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BIOM*3200. UOG > Term test 1- endocrine and renal > Flashcards

Term test 1- endocrine and renal Flashcards

1
Q

what is an endocrine gland?

A

a tissue which releases a substance into the blood stream; the substance then travels via blood to influence a target cell.

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2
Q

what is an exocrine gland?

A

a tissue which releases substances via ducts

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3
Q

name four kinds of hormones (ie what are hormones)

A

proteins & polypeptides
steroids
amines: catecholamines and thyroids

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4
Q

what are the 3 levels at which hormones can create an effect?

A

1) autocrine (sc=tc)
2) paracrine (tctc)
3) endocrine (SC -> TC)

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5
Q

how can hormones bind?

A

1) receptors in target cells, where very high specificity for a particular hormone, but non-specific binding does occur
* there is continuous trun-over of the receptor-hormone complex.

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6
Q

where are receptors located for most hormones?

A

on the transmembrane

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7
Q

where are receptors located for steroid hormones?

A

in the cytoplam

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8
Q

where are receptors located for thyroid hormones?

A

in the nucleus

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9
Q

explain how transmembrane receptors work.

A

a hormone binds to an extracellular domain which activates signal pathways. these can then use phosphorylation and enzyme activation, and follow through with DNA, mRNA and protein pathways to respond, and some will directly cause an effect.

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10
Q

explain adenylate cyclase pathways and give an example

A

1) hormone receptor, G-protein dissociate
2) a-subunit activates AC
3) catalyzes prod of cAMP
4) removes reg unit from PK
5) PK acitvates other molecule-hormonal response.
ie. epinephrine binds to b-adrenergic

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11
Q

explain phosphlipase C-Ca2+ pahtways

A

1)hormone and receptor
2)g=-proteins dissociate
2) activates PLC
3)causes breakdown of membrane phospholipid to IP3
4) IP3 binds endoplasmic reticulum
5) releases of stored Ca2+ into cytoplam
5)ca2+ activates other molecules-hormonal response
ie epinephrine binds alpha-adrenergic

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12
Q

what does Dopamine (PIH) do?

A

inhibits secretions of prolactin

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13
Q

what PRH: prolactin releasing hormone do?

A

stimulates release of prolactin

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14
Q

what TRH: thyrotropin-releasing hormone do?

A

regulates secretion of thyroid stimulating hormones

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15
Q

what CRH: caticotropin-releasing hormone do?

A

regulates secretion of adrenocorticotropic hormone [ACTH]

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16
Q

what does GHIH somatosin do?

A

it inhibits secretion of growth hormone [GH].

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17
Q

what does GHRH, growth hormone releasing hormone do?

A

it stimulates secretion of GH.

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18
Q

what does GnRH: gonadotropin-releasing hormone do?

A

regulates secretion of gonadotropin-releasing hormone, luterinizing [LH] and follicle stimulating hormone [FSH].

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19
Q

what is involved in the hypothalamus-anterior pituitary adrenal cortex axis?

A

hypothalamus releases corticotropin releasing hormone (CRH) which activates the anterior pituitary to secrete the adrenorcorticotropic hormone (corticotropin). this effects the adrenal cortext to increase cortisol levels, which regulates the secretion of hormones by the hypothalamus and the anterior pituitary through negative feedback.

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20
Q

what is cortisol?

A

its a glucocorticoid, which controls the chronic stress hormone.

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21
Q

explain the CRH synthesis and release. a

what is an inhibitory influence as well?

A

the central stimulatory stimulates pre-proCRH gene expression, which then stimulates pulsatile release of CRH. the inhibitory influence is that physiological levels of cortisol inbihits release of CRH (negative feedback)

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22
Q

what is the full name of POMC?

A

proopiomelanocorticotropin

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23
Q

what are some of the peptides off the POMC? (5) and explain them.

A

1) ACTH (regulates adrenal cortex function)
2) MSH (skin pigmentation in response to UV radiation)
3) EndL (analgesic roles in central nervous system
4) Enk (analgesic roles in fetus)
5) MC3,4,5 (hypothermia, hypotension, feeding behavior, appetite)

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24
Q

what is ACTH, what does it do, where does it move to?

A

adrenocorticotropic hormone, and it creates the bases for cortisol, and it moves through to the adrenal gland

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25
Q

where is the adrenal gland, and describe it.

A

located on top of the kidney. like a hat. and it i 2 embryological distinct tissues merged during development adrenal cortex + adrenal medulla.

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26
Q

describe the Adrenal cortex and the adrenal medulla

A

the cortex: steroid factory

examples: glucocorticoids, muneralocorticoids and sex steroids.
medull: modified sympathetic ganglia-secrete catecholamines* epinephrine

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27
Q

name the adrenal hormones released from the adrenal gland and how they are controlled.

A

1) glucocorticoids (cortisol) controlled by ACTH
2) sex steroids controlled by ACTH
3) mineralocorticoids controlled by the renin-angiotesin system. (NOT ACTH)

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28
Q

why is cortisol, an adrenal glucocorticoid essential for life>

A

it cases breakdown of skeletal muscle (gluconeogenesisi), supresses immune system, catabolic on bone, and affects brain function. It keeps the stress levels down. it is a natural regulator of the inflammatory response.

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29
Q

when cortisol levels are high it can lead to what?

A

cushing’s syndrome. can come from too much ACTH, and it causes changes in carbohydrate and proein metabolism, hyperglycemia, hypertension, muscular weakness.

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30
Q

cortisol helps with what? and what are its levels like during the day? what is its cycle pattern?

A

cortisol spikes in the morning to help get us up and running. People with insomnia secrete more cortisol around sleep time. it follows a continuous, pulsatile, circadian rhythm.

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31
Q

how does the hypothalamus- pituitary gland work (what is the process)?

A

the hypothalamus produces thyrotropin releasing hormone (TRH) which acts on the anterior pituitary. that then produces the thyroid-stimulating hormone (TSH) which acs on the thyroid. to produce thyroid hormones that grow the thyroid, and the thyoxine hormones. (this system is controlled by the thyoxines negative feedback where it inhibits responsiveness to TRH and inhibits secretion of TRH).

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32
Q

where is the thyroid gland located?

A

it is located just below the larynx, on either side of the trachea. Its composed of 2 lobes connected by isthmus. it is also the largest purely endocrine gland.

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33
Q

explain how t3 and t4 are made.

A

follicles take up iodide from the blood and in the colloid, the enzyme TPO helps attach it to a tyrosine residue in thyroglobulin. the attachment of one iodine produces MIT (monoiodotyrosine) and the attachment of two iodines produces DIT (Diiodotyrosine).enzymes in the colloid modify the structure (through condensation) of MIT and DIT to make thyroid hormones. T3 and T4.

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34
Q

what is the name of T3 and T4

A 
T3= triiodothyronine
T4= tetraiodothyronine
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35
Q

how are thyroid hormones transport in the body?

A

99% will transport in the blood system by means of a plasma carrir protein called thyroxin-binding globulin (TBG)
1 % (free fractions of TH) are biologically active.

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36
Q

what are some secretion properties of Thyroid hormones?

A

its pulsed because it increases our BMR (highest between 10 am and 2 pm), and it impairs with age. When you are stressed or cold, your thyroid hormones will increase.

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37
Q

what are physiological actions of thyroid hormones?

A

it elevates basal metabolic rate, needed for normal gonadal development and function, needed for normal embruonic/fetal development, and particularly for the development of the central nervous system.

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38
Q

explain the problem with hypothyroidism.

A

abnormally low BMR, and results in wright gain, lethargy and intolerance to cold

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39
Q

explain the problem with hyperthyroidism

A

increased BMR, and results in weight loss, muscular weakness, nervousness, and protruding eyes.

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40
Q

what is Cretinism, how can you avoid it, how was it done?

A

thyroid hormone is deendent in utero, without it there will be underdevelopment. treatment with T4 soon after birth, completely or almost completely restores development of intelligence. its usually due to innate maternal hypothyrodism, however it can also rise due to diet deficiency with iodine.

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41
Q

what can cause hypothyroidism and hyperthyroidism

A

insufficient dietary iodide, thyroid gland defect, impaired thyroid hormone pathway, insufficient ant. pit. TSH, insufficient hypothalamic TRH, mutant TSH or TRH receptors, mutant TH transport proteins.
hyper- common in cats
hypo- common in dogs

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42
Q

what are some treatments of thyroid disorders

A

1) surgery
2) hormone supplementation
3) radiation therapy
4) blockers (thiouracil derivatives-thiocabamides)
5) stimulants (furosemide)
6) diet, electrolyte infusions

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43
Q

describe Growth hormone

A

it is a protein, with a small half life. it is the most abundant ant. pit. hormone and plays a role in growth. It has insuline0like growth factors (somatomedins) IGF-1 and IGF-2.

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44
Q

describe the GH secretion patterns

A

GH secretion occurs as several large pulses or peaks each day. the largest GH peak occurs before sleep. over the years the GH secretion slows down (specially after 10 years).

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45
Q

how is GH transported in the flood?

A

is may be transported as a free hormone but much of GH is bound to binding protein GHBP.

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46
Q

name things that may increase GH secretion.

A

sleep, exercise, hypoglycaemia, high dietary protein, steroids, and ghrelin (hunger hormone)

47
Q

name things that may decrease GH secretion

A

hyperglycaemia, glucocorticoids, endocrine disruptors.

48
Q

how is IGF-1 transported in our bodies?

A

IGF-1 is almost entirely bound to transport proteins, but some (transport and binding proteins) have an endocrine function but there are receptors for these proteins.

49
Q

what goes GH stimulate?

A

it stimulate the synthesis and release of IGF-1 in many tissues. but also effects the adipos tissue by release of fatty acids and most tissues by decreasing glucose utilization.
ie. it stimulates growth of bone & cartilage growth, but also soft tissue growth by hypertrophy (increased cell size) and hyperplasia (increased cell number).

50
Q

what does IGF-1 stimulate?

A

cartilage and bone growth, and muscle and other organs by protein synthesis growth.

51
Q

what are the two ways bones can be formed?

A

by increasing their diameter, (growth around the bones) and the second by increasing the bone length (growth increases at the epiphyseal plates)

52
Q

what are osteoblasts?

A

they are bone forming cells.

53
Q

describe the steps to how bones are formed

A

the epiphyseal plate near the end of the bone contains chondrocytes- columns of collagen-producing cells. as the collagen layer thickens the old cartilage calcifies, and chondrocytes then degenerate. this is where osteoblasts invade and lay bone matrix on top of the cartilage base.

54
Q

how does GH stimulates bone growth.

A

it stimulates chondrocytes, and stimulates production of IGF-1 in liver. the IGF-1 helps stimulate chondrocyte & osteoblast activity, to promote bone.

55
Q

what does severe GH deficiency cause in childhood?

A

dawrfism

56
Q

what does severe GH oversecretion cause in children?

A

giantism

57
Q

what does severe GH oversecretion cause in adults?

A

acromegaly

58
Q

how would we treat GH deficiency in children?

A

by using rHGH. recombinant growth hormone.

59
Q

what 3 hormones regulate movement of calcium between bone, kidney and intestine?

A

they are parathyroid hormone (PTH), calcitriol and calcitonin.

60
Q

where and what is PTH?

A

it is made by the parathyroid gland and helps regulate calcium (by raising it when it is low)

61
Q

where and what is the parathyroid gland?

A

it is 2 pairs in the neck, and is associated but not part of the thyroid. there are 2 cell types: chief cells (produce PTH) and oxyphils

62
Q

how does PTH regulate calcium?

A

1) stimulates osteoclasts to resorb bone,
2) stimuylates kidneys to resorb Ca2+
3) stimulates kidneys to produce enzyme needed to activate vitamin D, which in turn promotes better absorption of Ca2+ from food and drink across the intestinal barrier.

63
Q

how do osteoblasts work?

A

they are part of bone deposition, where they secrete a matric of collagen protein, which becomes hardened by deposits of hydroxyapatitie.

64
Q

how do osteoclasts work?

A

they resorbe the bone, by dissolving the hydroxyapatites and return the bone calcium to the blood.

65
Q

what is the difference between hypocalcemia and hypercalcaemia and explain the reaction of PTH to these cases.

A

hypocalcaemia ([Ca] to low) and PTH secretions increases, where is hypercalcaemia is when the concentration of calcium is to high, and the secretion of PTH decreases

66
Q

how does Vitamin D, increase calcium levels?

A

it act on the intestines to absorb more Ca2+ from food and drink. its procudes from its precursor molecule (7-dehydrocholesterol) under the influence of UV’s. V D3, is sereated into the blood, and functions as a prehormone and is changed once again in the liver. it doesnt activate until a hydroxyl is added to C1. (done through PTH stimualtion)

67
Q

what is calcitonin, and where is it made?

A

its made in C cells of thyroid in response to increased [Ca2+], it play a minor roll.

68
Q

how is phosphate metabolism controlled?

A

same mechanisms that regulate Ca2+ metabolism.

69
Q

what happens from the lack of vitamin d?

A

poor bone mineralization, rickets disease in children, and osteomalacia in adults.

70
Q

hyperparathyroidism (PTH to active): name the effercts

A

hypercalcaemia, increased bone resorption, mineralization of soft tissue and increased thirst and urination

71
Q

hypothyroidism (PTH not active): name the effects:

A

hypocalcaemia, muscular weakness, and cardiac arrhythmias.

72
Q

explain osteoporosis, symptoms and treatment:

A

most common disorder of bones, reduction of quality of bine, high risk for fractures,
treatment would be calcium and vitamin D intake, hormone therapy, and exersice (to prevent)

73
Q

tested produce two kinds of cells what are they?

A

Sertoli cells and leydig cells

74
Q

which cells secreted testosterone?

A

leydig cells located between sminiferous tubules.

75
Q

why is there increased risk of infertility in males taking anabolic steroids?

A

anabolic steroids is a synthetic type of steroids. the idea is that you would be come infertile by using these steroids. (AAS mimic the effects of testosterone)

76
Q

how is the hypothalamic- anterior pituitary- testosterone axis controlled?

A 
through negative feedback:
excess androgens stimulate inhibin production, 
inhibins secreted by sertoli cells, 
inhibins inhibit FSH production
inhibins inhibit GnRH release also excess testosterone shuts down pathways
testes stop producing sperm
tested stop producing testosterone
Decrease Libido and fertility.
77
Q

what is a promising approach to male contraceptive?

A

plasma testosterone, given every 4 months.

78
Q

what two hormones are in focus when we talk about the ovarian Cycle?

A

FSH, and LH

79
Q

name the 13 components of the melanocortin system (plus 1 opoid)

A

1) menaocortin peptides: a-MSH, b-MSH, g-MSH and ACTH.
2) 5 melanocortin receptors: MC1R, MC2R, MC3R, MC4R, MC5R.
3) melanocortin AGRP
4) 2 proteins: mahogary and syndecon-3

80
Q

POMC is __________ specific?

A

tissue

81
Q

name the mutarion that follows:

1) a-MSH produce in brain inhibits food intake
2) a-MSH in skin acts on melanocytes
3) MCR (adrenal; skin; brain; penis)

A

1) mutation= early onset obesity
2) mutation= altered pigmentation
3) mutation= sexual function/ dysfunction

82
Q

HOW DOES A-MSH INCREASE BROWN/BLACK PIGMENT IN SKIN?

A

A. bind receptor (MCR)

b. Activate signal pathways
c. synthesis of MITF
d. Transcription Tyr. DCT influence pigmentation.

83
Q

What recent drug was discovered to replace a-MSH.

A

PT-141

84
Q

what is ADH and where is it stored?

A

antidiuretic hormone, vasopressin. and it is a hypothalamic hormone and is stored in teh posterior pituitary until it is needed.

85
Q

how does ADH work?

A

when you are dehydrated and there is high osmolarity in the blood stream (thick). this triggers the hypothalamus to send signals to release ADH which triggers your thirst, thins your blood, and tells your kidneys hold your H2O

86
Q

what happens when you are over hydrated?

A

you can get acute water intoxication, where plasma osmolarity is decreased therefore ADH production is reduced as well, and more water is excreted in the urine.

87
Q

what happens is ADH gene is mutated?

A

you’ll experience excessive thirst, and excess dilute urine, and diabetes insipids. (brattleboro rates lack ADH)

88
Q

When does ADH increase and decrease in every day life?

A

ADH levels increase at night, and therefore reabsorption of water increases, and nocturnal production of [urine] decreases.

89
Q

what is the balence (what a key partners involved) between water intake and loss?

A

intake: water produced by metabolism and drinking fluid.
loss: urine, feces, sweat and lungs

90
Q

where is all the water in the human body?

A

2/3 intracellular: (cytoplasm)

1/3 extracellular: (intestinal fluid, blood plasma-> kidneys, lungs and skin)

91
Q

what are some strategies for water regulaiton in special cases (animals)

A

stored lipid, so that lipid metabolism provides a significant amount of water, dry food provides some water, and kidneys of certain animals are very efficient at water recovery.

92
Q

how can an arabian camel regulate water when dehydrated?

A

1) super cooling during the night, overheating during the day (doesnt pant)

93
Q

how did the kangarro rate adapt?

A

obtains water from dry food, live in colonies underground (moist air reduces respiratory water loos), nocturnal, very dry feces.

94
Q

how do marine animals adapt to water regulation in salt water?

A

obtain water from their food (krill, fish, plankton), produces very [urine].

95
Q

how do hibernating animals accommodate to water regulation?

A

they reduce their BT (reduced metabolic rate), reduced heart rate, metabolic water from lipid balances respiratory water loss, urea recycled to produce protein, water reabsorbed from bladder.

96
Q

what 3 functions are the kidneys used for?

A

1 excrete metabolic waste products, water and electrolyte regulation, acid-base balance.

97
Q

describe the following anatomy titles of the kidneys: (ureters, urinary bladder, urethra)

A

UretersL drains urine from the kidneys
bladder: stores urine
Uretha: drains the bladder.

98
Q

name the 5 parts of the kidneys we use the most:

A

renal cortex, renal medulla, the major arteries and veins, papillae of the renal medulla (renal pyramids) renal pelvis.

99
Q

animals have different kinds of kidneys:

A

cattle have lobulated

marine mammals have reniculate

100
Q

what is and what does the nephron do?

A

it has frou regions:
Bowmans capsule, proximal convoluted tubule, loop of henle, distal convoluted tubule. there is also the collecting ducts but they are not considered part of the system (even though they are important)

101
Q

urine is formed in the nephron by 3 means: filtration, reabsorption and secretion. describe them

A

1) filtration is the movement of fluid from blood to lumen of nephron (renal corpuscle).
2) Reabsorption: after filtrate leaves bowmans its modified by reabsorption substances in the nephron tubules flow back into blood.
3) secretion: continues to remove select molecules from blood and adds them back into the nephron tubules filtrate.

102
Q

what is kidney disease?

A

this is where the nephrons dont work well anymore and a person has to go on dialysis.

103
Q

describe Bowman’s capsule

A

its two parts 1) podocyte cell body which intricate interdigitation of pedicels. the slits act as filters (they are negatively charged). only small proportions of plasma proteins are filtered, but smaller plasma solutes easily enter the glomerular filtrate.

104
Q

how does filtration in the Bowmans capsule work?

A

BHP (blood presure) forces blood plasma out of the glomerulus into bowmans capsule.

105
Q

explain the GFR and myogenic autoregulation.

A

glomerular filtration rape is determined by BHP, now BHP can change but GFR remains relatively constant, that ensures a constant flow of GF that allows reabsorption to occur.
(myogenic autoregulation)
when BHP ^, affarent arteriole constricts and efferent dilates, the opposite happens when BHP decreases

106
Q

what are juxtaglomerular cells?

A

smooth muscle cells in the afferent arteriole (JG)

107
Q

what are Macula Densa cells?

A

(MD) sensory cells in a region of the distal convoluted tubule (DCT)

108
Q

what are mesangial cells?

A

MC- connect JG and MD cells via gap junctions. they are communication cells

109
Q

what are plus sympathetic nerve fibers?

A

(SNFS) associate with affarent arterioles. they redirect blood from kidney to other organ systems.

110
Q

what happens with BP falls in the body?

A

JG cells secrete renin into the blood, and it acts on angiotensinogen to produce angiotensinogen to produce angiotensin 1, (ANG1). ANG1 is converted into ANG2 by ACE. ANG2 is a vasoconstrictor so it increases Bp.

111
Q

what is RAAS?

A

renin-angiotensin system

112
Q

what does ANG2 do?

A

it stimulates aldosterone secretion from adrenal cortex, to increase salt and water retention by the kidneys. (it increases blood volume)

113
Q

what is a problem with RAAS? how do we solve for it?

A

if your body has suffered from a heart attack or hypertension, then your RAAs goes out of control. we can give ACEi (ace inhibitors).

BIOM*3200. UOG (3 decks)

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