Endocrine Flashcards
The hypophysis is two parts, ….. & …..
Adenohypophysis (from somatic ectoderm “Rathke’s pouch”, devoid of innervation)
Neurohypophysis (from neuroectoderm “diencephalon”)
Pars nervosa is ….
part of the neurohypophysis, connected by the infundibulum to the hypothalamus (composed of nerve tracts from the latter)
The brain is connected to the adenohypophysis by ….
hypothalamic-hypophysial portal system
Each of these hormones stimulates:
- CRH
- TRH
- GnRH
- GHRH
- ACTH
- TSH & prolactin
- FSH & LH
- GH
Dopamin inhibits ….. release, while ….. inhibits TSH & GH
prolactin
somatostatin
* Dopamine is release by the hypothalamus in the hypothalamic-hypophyseal portal system
Oxytocin and ADH are produced by the ….., transported via the ….. and stored in …. to be released on appropriate stimulation
hypothalamus
nerve tracts (infundibulum)
pars nervosa
What is the difference between tropic and non tropic hormones?
tropic hormones have other gland as their target.
Non tropic hormones act directly on the target cell
* GH is both tropic and non tropic
Example of straight chain peptide with disulfide bridge are … & …
- GH: increases protein synthesis, increases lipolysis (to spare glucose & protein). Has diabetogenic effect
- Prolactin (PR): required for milk synthesis. Also called LTH (luteotropic hormone). Stimulates calcitriol & calcitonin production
see p. 428
What is the difference between gigantism & acromegaly?
Acromegaly: increase GH (A)fter fusion of growth plate
Gigantism: increase GH before closure of growth plates
How is the GHRH and GH are regulated?
by feed back mechansim
* They are secreted in pulses throughout the day
LH, FSH & TSH are example of ……
glycoproteins composed of alpha & beta subunits
What is the effect of LH on both sexes?
Males: testosterone synthesis by Lydig cells
Females: triggers ovulation
* secretion controlled by feed back mechanism
What is the effect of FSH on both sexes?
maturation of germ cells
Glucocorticoids …… GH secretion
inhibit
Example of straight chain polypeptide are … & …..
- ACTH: stimulates glucocorticoid release from adrenal cortex
- MSH: stimulates melanocytes
Addison’s disease is ….
(adrenal insuffeciency) causes high level of ACTH. Due to similarity with MSH, high ACTH causes pigmentation of the skin and oral mucosa
- There’s destruction of the adrenal cortex, most likely autoimmune
- Tx is cortisol (skin lesions disappear, but oral persist)
- Also called primary addison’s disease
Cushion syndrome is …
High ACTH due to pituitary tumor, steroid meds., or ectopic ACTH producing tumors, or adrenocortical adenoma
ADH & oxytocin are synthesized in …. & ….
SON & PVN (hypothalamus)
- unmyelinated axons from the hypothalamus terminate in the posterior lobe of the pituitary gland, where these two hormones are stored to be released on demand.
- These two hormones are synthesized by two different types of cells
Endorphins & enkephalins are ……
endogenous opioid agonists, act as neurotransmitters
Vasopressin primary site of action is ….. & ….. with its action being
DCT & collecting duct
increase permeability to water, leading to its reabsorption (by increasing Na retention)
ADH (vasopressin) release is controlled by …
osmoreceptors in the hypothalamus
- decrease osmolarity ===> decrease ADH release and vice versa
- Alcohol decrease ADH release
Low ADH leads to ….. urine
hypotonic
A small decrease in plasma osmotic pressure is needed to …… ADH, while it takes 10%…. in blood pressure for ADH to be released
decrease
decrease
In volume contraction, …… stimulates thirst
angiotensin II
What is diabetes insipidus?
Absence of ADH (central) or lack of response (nephrogenic), both which lead to hypotonic urine
* Lithium causes peripheral DI
Oxytocin effects are …..
- milk let down (stimulated by suckling)
2. Uterine contraction
The effect of aortic & atrial baroreceptors are transported via …, while those from the carotid sinus are via
vagus
glossopharyngeal
* aortic and carotid sinuses are high pressure receptors
* atrial receptor is low pressure receptor
see p. 430 & 419 for complete details
ADH increase leads to ….. urine volume
decrease
* urine will be hypertonic due to low water content
What are the zones of the adrenal cortex?
- Zona glomerulosa (outer): synthesizes aldosterone, controlled by renin-angiotensin system
- Zona Follicularis: produces glucocorticoids)
- Zona Reticularis: produces androgens precursor (DHEA)
* Follicularis and Reticularis are controlled by ACTH
* * mneomonic: GFR
Cortisol suppresses the release of …. & ….
CRH & ACTH
POMC is …
pro-opiomelanocortin is precursor of all corticotropins (MSH, ACTH & endorphines)
ACTH affects the cortex by ….
increasing cAMP
Glucocorticoid increase …. release from pancreas
glucagon
- Decrease sensitivity to insulin (glucogenic)
- Increases gluconeogenesis
- Increase lipolysis and proteolysis
- Increase glycogenolysis in the liver (not the muscles)
What is the effect of cortisol on inflammation?
Decrease inflammatory response by:
- Decrease release of arachidonic acid (inhibit phospholipase A2)
- Decrease histamin release from mast cells
- Inhibit interlukin 2 and T lymphocytes proliferation
High level of cortisol intake leads to ….
atrophy of the adrenal gland & ACTH cells in the pituitary
Addisonian crisis is caused by ….
sudden stop of cortisol intake, due to atrophied adrenals.
- could be fatal
- 6 to 9 months are required to regain normal cortisol secretion from the atrophied adrenals
- No skin or oral pigmentation
Cortisol ….. glycogenesis
decreases
- Promotes glycogenolysis
- Some sources says “increases”
Aldosterone ….. K & H release by kidney
promotes
How is the aldosterone secreted?
- Renin is released from juxtaglomerular appartus (due to sympathetic stim., low plasma vol., low BP etc..)
- Renin converts circulating angiotensinogen to angiotensin I
- ACE converts angiotensin I to angiotensin II, a potent vasoconstrictor (in the lung)
- Angiotensin II acts on the zona glomerulosa to produce aldosterone
* increased K also directly stimulates aldosterone release
What is the effect of ANF on renin secretion?
ANF inhibits renin release
Most of the catecholamines secreted from the medulla is ….
epinephrine, rest is norepinephrine
* adrenal medulla is neural crest derivative, while the cortex is mesodermal in origin
Catecholamines are transported to the periphery by ….., and then …..
microfilaments
exocytosed
Epinephrine and norepinephrine are stored in the same cell. T/F
False
Catecholamines are synthesized from …..
phenylalanine
see p. 433
Norepinephrine is converted to epinephrine by the action of …..
Phenylethanolamine N-methyltransferase
Pheochromocytoma is …..
tumor of the adrenal medulla, leading to high levels of catecholamines. May lead to hypertensive crisis and death
Iodide is ….. with Na against its concentration. At the follicular membrane colloid surface, the enzyme …. forms iodine
symported
thyroid peroxidase
Thyroglobulin is …. into the colloid space, then it is …… to form T3 and T4
exocytosed
* It is iodinated in the colloid space
T4 & T3 are formed in the ….., then they are …. back into the cell to be released into the blood stream
colloid (thyroglobulin)
endocytosed
* peptide bonds between the thyroglobulin and the iodinated tyrosin residues are hydrolyzed to release T3/T4
T3 & T4 inhibit further ….. release by negative feed back
TSH
What is the effect of TSH on the thyroid cells?
it increases cAMP level in the cells and controls all aspect of thyroid hormones synthesis
* TSH prevents thyroid gland atrophy
Between T3 & T4, the one more active is ….
T3 (has 10 times the effect of T4)
* however the one responsible for the negative feed back is T4, which is deionated at the pituitary to T3
Thyroid hormones decrease the responsiveness of pituitary to ….., along with decreased ….. secretion
TRH
TSH
Hypophysectomy causes …… , while thyroidectomy causes
- thyroid gland atrophy (Tx is TSH supply)
- pituitary enlargement due to lack of feed back and causes the appearance of thyrodectomy cells in the pituitary (Tx is T4 to prevent pituitary destruction)
What is the function of the intrathyroid regulatory mechanism?
maintain constant level of thyroid hormone production during time of low or high iodine concentration
T4 is carried in plasma while bound to …..
thyroxine binding globulin
What are the activities of thyroid hormone
increase metabolic rate, O2 consumption, glycogenolysis, gluconeogenesis, lipolysis.
It increases HR and inotropy
Increase BP, appetite, body temp, promotion of bone growth
* Acts on most tissues except spleen and testes (? unconfirmed)
Goiter is ….. thyroid gland. Its main cause is ….
hypertrophied
Iodide deficiency, goitrogens
* Can occur with hyper or hypothyroidism
What is the difference between the three types of hyperthyoidism?
What is the main cause for hyperthyroidism?
- Primary (TSH low/normal)
- Secondary (TSH increased) rare
- Tertiary (TRH increased)
Goiter is the main cause
What is Grave’s disease?? and what are its symptoms and treatement
the presence of antibodies against the TSH receptor on the thyroid gland causing hypertrophy
Symptoms: tremor, sweating, increased appetite, tachycardia, exophthalmos (enlarged eye muscles in response to IgG)
Tx is propythiouracil (inhibits oxidation of iodide to iodine)
Goitrogens that cause goiter are two types, …. & ….
- Inhibit iodide transport
2. inhibit binding and coupling process
What is the difference between the three types of hypothyroidism? and what is the main cause?
- primary (with normal or high TSH)
- secondary (with low TSH)
- tertiary (low TRH)
* there could be increase peripheral resistance to thyroid hormones
Main cause is immune thyroiditis and destruction of the thyroid gland
What are the main symptoms of hypothyroidism?
weight gain, lethargy, bradycardia, decreased appetite, dry skin & cold sensitivity
Thyroid hormone receptors are found in the ….
nucleus
Parathyroid hormone is secreted from ….., with its main function being ……
chief cells of the parathyroid gland
maintaining Ca & phosphate levels (low Ca increases PTH and vice versa)
Also stimulate the synthesis of calciferol in the kidney
The main sites for the action of PTH are …., …. & ….
bone, kidney, and the GIT (indirectly)
* The net effect is increased Ca and decreased phosphate
Osteoclastic activity is …… by PTH
increased
* there is increase in skeletal remodelling
The effect of PTH on the kidney is …..
- tropic: Increasing Ca reabsorption in the DCT, and increasing phosphate excretion
- Non tropic: In the PCT, it promotes the formation of calciferol
Define:
- Primary hyperparathyroidism
- Secondary hyperparathyroidism
- Hypoparathyroidism
- Pseudohypoparathyroidism
- Increase PTH secondary to adenoma
- Increase PTH due to low serum Ca (because of renal failure)
- Decreased PTH (causing low Ca & high PO4)
- PTH target tissue resistance (kidney, bone) which leads to (low Ca, high PO4). It is an autosomal recessive
The sources of vit. D are ….. or ….
diet, UV activation of 7-dehydrocholesterol
How is the active form of Vit D synthesized??
- 7-dehydrocholesterol is converted to cholecalciferol (D3) in the skin (by UV light)
- D3 is converted to 25-Hydroxycholecalciferol in the liver
- 25-hydroxycholecalciferol is converted to 1,25-dihydroxycholecalciferol by the kidney PCT(active form)
* Vit D is the most toxic of the fat soluble vitamins
What is the effect of 1,25 (OH)2 D3 on intestine?
increases Ca & PO4 absorption from the intestine
Most common vit D deficiency is …. & ….
ricket (children) & osteomalacia (adults)
- There is accumulation of unmineralized bone (osteoid)
- Normal ossification requires vit D acting directly on the bone
- 99% of Ca is reabosorbed by the kidney when vit D is insufficient
In vit D deficiency, there is decrease in the number of osteoclasts. T/F
True. This is despite the normal level of PTH
The actions of Vit D on the bone seem paradoxical.. Explain
Although vit D increases osteoclastic activity, this activity is in balance with formation of new bone (remodeling). So the osteoclastic reabsorption is in equilibrium with osteoblastic mineralization of new bone
What are the main causes of vit D deficiency?
malnutrition, renal disease, liver disease, inadequate sun exposure
Calcitonin is secreted by …..
parafollicular cells (C- cells) in thyroid, parathyroid and thymus
What is the stimulus for Calcitonin release?
increased serum Ca
* calcitonin decrease both serum Ca & PO4 (by decreasing bone reabsorption & intestinal absorption of Ca)
Calcitonin is an effective treatment for ….
osteoporosis
Calcitonin also regulates serum Ca level, just like PTH and VIt D. T/F
True, however not on a daily basis
Gastrin & prolactin, both ….. calcitonin secretion
increase
The functional unit of the pancreas is ….., which has four cell types
The pancreas receives …….. innervation
isles of Langerhans Mixed innervation * Cell types are: 1. alpha: glucagon 2. beta: insulin 3. delta: somatostatin 4. F cells: pancreatic polypeptide
The precursor for insulin is …..
preproinsulin
* This one is cleaved to proinsulin
What are the stimuli for insulin release?
- Hyperglycemia
- fatty acids (palmitic & stearic acids)
- amino acids (especially arginine)
- GIT hormones (gastrin, GIP, secretin)
- Acetylcholine
- GH & cortisol
Why oral glucose causes faster release of insulin than IV glucose?
because of presence of many GIT hormones to activate its release
What are the inhibitors for insulin release?
- epi & nor epi
- hypoglycemia
- somatostatin
Insulin increases the activity of the hormone …… to enhance fatty acids uptake by the tissues
lipoprotein lipase
Insulin ….. protein synthesis
increases
- decreases protein degradation by decreasing lysosome activities
- Also increases ribosome synthesis
Hyperkalemia can be treated with ….
IV insulin with glucose
* Insulin enhance K uptake by cells
What is the precursor for glucagon? and where is it synthesized?
preproglucagon
* synthesized in the pancreas, some brain cells & GIT
Glucagon release is stimulated by ….
- hypoglycemia
- Arginine (this AA also stim. insulin release)
- Epi & nor Epi
- CCK& Ach
Glucagon release is inhibited by ….
- Hyperglycemia
- Fatty acids & ketones
- insulin
- Somatostatin
Glucagon inhibits glycolysis by inhibiting the enzyme …..
pyruvate kinase
Glucagon ….. the level of ammonia
increases
* activates the urea cycle
Somatostatin inhibits both …. & ….. release from their cells, due to its ….. role
glucagon & insulin
paracrine
What is the criteria for DM diagnosis??
elevated blood glucose (>140 mg/dl) after overnight fasting
Type II DM could be due to ….. or ….. . It is treated with ……
- decreased peripheral response to insulin
- Decrease secretory response in the pancreas itself
* Insulin level could be high, normal or low.. The main cause is cellular resistance to insulin
* Treated with sulfonylurea
The pineal gland produces ….., receives …. innervation. It is located …….
melatonin
- it is a derivative of serotonin
- production stimulated by dark/light
- The gland receives both symp & parasymp innervation
- The gland is located dorsal to the superior colliculus
All peptide hormones are transported in the blood ……., and bound to membrane receptor, generating a …..
unbound
second messenger inside the target cell
* Note: Sex hormones are not peptide hormones, and they bind to SHBG for transportation
Tyrosine kinase is ……., with its function …..
is a subclass of protein kinase. Causes phosphorylation of intracellualr enzymes * Functions as an ON/OFF switch * Insulin binds to a transmembrane receptor, which in turn is linked to Tyrosine Kinase
Steroid hormones bind to ……., while peptide hormones bind to ….
intracellular receptor
membrane receptors
Corticosteroids include both ….. & ……
glucocorticoids + mineralocorticoids
TRH release is inhibited by stress. T/F??
True
Tetany is caused by …..
Low serum Ca due to low PTH (this will cause opening of Na channels, leading to progressive depolarization)
* Tetanus is different than tetany. It is caused by Clostridium tetani toxins, which inhibits muscle relaxation
Hypercalcemia causes ……
Hypocalcemia causes …….
- cardiac and CNS depression, anxiety
* irritability/excitability, tetany
