
name 2 disorders of phosphate homeostasis?
- hypophosphataemia | - hyperphosphataemia
194
what are the features of hypophosphataemia?
- decreased intestinal absorption - increased renal wasting - redistribution of ECF into cells
195
what are the clinical consequences of hypophosphataemia?
- 5% of hospitalised patients/ 30% in alcoholics - poor growth in children - fatigue, weakness, loss of appetite - bone pain/ fragile bones
196
what are the features of hyperphosphataemia?
- decreased renal excretion - acute exogenous phosphate load - redistribution of intracellular phosphate to extracellular space
197
what are the clinical consequences of hyperphosphataemia?
- hypocalcaemia - soft tissue calcification - calcification of arteries and heart valves
198
where are the parathyroid glands situated and how many are there?
-4 small glands on posterior part of thyroid gland
199
name the 2 cell types which make up the parathyroid gland.
- chief cells | - oxyphil cells
200
what are chief cells of the parathyroid responsible for?
synthesising and secreting parathyroid hormone-PTH
201
where do the parathyroid glands develop from?
-develop from endoderm of 3 and 4 pharyngeal pouches
202
what is the role of the parathyroid glands during gestation?
control calcium balance in foetus
203
how does PTH act on bones?
PTH---->stimulates osteoblasts---->stimulates RANK ligand------>allows differentiation from osteoblast to osteoclast------->cause resorption of bone----->Ca released into blood stream
204
how does PTH act on kidneys?
- Increases Ca reabsorption----->decreased phosphate reabsorption - increases activation of Vit D
205
describe the indirect effect of PTH on small intestines.
- increase in active Vit D due to its action on kidneys | - Vit D increases absorption of Ca and phosphate from intestines
206
what are 3 disorders of the parathyroid?
- hyperparathyroidism - hypoparathyroidism - pseudohypoparathyroidism
207
what is hypoparathyroidism due to?
-high levels of PTH and Ca
208
what are the 3 different types of hyperparathyroidism?
- primary (PHPT)-abnormality of parathyroid gland itself - leads to loss of bone tissue - secondary (SHPT)-in response to low calcium - tertiary (THPT) -after secondary HPT is treatment-very rare
209
what are the clinical features of hyperparathyroidism (and hyperCa)?
- nausea/ vomiting - constipation - ECG changes-short QT interval - kidney stones - bone pain - osteoporosis - psychosis/ altered mental state
210
what are the clinical features of hyperparathyroidism (and hyperCa)?
- nausea/ vomiting - constipation - ECG changes-short QT interval - kidney stones - bone pain - osteoporosis - psychosis/ altered mental state
211
what does hypoparathyroidism suggest about PTH and Ca levels?
-low Ca -low PTH (most likely caused by autoimmune disorders)
212
what are the clinical features of HypoPTH and HypoCa?
``` -muscle weakness and cramps Nerve function: -peroral numbness and tingling -Chvostek’s sign -Trousseau’ sign -Tetany ```
213
what is pseudohypoparathyroidism due to?
- target organ is resistant to PTH | - PTH is present just not effective so pseudo
214
what are the roles of sex steroids?
- promote sexual differentiation - development of secondary sexual characteristics - regulate sexual behaviour - supporting normal reproductive function - support bone growth and maintain bone mass
215
which enzyme converts testosterone and androstendone to oestrogen?
aromotase
216
describe the actions of steroid hormones
- enter cell (lipid soluble) - bind to receptors in nucleus - then bind to DNA sequences-creating a hormone response element - this response then induces a transcription of mRNA in order to produce effector proteins-bring about physiological effects in several organs in body
217
what do steroid hormones act as?
transcription factors
218
which cells produce testosterone?
-Leydig cells in testicles
219
which hormone can control testosterone release?
LH (stimulates Leydig cells to secrete test)
220
when are testosterone levels highest and lowest?
- highest-waking up and midnight-when melatonin peaks | - lowest in afternoons/ evenings
221
what are the functions of testosterone in males?
- primary sex hormone in males | - influences sexual characteristics and increases bone building-increases bone thickness/ increases basal metabolic rate
222
what are the functions of testosterone in females?
- tends to be used as a precursor to make estrogens - small influence on sexual characteristics - increases bone building
223
what are the 3 types of estrogens?
- estrone - estradiol-main type - estriol
224
where are estrogens generally produced?
ovaries by granulosa cells
225
how is estradiol produced?
from conversion of circulating androgens by aromatisation
226
what is estrogen secretion under the influence of?
LH | FSH
227
where are LH and FSH secreted from?
anterior pituitary gland
228
what type of hormones are LH and FSH?
gonadotropin hormones
229
what are the functions of estrogens?
- influences sexual characteristics - responsible for secretory activity within genital tract - regulates GnRH secretion - responsible for ovulation during menstrual cycle - regulates cardiovascular physiology and neuronal growth - decreases bone breakdown
230
describe the hypothalamic-pituiutary-ovarian axis
- hypothalamus secreted GnRH - stimulates anterior pituitary to secrete LH anf FSH - LH causes theca cells to secrete androgens (test) - androgens and FSH cause granulosa cells to secrete estrogens
231
where is progesterone secreted from?
corpus luteal cells
232
what are the roles of progesterone?
- embeds a fertilised ovum and maintains pregnancy - encourages growth of the endometrial wall-allows rooting of ovum and forming of bed for its development - inhibits uterine contractions - increases viscosity of cervical mucus - promotes breast development - increases body temperature - inhibits GnRH release
233
what cells secrete testosterone in the ovaries?
theca interna cells of ovary
234
which cells of testis secrete estradiol?
sertoli cells of testis
235
what are the 2 phases of the ovarian cycle and what days of the cycle do these include?
- follicular-days 0-14 | - luteal-14-28
236
which tissues is aromatase present in?
- gonads - vascualr endothelium - endometrium - skin - bone - brain - adipose tissue - placenta
237
which hormone conversions is aromatase responsible for?
androstenedione----->estrone | Testosterone----------->estradiol
238
what does aromatase deficiency in peripheral tissues lead to and how does this differently affect females and males?
- results in overproduction of testosterone - less oestrogen production - females: ambiguous genitalia - males: not enough oestrogen can affect skeletal growth and final height
239
what is hypogonadism?
inability of testicles or ovaries to produce enough testosterone or oestrogen
240
what are the 2 types of hypogonadism?
- --->primary-due to defect at level of the gonad-ie testicles or ovaries - ---->secondary-due to defect at level of pituitary or hypothalamus-causing reduced amplitude or pulsality of FSH/ LH or GnRH secretion
241
what is the effect of oestrogen on LH/FSH in the follicular phase?
oestrogen has stimulatory effect on LH /FSH
242
what is the effect of oestrogen in the luteal phase?
oestrogen inhibits LH and FSH in luteal phase
243
what is the effect of progesterone in the luteal phase?
progesterone has inhibitory effect on pituitary LH and FSH secretion
244
what happens to the corpus luteal cells is pregnancy occurs?
corpus luteum is maintained by HCG secreted by trophoblast
245
what happens to the corpus luteum if there is no pregnancy?
corpus luteum is degenerated into corpus albicans-by luteolysis
246
what is ovulation triggered by?
- ovulation is triggered by rapid rise in oestradiol level | - positive feedback of oestradiol at pituitary and hypothalamus results in LH surge-causing ovulation
247
what is the LH surge essential for in the menstrual cycle?
release of ovum and formation of corpus luteum
248
in the luteal phase do oestrogen levels fall or rise again?
rise again
249
what are the 2 types of adipose tissue?
- white adipose tissue | - brown adipose tissue
250
what is the structure of white adipose tissue?
-contains single large fat droplet, forces the nucleus to be squeezed into a thin rim at the periphery
251
what are the functions of white adipose tissue?
- lipid storage tissue | - has receptors for insulin, adrenaline and sex steroids-these can trigger lipolysis-breakdown of WAT to generate energy
252
what is the structure of brown adipose tissue?
small lipid droplets and numerous-iron rich mitochondria giving the brown appearance
253
what is the function of brown adipose tissue?
- helps them survive cold temperatures-transfer energy from food into heat - may contribute to energy homeostasis in adults
254
what does the ovarian cycle involve?
involves the growth of the ovum and follicle
255
what does the uterine cycle involve?
involves breakdown and growth of the endometrial wall
256
when are ghrelin levels high?
before a meal when stomach is empty
257
when do ghrelin levels decrease?
shortly after eating when stomach is full
258
what are the 3 stages of the uterine cycle and what days these include?
- menses days 0-7 - proliferative phase days 7-14 - secretory phase days 14-28
259
where does aromatisation usually occur?
reaction tends to occur in the peripheral fat of the body
260
describe the hypothalamic -pituitary-testicular axis
- hypothalamus releases GnRH - stimulates anterior pituitary to release LH and FSH from gonadotrophs - LH stimulates testes-Leydig cells to secrete testosterone - FSH stimulates sertoli cells-stimulating spermatogenesis and estrogen production
261
what is an example of negative feedback in the hypothalamic-pituitary-testicular axis?
sertoli cells in testes (stimulated by FSH) release inhibition B to stop the release of FSH and LH (negative feedback loop)
262
what is an example of negative feedback in the hypothalamic-pituitary-ovarian axis?
granulosa cells of the ovaries (stimulated by FSH) | release inhibition B to stop the release of FSH and LH-negative feedback loop
263
what is the role of FSH in males?
stimulates spermatogenesis in sertoli cells
264
what is the role pf FSH in females?
stimulates oogenesis in the granulosa cells
265
what are eicosanoids (FA derived hormones) made from?
arachidonic acid
266
what are examples of eicosanoids?
prostaglandins
267
what hormone types are hydrophobic?
steroid hormones | amino acid derived hormones
268
which family of receptors do catecholamines bind to?
GPCR-specifically alpha and beta adrenergic receptors
269
which hormone is hydrophilic?
peptide-mostly use receptors embedded in membrane
270
which receptors do steroid hormones use?
nuclear/ intracellular
271
what is adipose tissue?
-tissue deicated to lipid storage-safely stores fatty acids as triglycerides
272
why are fatty acids an important energy molecule?
- they undergo beta-oxidationo to produce acetyl CoA | - must be stored if not used as toxic in blood
273
what is the difference between fasting and post-prandial phase?
- fasting-triglyceride undergoes lipolysis to FAs and glycerol-produce ATP - post-prandial-ATP and glycerol undergo lipogenesis to form triglyceride to store
274
what are the 4 important adipose tissue regulators?
- Adiponectin - Leptin - Ghrelin - Insulin
275
where is adiponectin released from and where does it bind to?
released from: adipose tissue binds to: - ADIPOR1-skeletal muscle - ADIPOR2-liver
276
where is leptin released from and where does it bind to?
released from: adipose tissue binds to: hypothalamus
277
where is ghrelin released from and where does it bind to?
released from: stomach | binds to: hypothalamus NPY and AgRP receptors
278
insulin is released from beta cells of pancreas, where does it bind to?
hypothalamic arcuate nucleus | -GLUT receptors
279
what is the function of adiponectin?
- enhances cells sensitivity to insulin - makes it easier to uptake glucose - good marker for whether or not someone has developed insulin resistance
280
what is the function of leptin?
- anorexigenic hormone-released after you eat high fat food-tells you to stop eating by binding to hypothalamus-activate thyroid and HPO axis - increases lipolysis
281
what would a mutation in leptin gene cause?
hyperphagia- overeating
282
what is the function of ghrelin?
orexigenic hormone-hunger hormone - binds to NPY and AgRP receptors in hypothalamus to stimulate you to eat and store fat you eat in meals - increased lipogenesis
283
what is released after eating to stimulate insulin?
Glucagon-like peptide 1
284
what type of hormone is insulin in eating?
anorexigenic hormone-binds to arcuate nucleus in hypothalamus and promotes glucose storage
285
what is the hypothalamic arcuate nucleus (ARC)?
an area of the hypothalamus that is key for regulation of appetite
286
what 2 peptide types does ARC express?
- orexigenic-NYP and AgRP-encourages eating (ghrelin binds) | - anorexigenic-POMC-discourages eating
287
which other nuclei in the hypothalamus does ARC work with?
- ventromedial nucleus-satiety centre - -stimulation decreases eating - -lesion or disease results in overeating - dorsomedial nucleus - paraventricular nucleus
288
what are the roles of androgens in males and females?
released from zona r. of adrenal gland-used to make testosterone and oestrogens (precursor to sex cells)
289
what are the effects of angiotensin II?
- aldosterone production - stimulates ADH release-increases BP - arterial vasoconstriction-increases BP (binds to AT-R receptor on vascular endothelium) - degrades bradykinin
290
how does bradykinin cause vasoconstriction?
- bradykinin synthesises nitric oxide-NO - NO is vasodilator - ACE degrades bradykinin - so less vasodilation-more vasoconstriction
291
where do all female estrogens come from after menopause?
the conversion of adrenal androgens
292
what is Addison's disease caused by?
autoimmune disease that attacks the adrenal cortex (primary adrenal insufficiency)
293
How does Addison's disease cause hyperpigmentation?
- low cortisol triggers release of ACTH - excess ACTH binds to melanocytes - stimulates melanocytes to secrete melanin
294
why does secondary adrenal insufficiency not cause hyperpigmentation?
the secretion of ACTH is not increased
295
what is tertiary hypothyroidism?
insufficient TRH production form hypothalamus
296
how is vitamin D synthesised?
- UV converts 7-dehydroxycholestrol to vit D in keratinocytes in skin (lipid soluble as steroid) - can be absorbed in GI tract via dietary sources
297
what are the effects of vitamin D?
in liver: - vit D is converted to calcidiol via 25-hydroxylase - calcidiol is converted to active calcitriol in the kidney-stimulated by PTH - vit D increases osteoclast activity and increases osteoclast uptake from GI tract
298
what is the stimulator and inhibitor of calcitonin?
- stimulus= high Ca+ | - inhibitor= low Ca+
299
what type of hormone is calcitonin?
peptide
300
what is calcitonins, PTH receptor type?
GCPR
301
what is T3/T4 receptor type?
nuclear
302
what is Vit D receptor type?
nuclear
303
what is the stimulus and inhibitor of GH?
stimuli - hypoglycaemia - low FAs - high aas - ghrelin inhibitor -somatostatin
304
what is the stimulus and inhibitor of ACTH?
stimuli - stress - low glucose inhibitor -cortisol
305
what is the stimulus and inhibitor of TSH?
stimuli -low T3/ T4 inhibitor - T3 - T4
306
what is the stimulus and inhibitor of LH/FSH?
stimulus -oestrogens inhibitors - oestrogen - progesterone
307
what are is the stimulus and inhibitor of prolactin?
stimuli - low dopamine prior to menses - baby sucking on nipple inhibitor -dopamine
308
what is the stimulus and inhibitor of oxytocin?
stimuli -uterine stretching during labour inhibitor -catecholamines
309
what is the stimulus and inhibitor of vasopressin?
stimuli -osmoreceptors in the hypothalamus detect high blood osmolarity-low water levels inhibitor - alcohol - low blood osmolality-high water levels
310
what are the locations of GLUT1?
brain RBCs placenta fetal tissue
311
what are the locations of GLUT2?
liver kidney intestine beta cells
312
what is the location of GLUT 3?
brain
313
what are the locations of GLUT 4?
muscles and adipose tissue
314
what are the locations of GLUT 5?
jejunum
315
describe the mechanism of GLUT 2
- glucokinase sites become occupied with glucose=converting glucose to glucose-6-phosphate - increase in glucose-6-phosphate and insulin action leads to build up of glycogen stores in liver - this glycogen can be released as glucose when blood glucose levels are low - inulin accelerates uptake of glucose not necessary
316
describe the mechanism of GLUT4
1-insulin binds to tyrosine kinase receptor 2-triggers protein kinase cascade 3-glut4 transporters travel to cell surface membrane by exocytosis 4-glucose enters cell adipose-glucose to FAs muscle and liver-glucose to glycogen
317
what are SDGLTS?
sodium dependent glucose transporters -contribute to renal glucose absorption -found in small intestine and proximal tubule of nephron
318
what do pancreatic polypeptide cells do?
inhibit secretion of spomatostatin
319
how do beta cells work?
- glucose enters cell via GLUT2 - glucose to glucose-6-phosphate via glucokinase - G6P stimulates glycolysis to produce ATP - ATP sensitive K+ channels close - K+ builds up in cell-change in potential differnece causes V.G. Ca2+ channels to open - increased calcium induces secretion of insulin
Medicine yr1
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