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pharm 110 > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q

What are the main endocrine organs

A

pineal, hypothalamus, pituitary, thyroid, PTH, thymus, pancreas and ovary/testis

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2
Q

What are hormones

A

chemicals that are released by 1 part of a cell and affect cells in a different body area
——- secreted

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3
Q

Difference between endocrine and Neuroendocrine

A

Endocrine: secreted into BS
Neuroendocrine: made by neurons + secreted into BS

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4
Q

What does exocrine mean

A

secreted into a duct which then goes into the BS
- not direct secretion into the BS

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5
Q

T or F: autocrine and paracrine chemicals are hormones

A

F- work locally not in a different part of body

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6
Q

What is autocrine

A

chemical that effect the same cell (or type of cell) that secretes it

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7
Q

What is a paracrine chemical

A

chemical that affect nearby cells; responses to allergens, tissue repair, and blood clotting

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8
Q

T or F: a chemical can be autocrine and paracrine

A

True

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9
Q

How do hormones work (general)

A

bind to target cell receptor and alter its activity by…
1) activating secondary messengers
2) direct gene activation (ex// steroid) —- go into cell directly

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10
Q

Effects of hormones on cells (general)

A

increase PM permeability, change protein synthesis, change enzyme states, stimulate mitosis

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11
Q

Where does hormone specificity come from

A

come from receptor binding; hormone binds to a specific receptors
- receptors can be found on only 1 cell type or can be on multiple tissues

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12
Q

What impacts receptor and hormone binding/activation

A

blood hormone levels, number of receptors on target, and affinity of hormone for receptor

—- can upregulate or downregulate receptor amount on target cell in response to hormone-receptor binding

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13
Q

T or F: hydrophobic hormones freely circulate in blood

A

F —- hydrophobic hormones need to be bound to protein

hydrophilic —- freely circulate

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14
Q

What controls hormone level in the blood

A

controlled by negative feedback loops
- vary within desired range
- concentration represents the rate of release, speed of inactivation and removal of hormone from the body

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15
Q

What stimulates hormone synthesis/release

A

1) humoral: ion/nutrient stimulated release; released based on changes in levels (Ex/// Calcium and PTH)

2) Neural: nerve fibers stimulate release (Adrenal medulla — NE + E)

3) Hormonal: release in response to different hormones (tropic — hormones that cause the release/effect other hormones)

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16
Q

Types of interactions of hormones with target cells

A

1) Permissiveness: 1 hormone doesn’t work without the others (allow each other to work)

2) Synergism: 2 hormones have the same effect

3) Antagonism: work against each other

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17
Q

T or F: The NS can override and take control of the endocrine system (ex// release of hormones —— go outside of normal range)

A

T
- NS can modify the stimulation of the endocrine glands and their negative feedback loops
—- if we really need something (ex// need more glucose due to stress) : NS can kick in and increase glucose amounts outside of the normal range set by the endocrine organs

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18
Q

T or F: Eicosanoids are true hormones

A

F - they are autocrine and paracrine

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19
Q

Types of Eicosanoids (general classes)

A

prostaglandins - inflammation , fever, induce labour, prevent BC

thromboxane - promote BC

leukotrienes - allergic rxn

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20
Q

T or F: Eicosanoids are derived from AA

A

true —- from AA in PM
- AA produced from alpha-linolenic acid (omega 3) and linoleic acid (omega 6)——— don’t make these

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21
Q

T or F: AA is converted into prostaglandins by LOX enzyme

A

F - Membrane PL —— AA (by phospholipase) —- PGH2 (COX) —— prostaglandins + thromboxanes

AA——- Leuokotrienes by LOX

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22
Q

What inhibits the COX enzyme

A

NSAIDS

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23
Q

What specifically inhibits COX2

A

VIOX — increase CVD risk

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24
Q

Different eicosanoids produced in the prostanoid path and their effects

A

Prostaglandins- induce labour, vasodilator, pain , pyretic
prostacyclins- inhibit BC, vasodilation
thromboxane - promote BC, vasoconstrictor

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25
Q

What are the AA hormones

A

amines, thyroxines, peptides, protein hormones

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26
Q

What does Gs do when activated

A

activated adenylate cyclase —— converts ATP to cAMP —- activate PKA

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27
Q

What does Gi do

A

inhibits adenylate cyclase —- decrease cAMP and PKA activation

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28
Q

What is the PIP2 path

A

hormone + receptor —- activate Gq —- activate PC

PC- cleaves membrane bound PIP2 into IP3 (free) and DAG
— IP3: causes release of Ca from ER—- Ca interact with calmodulin
— DAG: activate PKC

** together trigger cell response

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29
Q

T or F: cAMP, DAg and IP3 are synergistic

A

T- cause insulin release from cell

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30
Q

T or F: steroid hormones are hydrophobic and can just move into the cell and through the PM and NM

A

T-just move into the nucleus and interact with receptor/chaperone complex
—— this complex (minus chaperone - leaves once hormone binds) binds to DNA and causes changes in gene expression
—— need 2 hormone+receptor complexes to bind to DNA to get effect

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31
Q

T or F: steroid hormones and AA hormones cause immediate cell response

A

F — steroid takes longer because cause changes in gene expression —- change proteins etc

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32
Q

E2 and Breast cancer

A
  • E2 levels are higher in BC — drugs look to modulate and target this pathway
  • block the interaction bw the 2 receptors
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33
Q

How do Tamoxifen and Raloxifiene work - BC

A

block the e2 binding by changing receptor shape

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34
Q

How does herceptin work

A

AB used to treat BC with HER2 (found in more metastatic BC)
— prevents dimerization of HER2 + targets cell for destruction

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35
Q

T or F: Neurohypophysis is found in the anterior lobe

A

F
Neurohypophysis : posterior lobe, neural tissue — extension of hypothalamus into PG ( cell body in hypo and axons release hormones here
—- fxn to receive, store and release hypothalamus hormones

Adenohypophysis: anterior lobe, glandular tissue that make and secrete their own hormones

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36
Q

What connects the PG and the hypothalamus

A

infundibulum

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37
Q

Posterior Lobe pathway

A

cell bodies in PVN and SON (hypothalamus )- axons pass through infundulum
—- hypothalamic - hypophyseal tract
—— synapse in Posterior lobe

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38
Q

Anterior lobe pathway

A

cell body in VH of hypothalamus —- secrete hormones into the blood via hypophyseal portal system (how Anterior lobe and hypo connected)
—- primary capillary plexus —- hormone travels along hypophyseal portal veins to anterior pituitary glands where stimulates or inhibits hormone release from anterior lobe— anterior lobe releases hormones in the 2nd capillary plexus

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39
Q

What connects the hypothalamus and anterior lobe

A

vascular connection vis hypophyseal portal system

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40
Q

What hormones are released from Anterior lobe of pituitary

A

TSH
FSH
LH
ACTH
GH
PRL

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41
Q

Tropic anterior lobe hormones

A

TSH, ACTH, FSH, LH, GH,

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42
Q

What does hypothalamus CRH stimulate release of in AL

A

corticotroph cells release ACTH

43
Q

What does hypothalamus TRH stimulate release of in AL

A

stimulate TSH (Thryotroph) and PRL (Lactotroph) secretion

44
Q

What does hypothalamus GHRH stimulate release of in AL

A

stimulate GH release by somatroph

45
Q

What does hypothalamus GHIH stimulate release of in AL

A

inhibits release of GH by somatotroph cells

46
Q

What does hypothalamus GRH stimulate release of in AL

A

release of LH and FSH by gonadotroph cells

47
Q

What does hypothalamus prolactin releasing hormone stimulate release of in AL

A

stimulate PRL release (along with TRH) by lactotroph

48
Q

What does hypothalamus dopamine stimulate release of in AL

A

inhibit release of PRL by lactotroph

49
Q

Growth hormone function

A

anabolic tissue building —- increase size, division and metabolic activity

targets- liver (primary target) bone and skeletal muscle

Directly - affects the metabolic activity, fat breakdown and carb metabolism in liver, SM and bone

Indirectly - stimulate release of IGF-1 by liver: IGF-1 stimulates cartilage growth and extra skeletal protein synthesis and division

50
Q

Affect of IGF-1 on GH release

A

negative feedback loop—- inhibits GHRH release by hypothalamus and increase release of GHIH by hypo

51
Q

What is Acromegaly

A

when make too much GH; occurs after puberty (epiphyseal plates fused)
—- tissue swelling, changes in pigment and skull expansion

52
Q

Gigantism

A

excess GH secretion that occurs before puberty —- bone elongation and tissue swelling

53
Q

Impact of ACTH

A

released by corticotropin cells in anterior lobe
—- stimulated by internal and external stressors
— target the adrenal gland

*stimulate release of cortisol by cortex (long term stress)
*Medulla: not regulated by NE and E

54
Q

What do FSH and LH do

A

regulate function of ovaries and testes
- FSH is not released until puberty

FSH - stimulate gamete production

55
Q

FSH and LH: females

A

cause maturation of ovarian follicle

LH: trigger ovulation on its own , mediate synthesis and release of estrogen and progesterone

56
Q

FSH and LH: males

A

make and mature sperm

57
Q

What does Prolactin do

A

stimulate milk production in females (release triggered by PRH and inhibited by PIH)
—- levels increase near end of pregnancy
— sucking stimulate release of PRH —- increase PRL and milk production

58
Q

What hormones are released at posterior lobe

A

oxytocin and ADH
- made in PVN and SON of hypothalamus — travel along axons via hypothalamic and hypophyseal tract —— released from posterior lobe when stimulated
—- released directly into blood (axons synapse with BS)

59
Q

T or F: Oxytocin is regulated by a negative feedback loop

A

F - positive feedback loop
—- leads to increased intensity of uterine contractions during birth
—- used to induce labour + trigger milk ejection (let down reflex)

60
Q

Roles of oxytocin

A

increase intensity of uterine contractions

let down reflex : increase in levels cause milk to spit out : cause mammary lobes to contract and eject milk (will keep going till no more sucking)

role in sexual arousal in M+ F

61
Q

Role of ADH : posterior lobe hormone

A

helps maintain plasma osmolarity
— osmoreceptors in hypo
—-High solute: ADH release —— increase water preserved (increase uptake at kidney, decrease )
— Low solute: inhibit ADH release

62
Q

T or F : alcohol inhibits ADH release

A

T

63
Q

Cells that make up the thyroid gland and their roles

A

Follicle cells - produce glycoprotein thyroglobulin (thyroid hormone precursor)
Parafollicular cells : fill space bw follicle and colloid
colloid : fluid filled space

64
Q

What does thyroid hormone do

A

targets a lot of cells
- concerned with glucose oxidation , increase metabolic rate, heat production
- maintain BP, regulate tissue growth, develop skeletal and NS (not adult brain)

**elevated and maintain normal body fxn

65
Q

What tissues does thyroid hormone not affect

A

USTAT
- uterus, spleen, thyroid gland, adult brain, and testes

66
Q

T or F: there are two types of TH iodine compounds

A

T
T4 : thyroxine , 2 tyrosine + 4 iodine (less active)
T3: Triiodothyronine: 2 tyrosines + 3 iodines ( more active)

67
Q

Steps to TH synthesis

A
  • thyroglobulin (134 tyrosine) synthesized in follicle and discharged into the lumen —- sent to the colloid via exocytosis
  • Iodides (I-): actively taken into the cell, oxidized into I2 + release into lumen (colloid)
  • Thyroid peroxidase (made by follicle) : sent into colloid, attaches iodine to tyrosine —- T1 and T2 in lumen
  • Link them together to make T3 and T4 in colloid
  • Endocytosis of T3 and T4: cleaved in follicle cell lysosome; diffuse into BS (taken up by carrier protein)
68
Q

Who makes the thyroid binding protein

A

liver ; binds to T3 and T4
- binds to t3 better

69
Q

T or F: peripheral tissue can convert T4 to T3 if need more TH

A

T

70
Q

Mechanism of TH activity

A

steroid like
- bind to receptor in cytosol or nucleus —- bind to DNA

71
Q

Hypothyroidism

A
  • low levels of T4 (and T3) —- increased release of TSH by pituitary
    —- stimulating thyroid to make shit but not enough iodine to make TH
    —- stimulating formation but not making cuz cant

Effects: decrease metabolic rate, lethargy, goiter (enlarged gland)

Infants —- Cretinism

72
Q

Graves’ disease

A

autoimmune
AB mimics TSH : so keeps stimulating TH release
—- symptoms caused by high levels of T4 and T3

Symptoms: high heart rate, muscle weakness, disturbed sleep, goiter exophthalmos

73
Q

What is Calcitonin

A

peptide hormone produced by parafollicular cells
- helps decrease blood Ca levels in children
- inhibit osteoclasts activity and stimulating Ca incorporation in bone matrix

74
Q

T or F: PTH oxyphil cells release PTH

A

F. chief cells secrete it

75
Q

Function of PTH

A

regulate Ca levels in the blood : increases Ca levels in the blood
- works against calcitonin
- stimulating osteoclasts, enhancing reabsorption of Ca + increase P secretion by kidneys; promotes Vit D activation to calcitriol

—- negative feedback loop: inhibits its own release as Ca levels rise

76
Q

T or F: the adrenal medulla is the external neural tissue part of the adrenal gland and the adrenal cortex is the endocrine tissue on the inside of the gland

A

F
medulla: internal and neural tissue; part of the SNS (release NE +E)

cortex: external and release steroid hormones — corticosteroids

77
Q

Layers of the adrenal cortex

A

Zona glomerulosa: top, release mineralocorticoid
Zona Fasciculata: release glucocorticoids
Zona reticularis: bottom , release gonadocorticoids

78
Q

What are the classes of hormones released by the adrenal cortex? what is the precursor

A

precursor: cholesterol

classes;
progesterone
Glucocorticoid: cortisol, and corticosterone (long term stress)
Androgens: Testosterone + DHEA, DHT
Estrogens: E1-3
Mineralocorticoids: aldosterone

79
Q

Connections between the different classes of adrenal cortex hormones

A

cholesterol ——- progesterones ——- glucocorticoids — mineralocorticoid

progesterones —— androgens —— estrogens

80
Q

Fxn of Aldosterone

A

regulate Na levels: maintain levels by decreasing excretion + stimulating resorption by kidneys

4 regulators
1) Renin angiotensin : decrease in BV/BP — causes renin release by kidneys —- angiotensin II release — stimulate aldosterone
2) increase K- influence zona g. cells
3) ACTH: released by Anterior PG due to stress to increase
4) ANP - inhibit release (made by heart; detect increase in BP/BV)

81
Q

Functions of glucocorticoids (cortisol, cortisone and corticosterone)

A

help body resist long term stress
- help keep glucose levels constant + BV constant; prevent water shift to tissue
- provoke gluconeogeneis : increase glucose, AA and FA —— energy motivator

=if high for a long time : negative impacts (decrease bone formation , inhibit inflammation and immune)

82
Q

Fxn of Gonadocorticoids

A

Mostly androgens (test)
- contribute to start of puberty, appearance of 2nd sex traits + female sex drive

androgens convert to estrogen after menopause

83
Q

What cells release hormones in adrenal medulla

A

chromaffin cells — release the catecholamines (NE, E and dopamine)
— strong term stress

84
Q

NE fxn

A

peripheral vasoconstriction and increase BP

85
Q

E fxn

A

increase HR, dilate bronchioles, increase BF to skeletal muscle, brain and heart
- liver breaking down glycogen —- glucose

86
Q

What has a more rapid onset: cortex or medulla

A

Medulla —- nervous system
cortex —— hypothalamus —- CRH —— ACTH —- cause release of hormones at cortex

87
Q

Paracreas : cell types

A

exocrine : produce enzymes and buffers for digestion
endocrine ; form islets which release hormones (islets made from alpha cells, beta and delta cells

88
Q

What does the pancreas alpha cells make and what does it do

A

glucagon made by alpha cells (exterior of pancreatic islets)
- hyperglycemic agent
- released in response to low glucose: causes increase in glucagon breakdown, glucose synthesis
- glucagon inhibits B cells
- negative feedback

**Long term hypoglycemia — liver produces ketones from FA as energy source to use in place of glucose *

89
Q

What does B cells secrete and its function

A

insulin + amylin secreted by internal B cells

insulin: made from proinsulin (contains A,B.C peptides: cleave off C; so 2 AA chains with disulfide bonds

  • function : increase glucose transport in cells/ decrease blood glucose levels
  • release when glucose is high: causes liver to increase making/storing glucose as glycogen )
  • inhibit alpha cells
90
Q

differences between Type 1 and Type 2 diabetes

A

Type 1: early onset, more severe — autoimmune so attack and kill B cells (can’t make insulin) , eating —- but wasting away

Type 2: adult onset, cells don’t respond right to insulin (disregulation of insulin secretion , increase or decrease release); diet and exercise help

91
Q

Cardinal symptoms of Type 1 diabetes

A

polyuria, polydipsia and polyphagia

92
Q

Main targets of insulin

A

liver, skeletal muscle and adipocytes

93
Q

Impacts of low insulin: diabetes

A

Liver (break down glycogen) + SM (breakdown protein) —- increase in blood glucose levels —- increase in glucose in urine which pulls more water out of the body
—— causes polyuria and polydipsia

adipocytes; increase breakdown of fat + SM break down protein —- polyphagia
—- increase fat breakdown also converted into ketone bodies in liver, decrease blood pH=== more ketones in blood which pulls more ions with it

**increase in glucose and ketones in urine —- pulls water and ions in urine —— give symptoms

94
Q

What do ovaries produce and what does it do?

A

produce estrogen and progesterone — help maturation reproductive organs,2nd sex traits, breast development and cyclic changes

— cyclic release of FSH and LH which impacts estrogen and progesterone
-increase in estrogen during follicular phase
luteal —- high progesterone

95
Q

What do the testes produce and what does it do

A

produce testosterone —- starts maturation of reproductive organs, sex drive, 2nd sex traits and sperm production

96
Q

What does the pineal gland produce and how is its release controlled?

A

produces melatonin- helps with rhythmic control of body temp, appetite and day/night cycles

  • has neural projections from SCN: gets light signals
  • melatonin helps SCN sense length of night
  • circadian pacemaker — SCN (regulates melatonin release to ensure right levels at right time
97
Q

What does the thymus produce and its function

A

thymopoietins and thymsins - T cell maturation

98
Q

Adipose produces..

A

leptin, resisted, adiponectin

99
Q

GI produces…

A

gastric, intestinal gastric, secretin, CCK and incretins

100
Q

Heart produces

A

atrial natriuretic peptide

101
Q

kidney produces..

A

EPO and Renin

102
Q

skeleton produces..

A

osteocalcin

103
Q

skin produces…

A

cholecalciferol

pharm 110 (4 decks)

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