Endocrine 1 Flashcards
Major Hormones of the hypothalamus
- GnRH —> inc LH and FSH
- CRH (corticotropin rh) —> inc ACTH
- TRH (thyrotropin rh) —> inc TSH
- PIH (prolactin Ih) —> dec PRL
- GHRH (GH rh) —>inc GH
- GHIH (GH ih or SS) / somatostatin —> dec GH
Major hormones of the anterior pituitary
- FSH —> stimulate follicle growth
- LH (luteinizing hormone) —> spermatogensis
- ACTH (adrenocorticotropic hormone) —>inc testosterone sec
- TSH (thyroid stimulating hormone) —> inc adrenal steroid sec (T3 and T4)
- PRL (prolactin) —> produce milk
- GH —> inc protein synthesis
Major hormones of the posterior pituitary
- oxytocin (OXY) —> expulsion of milk
- ADH —> increases H2O reabsorption, decrease urine volume.
Major hormones of the adrenal cortex
- glucocorticoids (cortisol) —>
- Mineralocortoids (aldosterone) —> effects metabolism and increases Na+ reabsoption in nephron
(Counter regulatory)
Major hormones of the thyroid hormone
- T3 —> metabolism and growth
- T4 —> metabolism and growth
- calcitonin —> decrease blood Ca+
Major hormones of the parathyroid glands
- parathyroid hormone (PTH) —> increases blood Ca+
Major hormones of the pancreas
- insulin —> lowers blood glucose
- glucagon —> raises blood glucose
(Counter regulatory)
Classifications of hormones based on structure?
1) proteins
2) lipid
3) monamines
Types of protein hormones
1) small peptide (TRH, oxytocin, ADH)
2) polypeptides (insulin, glucagon, GH)
3) glycoproteins (FSH, LH and TSH)
Types of lipid hormones
1) steroids (cortisol, aldosterone, sex hormones)
2) eicosanoids (prostaglandin, leukotriens)
Types of monamine hormones
1) catecholamines ( dopamine, noradrenaline, adrenaline)
2) thyroid hormone ( T3 and T4)
What are steroid hormones made form ? And what is the pathway?
Cholesterol.
Cholosterol —> pregnenolone —> progesterone —> aldosterone, cortisol and (testosterone —> estrogen)
What are eicosanoids made form?
Form arachidonic acid
What are catecholamines made form?
From tyrosine
What are thyroid made form?
From Tyrosine
The four types of ways hormones reach their target
1) endocrine (via blood to distant target)
2) paracrine (via blood to Nearby target)
3) neuroendocrine (AP = stimulates nerve to sec hormone, moves via blood and stored in cell terminal of nerve cell)
4) autocrine (self stimulating, act on itself)
Types of hormone receptors
1) cell surface receptors
2) intercellular receptors
What kind of hormones bind to cell surface receptors ?
Proteins which bind protein hormones and to catecholamines
What kind of hormones bind to cell intracellular receptors ?
Proteins which bind to steroid hormones, and to Thyroid hormones, t3 and T4
Protein hormones are soluble where and not soluble where?
- soluble in aqueous environment
- insoluble in lipid environments
Lipid hormones are soluble where and not soluble where?
- soluble in lipid environments
- insoluble in aqueous environments
Why are surface receptors not inside the cell?
Because they are insoluble in lipid/fat env and cant pass through cell membrane = stay outside
Why are intracellular receptors inside the cell and not outside
They are insoluble in aqueous env but soluble in lipid/fat env, so they can pass through the cell memb
Types of cell surface receptors
1) G-protein receptor: G protein regulate second messenger
- (receptors for adrenaline and glucagon)
2) Catalytic receptors: reactors have enzymatic activity (tyrosine kinase),or closely associated with enzyme after binding to ligand
- (receptors for insulin and GH)
Role of second messenger
Hormone binds to surface receptor = change receptor conformation = G protein change conformation = inc/dec enzyme inside cell = produces second messenger (cAMP) = acts on protein kinase (PKA) = phophsorylation of protein = respond of target cell.
Types of intracellular receptors (3X)
1) mainly in cytoplasm (receptors for steroid hormones)
2) mainly in nucleus (receptors for sex steroids)
3) bound to DNA in the nucleus (thyroid hormones, T3 and T4)
All these receptors end up i the nucleus as transcription factors
Where do all intraceullar receptors end up?
All intraceullar receptors end up in the nucleus as transcription factors
What’s the pathway for intracellular receptor pathways
Steroid hormone passes through cell memb to bind to receptor either in the cytoplasm or nucleus, either why end up in a receptor in nucleus to act as transcription factor to porduce protein that act on the target cell.
What happens to hormones bind to plasma proteins
It solublizes it / becomes bound and inactive, balance between bound (inactive) and unbound (active) hormones regulate hormone amount
Catecholamines come from the
adrenal medulla.
Proteins hormone (& catecholamines)
1) solubility
2) synthesis
3) storage/Secretion
4) transport
5) hormone receptors
6) mechanism of action
7) time course
1) solubility : water soluble
2) synthesis : from amino acids (from tyrosine)
3) storage/Secretion : in granule / exocytosis
4) transport : doesn’t need solubilization in blood
5) hormone receptors : surface receptor
6) mechanism of action : intracellular signalling pathways
7) time course : FAST
Steroid hormone ( & T3 and T4)
1) solubility
2) synthesis
3) storage/Secretion
4) transport
5) hormone receptors
6) mechanism of action
7) time course
1) solubility: lipid soluble
2) synthesis: from cholesterol (from tyrosine)
3) storage/Secretion: not stored / diffusion
4) transport: bound to plasma proteins
5) hormone receptors: intracellular
6) mechanism of action: gene regulation
7) time course: SLOW
Examples of protein and catecholamine hormones
Most hormones of the hypothalamus, pituitary, pancreas, parathyroid, GI tract, adrenal medulla
Examples of steroid and thyroid hormones
Most hormones form the adrenal cortex, ovaries and tests and thyroid gland.
The hypothalamus-pituitary unit is composed of
composed of the:
- anterior pituitary (up growth to mouth)
- posterior pituitary (downstream growth)
- connected by the pituitary stalk
Is the blood supply to ant pit direct or indirect? Explain pathway
Indirect.
(Blood comes in) Artery —> primary plexus —> Portal blood vessel —> secondary plexus (inside the ant pit) —> vein in anterior (blood leaving)
The two nucleus within hypothalamus that communicate with pituitary glands are:
- Supraoptic nucleus (SON)
- Paraventricular nucleus (PVN)
These are the regions where there are cells bodies which communicate with the posterior pituitary
• Supraoptic nucleus (SON) and the Paraventricular nucleus (PVN) produce 2 different hormones, they both travel down the
nerve axon and into the posterior pituitary which are then stored in the terminals and will be released for a AP or stimulus.
Then the vein carries these hormones away.
Is the blood supply to the post pit direct or indirect? What’s the pathway
Direct.
(Blood come in) artery —> SON/PVN axons reach all the way down to the and insert their hormones —> vien (blood leaving) exits with the hormones from the SON/PVN
Where are hormones stored in the SON / PVN?
In the nerve terminus within the post pit.
How does the ant pit receive hormones and where
They receive hormones within the secondary plexus via anterior glands
Neurons in hypothalamus produce hormones via
cell bodies.
Main regions of the bone
- epiphysis (round-head end of bone)
- Epiphyseal plate (cartilage)
- Diaphysis (shaft)
When is the epiphyseal plate present? what does being open mean?
In bones of children who are growing.
Being open means when its responsive to hormones and it can cause bone to grow LONGER.
When we stop growing in height, its due to the
cartilage/ephyiseal plate isn’t no longer able to contribute to that growth and so it said to be in a CLOSED state.
Progenitor cells (Fibroblasts)
able to differentiate into cartilage cells.
Cartilage cells (chondrocytes)
Can perform proliferation (cell division) and ossification (bone formation)
Where are progenitor cells (fibroblasts) located in the bone?
Within the epiphyseal plate
If this child has a deficiency in GH and is much smaller then average.
Take growth hormone and inject it in vivo. Then the child will grow.
If you took a sample of bone cartilage and put in in vitro (in a test tube or beaker), you
wont see any growth.
Does GH work in VIVO or in VITRO or both? Why?
It works only in vivo (inside body).
Because inside body it require insulin light growth factor (IGF) in order to work. Outside the body IGF isn’t present and therefore GH wont work.
Where is IGF produced?
In the liver
In vitro, insulin light growth factor isn’t produced and is missing, therefore there is
NO GROWTH.
Effects of GH on metabolism
1) fats
2) carbohydrates
3) proteins
1) fats: increases lipolysis, increases free fatty acids for E.
2) carbohydrates: decrease glucose uptake = hyperglycaemia (“diabetogenic”)
3) proteins: increases protein uptake, synthesis and cell size.
Growth hormone secretion is
increased by:
- GHRH
- Ghrelin
- hypoglycaemia (low glucose in blood)
- increase in amino acids
- deep sleep
Growth hormone decreased by
- somatostatin (GHIH)
- GH
- IGF
- hyperglycaemia
- increase fatty acids
- aging
Too much GH can lead to what conditions
1) gigantism: in children, increased linear growth. Keep on growing.
2) acromegaly: in adults, thickening of bones, large hands and feet, jaw.
Too little GH can lead to what conditions ?
1) dwarfism: in children, stunted growth due to low GHRH, low GH, low IGF, low receptor #
Post pit hormone secretions form which neurons ?
SON: ADH —> kidney and blood vessels
PVN: oxytocin —> uterus and mammary glands
Where is ADH produced and what is its target cells
Produced in the post pit and targets the principle cell within the kidneys.
How does ADH function, what’s its mechanisms?
ADH in blood binds to cell G-protein surface receptors = cAMP second messenger acts on vesicle with inactive water channels = activates AQP2 channels = water passes through APQ2 from lumen to the blood = less volume of urine, more volume in blood. Hence antdieretic effect
What kind of receptor does ADH increase to increase water reabsorption in principle cells within the kidney?
Increases AQP2 receptors
What are the 2 factors effecting secretion of ADH? Which is more effective ?
1) increase osmotic pressure detected by osmoreceptors in hypothalamus (dehydration) [more effect stimuli]
2) decrease blood volume detected by baroreceptors in cardiovascular sys.
• An increase in osmotic pressure and decrease in volume = release of.
ADH
Too much ADH
Syndrome of inappropriate ADH secretion (SAIDH):
- Increased H2O retention
- increased blood volume
Too little ADH
1) central or neurogenic diabetes insipidus (lack of ADH, large volumes of dilute urine)
2) nephrogenic diabetes insipidus (abnormal ADH receptors in kidney; large volumes of dilute urine)
• Central diabetes insipidus:
due to lack of ADH (abnormal production)
• Neurogenic dramatic insipidus:
problem in the kidney, so ADH is produced just not able to do its function. Could be due to lack of ADH receptors or to much urine
Factors effecting oxytocin secretion
1) Partition: giving birth
2) lactation: release of milk
Actions of oxytocin in partition
Baby’s head puts pressure on the uterus opening = uterine stretch of smooth muscle cells = signals hypothalamus = post pit releases OXY = contraction of uterus = baby exits
(+) feedback system, prevents blood loss as muscles stretch.
Actions of oxytocin during action
As baby suckles, sends single to hypothalamus = posterior pituitary releases oxytocin = milk ejection reflex
Is oxytocin responsible for production of milk?
The production of milk is NOT dependant on the production of oxytocin, prolactin is responsible for the production of milk. Oxytocin only is reasonable for the release of milk.
Structure of adrenal gland is composed of what 3 main sections
1) zona glomerulosa
(outer most, thinnest layer)
2) zona fasciculata
(middle, thickest layer)
3) Zona Reticularis
(Innermost, thin layer)
Each produce hormones
Where is the adrenal gland located?
On top of both kidneys
What kind of cell are within the medulla of the adrenal gland?
Chromatin cells of adrenal medulla
Hormones of the adrenal cortex
1) zona glomerulosa: aldosterone (mineralocorticoid)
—-> control electrolyte / salt levels
2) zona fasciculata: cortisol (gluco-corticoids)
—> control sugar
3) Zona Reticularis: DHEA and andro-stenedione (androgens)
—> regulate sex
How are corticosteroids made?
From cholesterol —> pregnenolone —> progesterone —-> (cortisol, aldosterone, adrenal androgens)
Major actions of aldosterone
1) increased Na+ reabsorption by kidney (primary action)
2) increased H2O retention by kidney
(Secondary)
3) increased H+ secretion by kidney
(loss of H+ in urine)
4) increased K+ secretion by kidney
(loss of K+ in urine)
What cells does aldosterone act on?
Principle and intercalated cells that form the lining of the lumen, where fluid flows to become urine.
Mechanism of action for aldosterone
Aldosterone is a steroid hormone that can pass through the cell membrane to bind to the receptor in the nucleus, act as a transition factor to regulate Protein synthesis.
These proteins assist in regulating the transport channels of ions, causing the movement of H+ and K+ towards the urine (duct lumen), and Na+ towards the blood. As Na+ moved in the blood, so does H2O = increasing water reabsorption = increasing blood volume.
Control of aldosterone secretion
Decrease in volume of ECF / decrease blood pressure / decrease in Na+
= activate the sympathetic nerve.
= stimulate the release of renin from kidney.
= renin (enzyme) converts angiotensinogen to angiotensin I (inactive peptide).
= ACE (enzyme) converts angiotensin I to angiotensin II (active peptide).
= angiotensin II increases blood pressure and acts on the adrenal gland to secrete aldosterone
= aldosterone from adrenal gland increases Na+ and H2O reabsorption into the blood
= increase blood volume, Na+, blood pressure, volume of ECF, and a decrease in K+
Major actions of cortisol
1) metabolism
2) on immune system
1) metabolism:
- increase protein breakdown
- increase fat break down
- increase glucose formation in liver
- increase glycogen (hyperglycaemia)
- increase glucose available for CNS
- decrease glucose utilization by peripheral tissue
2) on immune system
- Decrease lymph node size
- Decrease lymphocyte number
- Decrease humoral/cellular immunity
- Decreaseproduction of inflammatory substances
- Increase infections
Effects of cortisol on metabolism
Glucose is secreted from the blood and effects 4 different sites.
1) LIVER —> cortisol increases uptake of glucose form liver to the blood. glycogen (storage form) leaves liver and enter blood, Gluconeogenesis occur at the liver. Amino acids from Proteins and glycerol+FFA form adipose tissue both come to liver to increase glycogen.
2) ADIPOSE TISSUE: uptake of glucose is decreased by cortisol, release glycerol+FFA=E
3) muscle, bone, skin: uptake of glucose is decreased by cortisol, releases amino acids.
4) CNS: uptake of glucose is increased by cortisol.
What does cortisol do to glucose in the blood
It increases it
Control of cortisol secretion
Stress = activates hypothalamus = releases CRH (corticotropin releasing hormone = activate ant pit - release of ACTH blood = activate adrenal cortex = released of CORTISOL
Cortisol has why kind of feedback system, and on what?
(-) feedback on both the hypothalamus and Ant Pit.
Catecholamines synthesis
Tyrosine = DOPA = dopamine = noradrenaline (noradrenaline) = adrenaline (epinephrine)
Too much aldosterone
Conns syndrome —>
- increased vol of ECF
- increased blood pressure
- hypokalemia
- metabolic alkalosis
Too little aldosterone
Addison’s disease —>
- hypotension
- metabolic acidosis
- hyperkalemia
Too much cortisol
Cushing’s disease —>
- increase blood glucose
- muscle wasting
- moon face
- decrease resistance to infection
Too little cortisol
Addison’s disease —>
- decrease blood glucose
- increase skin pigmentation
To much adrenal androgens
- verilization in females (look more masculine)
Too little adrenal androgen
- decrease sexual hair growth
- decrease libido in female
Major actions of catecholamines (adrenaline and noradrenaline)
1) cardiovascular system:
2) smooth muscle
3) metabolism
1) cardiovascular system:
- increase heart rate
- increase force of contraction
- increase cardia output
- redistribution of blood flow
2) smooth muscle:
- dilation of pupils
- bronchodilatation
- decrease GIT motility
3) metabolism:
- increase glygonenolysis (skeletal muscle and liver)
- increase lipolysis
- increase gluconeogensis
Control of catecholamines secretion
Stimulation of the splanchnic nerve = releases Ach = stimulates the chromaffin cells inside adrenal cortex = release of catecholamines = increase in adrenaline and noradrenaline
Glycolysis
Conversion of glucose to pyruvate acid
Glycogenesis
Synthesis of glycogen from glucose
Glycogenolysis
Breakdown of glycogen to glucose
Gluconeogenesis
Synthesis of glucose from amino acids
Lipogenesis
Synthesis of fats
Lipolysis
Breakdown of fats
Ketogenesis
Formation of keytone body from break down of fatty acids
Anabolism and catabolism
Anabolism = formation of new mol.
Catabolism = breakdown of mol.
