module 3- endocrine Flashcards
1
Q
hormone function
A
allow cells that are not beside each other to communicate in synchronized functions
2
Q
paracrine vs neurotransmitter communication
A
P- short, local
N- long, distant
3
Q
endocrine cells function
A
dump message into blood & only effector will be the cell that has a receptor for that message
4
Q
neurohormone
A
nerve cell that drops a neurhormone into blood & communicates with faw away cells
5
Q
parahormone function
A
messages to another animal
6
Q
3 types of hormones
A
1) peptides & proteins
2) amines
3) steroids
7
Q
amines are derived from
A
tyrosine
8
Q
steroids
A
neutral lipids derived from cholesterol
9
Q
peptides
A
chains of amino acids- long or short
10
Q
what are all steroids derived from?
A
cholesterol
11
Q
T or F: steroid structures are similar but have very different affects on the body
A
T
12
Q
4 types of steroids & what they are
A
1) testosterone- male
2) estradiol- fermale
3) corticosterone- stress
4) aldosterone- water retention
13
Q
why does insulin get injected, not taken in pill form
A
b/c peptides get denatured in the stomach
14
Q
why can estrogen for birth control be taken using pills?
A
estrogen does not get denatured in the stomach
15
Q
peptides & catecholamines are ( ) and steroids & thyroid hormones are ( )
A
hydrophilic, lipophilic
16
Q
where are peptides produced
A
ribosomes on rough endoplasmic ret
17
Q
preprohormone
A
long chain of amino acids
18
Q
how are peptides synthesized steps
A
1) preprohormone is synthesized
2) pruned to prohormone
3) cut to active hormone in golgi complex
4) gets concentrated in golgi complex & packaged into vesicles to be ready for use
5) released into body via exocytosis when stimulated
19
Q
where do the bits from cutting of the peptide hormone go?
A
used to make other things from POMC
20
Q
steroid hormone synthesis steps
A
1) cholesterol from diet or LDL
2) enzymes modify cholesterol into hormone
3) steroid hormone is produced & secreted right away b/c they cannot be stored
4) diffuse through membrane into blood & some undergo further modifications
21
Q
amine hormone synthesis
A
1) derived from tyrosine
2) undergoes modification
3) stored until needed
4) thyroid hormone undergoes further processing after release
22
Q
peptides, steroids & thyroid hormone transport
A
peptides: freely in plasma or bound to carrier
steroids & thyroid hormones: dragged by plasma protein b/c they cannot dissolve
23
Q
T or F: only free lipophilic hormones are active
A
T
24
Q
what is the goal of hormone transport?
A
maintain hormonal equilibrium through feedback loops
25
what occurs after a free hormone has interacted with its target cell
it gets inactivated
26
tropic vs non-tropic hormones & their targets
tropic- regulate production/secretion of another hormone by acting on it
target: endocrine tissues
non-tropic: final product, acts on regular cells & does not regulate other hormones
target: non-endocrine tissue
27
T or F: hormones act like key & lock system
T
28
2 categories of receptor & hormone interactions
1) membrane receptors
2) internal receptors
29
membrane receptors
bind a receptor outside plasma membrane to start a chain of reactions
30
internal receptors
bind to specific receptors inside the cell, often produce new protein
31
where does hormone binding occur?
HRE (hormone response element)
32
hormone effects on transcription steps
1) hormone gets dropped & tries to leave cell
2) finds specific receptor & binds = activates it
3) goes to nucleus & finds HRE to activate some gene
4) cell makes a new protein
33
negative feedback loops
counteracts any change
34
TRH, TSH, TH- tropic or non-tropic
TRH & TSH= tropic
TH= non-tropic
35
when are neuroendocrine reflexes used for hormonal regulation?
to produce a sudden increase in hormone secretion in response to an external stimulus
36
catecholamine vs cortisol release time
cat- released within seconds, very fast so cannot measure
cort- peaks after 1 hour
37
what is circadian control and when is it used to regulate hormone secretion?
anticipatory regulation allows your body to adjust cyclical changes
example- cortisol cycle
38
when is cortisol the highest?
early morning
39
hasimotos disease
destroys thyroid hormone =no thyroid hormones
40
hormone elimination is primary through
urinary excretion
41
human chorionic gonadotropin hormone (hCG)
detecting hormone produced by the fetus
42
the response of a cell to hormone is correlated with
number of receptors
43
downregulation of hormones & example
presence of hormones reduces number of receptors on the cell
example-type II dabetes
44
type II diabetes
too much insulin so your cells stop responding
45
pineal gland
controls circadian rhythm via light/dark and secretes melatonin
46
in low light ( ) melatonin is produced
more
47
melatonin effects
sleep, blood pressure, & anti-imflammatory
48
ADH & oxytocin are released by the ( ) but produced in the ( )
posterior pit, hypothalamus
49
what type of diabetes is caused by ADH deficiency
diabetes insipidus
50
central vs nephrogenic diabetes insipidus
c: no ADH secretion
n: kidneys do not respond to ADH
51
prolactin vs oxytocin in relation to milk
p- milk production
o- milk delivery
52
what 2 hormones stop milk from being produced when not needed
progesterone & estrogemn
53
what hormone increases during pregancy
prolactin
54
how many hormones does the anterior pit produce?
6
55
portal system
2 capillary beds back to back without going through the heart
how hormones travel
56
portal system pathway
heart, artery, capillaries in hypothalamus (picks up hormone), veins, capillaries in anterior pit (drops hormone & picks up new one, veins, heart
57
if hypothalamus drops TRH, the anterior pit stimulates ( ) TSH
release of
58
hypothalamus secretes its own tropic hormone in response to
stress
59
what occurs if you do not have stress
corticosteroids have antigrowth effects
60
when does GH get released
when body is running out of glucose
61
overall effect of GH on metabolism
mobilize fat stores & keep glucose for the brain
62
indirect effect of GH on growth
effects are mediated by IFGs
63
how are IGF-1 stimulated
by GH
64
what is the most important IGF for growth
IGF 1
65
IGF-2 is important for
muscle growth
66
T or F: IGF-2 is independent of GH
T
67
hyperplasia
increase number of cells
68
hypertrophy
increase in the size of the cells
69
IGF-1 is important for
soft tissue and bone growth
70
T or F: bone is a living tissue
T
71
what are the 2 components of bone
cells & extracellular matrix
72
why is a bone strong
it is calcified
73
what is a long bone made of?
diaphysis, epiphysis & epiphyseal plate
74
long bone formation steps
1) cylindrical shaft- diaphysis
2) articulating knobs at both end- epiphysis
3) layer of cartilage separating the 2- epiphyseal plate
75
how do bones grow thicker vs longer
thicker- adding new bone on top of old bone
longer: proliferation of cartilage cells in epiphyseal plates
76
T or F: thickness of cartilage reflects how much growth you have left
T
77
what is the epiphyseal plate made of
chondrocytes (non-calcified)
78
how does a bone grow?
1) chondrocytes divide & start creating a new layer
2) everything gets pushed down to grow the knob
3) calcification of extracellular matrix
4) dead chrondocytes are cleared by osteoblasts
5) osteoblasts deposit bone over top of everything, die & become regulate bones
6) plate shifts up & bone gets longer
79
osteoblast vs osteoclasts
osteoblasts- builds
osteoclasts- blasts
80
GNRH vs GHIH stimulatory or inhibitory? where do they come from?
GNRH- stimulatory
GHIH- inhibitory
comes from hypothalamus
81
high amino acid concentration & low fatty acid concentration does what to GH
increase
82
growth hormone deficiency
- cause
- effect on newborn vs adult
- treatment
caused by pituitary issues or congential
newborn: dwarfism
adult: no effects on growth, but see effects on soft tissues
treatment: injection of GH
83
provacative test
tests for GH deficiency
injects insulin & if peaks then normal, but if no peak then GH problems
84
growth hormone hyperproduction
- cause
- effect on children vs adults
- treatment
- how to diagnose
cause: pit issues or congenital
children: gigantism
adults: acromegaly - soft tissue overgrowth
treatment: injection of GHIH
diagnose: if given glucose, GH will not drop
85
acromegaly
constant production of GH & causes soft tissue to continue growing
86
what is considered gigantism
over 2.2 meters
87
T or F: HGH (human growth hormone) does not have performance enhancement
T
88
thyroid gland shape/location
sits like a bowtie down the front of the neck
1 gland- 2 lobes
89
follicular cells
spheres full of fluid that stores TH
90
what is the backbone to TH
thyroglobulin
91
where is iodine stored
colloid of thyroid gland
92
follicular cells produce what 2 iodine containing hormones?
T3 & T$
93
to make TH, you need
tyrosine & iodine
94
what form of TH is the major biologically active form?
T3
95
T or F: most TH is bound to plasma proteins
T
96
3 main things TH are supposed to do:
metabolic effects, cardiovascular effects & growth/nervous system effects
97
what can be used to measure BMR
O2 consumption
98
endotherms vs ectotherms TH levels
en- high
ec- low
99
3 cardiovascular effects of TH
increase HR, cardiac output & heat production
100
T or F: GH cannot be secreted properly if not enough TH
T
101
T or F: AP transmission can be slowed down if not enough TH
T
102
dwarfism on GH levels
GH is normal, but b/c there is not enough TH, the GH could not do its job
103
T or F: hair loss occurs with low TH
T
104
SNS effect on TH
increase
105
T or F: TH controls metamorphosis
T
106
what is the most important regulator of the TH secretion
TSH (thyroid stimulating hormone)
107
how to increase TH
size & number of cells
108
T or F: TH release is slow
T
109
why does TRH production increase in cold newborn mammals?
kickstarts negative feedback loops to increase TH b/c they cannot thermoregulate on their own
110
hypothyroidism
- what is it
- causes
- symptoms
low TH levels
not enough TRH, damage to thyroid gland itself, no iodine
cold, weight gain, hair loss
goiter
111
disease formed when hypothyroidism from birth
cretinism
112
why does hypothyroidism from birth lead to cretinism
GH needs enough TH to do its job so with too little TH=GH cannot do its job
113
cretinism
physical & mental growth impairment
114
treatment to hypothyroidism
thyroxine & iodine supplement
115
hyperthyroidism
too much TH, more signalling for TSH which causes thyroid gland to grow = goiter
116
how to treat hyperthyroidsm
remove thyroid gland & low iodine diets
117
2 layers of adrenal glands
1) outer: adrenal cortex- secretes steroids
2) inner: adrenal medulla - secretes catecholamines
118
3 layers to adrenal cortex
1) zona glomerulosa (outermost)
2) zona fasiculata (middle & largest)
3) zona reticularis (inner)
119
3 main jobs of the adrenal glands
salt, sugar, sex
120
3 main categories of steroids
1) mineralocorticoids
2) glucocorticoids
3) sex steroids
121
mineralcorticords
electrolyte balance, aldosterone, produced by glomerulosa
122
glucocorticoids
glucose, lipid & protein metabolism
- cortisol & corticosterone
- produced by fasicultata & reticularis
123
most important sex steroid
DHEA
- produced by fasiculata & reticularis
124
what carries only glucocorticoids
transportin
125
4 metabolic effects of glucocorticoids
1) stimulate gluconeogenesis
2) inhibit glucose uptake
3) stimulate protein degradation
4) facilitate lipolysis
126
permissiveness
one hormone must be present in adequate amount for full exertion of another hormones effect
127
lack of cortisol can cause
hypovolemia = not enough blood flow
128
stress
generalized response to any factor that overwhelms the bodys ability to maintain homeostasis
129
how to glucocorticoids help manage stress
release of them increases the availability for blood glucose to protect the brain from malnutrition
130
lymphocytes release ( ) when activated
ACTH
131
low, high, very high stress effects
low: no anti-inflammatory effects
high: anti-inflammatory effects
very high: immunosuppression
132
glucocorticoids inhibits the secretion of ( ) and ( )
CRH & ACTH
133
what factors influence secretion of glucocorticoids
stress & circadian rhythm
134
HPA suppression on glucocorticoids
inhibits release of ATCH = adrenal gland is not stimulated = little cortisol available
135
ATCH is responsible for the adrenal cortex ( )
size
136
what can occur if a steroid drug is stopped immediately
vomiting, fatigue, low BP
137
T or F: adrenal cortex produces androgens & estrogens in both sexes
T
138
the only adrenal sex hormone that has significant biological effects is
DHEA
139
what does androgens in females cause
pubic hair, armpit hair, sex drive & puberty growth spurt
140
hyerpadrenocorticisim
- what is it
- disease example
- cause
- symptoms
- treatment
- too much cortisol caused by too much CRH or ATCH
- cushings
- increased appetite = weight gain & high BP
- destroy adrenal cortex to stop producing cortisol
141
hypoandrenocorticism
- what is it
- disease example
- cause
- symptoms
- treatment
too little cortisol
- addisons disease
- aldosterone deficiency
- weak & lethargic
- glucocorticoids & mineralcorticoids (aldosterone)
142
how do chromaffin cells work in the adrenal cortex
dump their neurohormones directly into the blood & do not send signals to other neurons
143
what do chromaffin cells release
epinephrine & some NE
144
only ( ) is released as NT from post-ganglionic fibre but ( ) and ( ) are released as hormones from adrenal medulla
NE, NE & epinephrine
145
how is NE released from chromaffin cells
exocytosis
146
how is catecholamine secretion from adrenal medulla controlled
SNS input
147
5 effects of epinephrine
1) cardiac effects = increase CO
2) a-1 = vasoconstriction & b-2 causes selective vasoconstriction
3) respiratory effects = bronchodilation
4) metabolic = glycogenolysis & increase metabolic rate
5) less salivation = no need to digest
148
catecholamine function
TH increase adrenergic receptors & cortisol
149
T or F: everything increases blood glucose level but not insulin
T
150
slow vs rapid stress responses
slow= CRH
rapid= CNS
151
epigenetic effects
infant rearing modifies activation of HPA axis = can transfer via genetics
152
the number of glucocorticoid receptors is related to
HPA axis
153
3 fuel molecules
protein, carbs & fats
154
2 complications to interconversion of nutrients
1) need energy released during fasting periods
2) brain needs continuous energy but only can use glucose
155
normal range of glucose
70-100mg/ml
156
sorbitol
stays in eyes & causes cataracts due to long term high concentrations of glucose
157
glucose homeostasis prevents ( hypoglycemia) and ( ) hyperglycemia
short term, long term
158
HbA1c test
tests blood glucose level over last 3 months
more free glucose = good at controlling glucose
159
3 alternate energy sources
glycerol, lactate, ketones
160
when is the only time the brain can use a non-glucose energy source
use ketones during starvation
161
beta vs alpha cells
b- insulin synthesis & secretion
a- glucagon
162
when are delta cells released
high glucose & AA in blood
163
overall effect of insulin
decrease blood glucose concentration, AA & FA
164
GLUT
glucose transporter, moves glucose into a cell so it gets methylated & trapped
165
GLUT 1, 3 & 4
1- moves glucose through blood brain barrier (insulin-independent)
3- transport glucose into neurons (insulin-independent)
4- release via exocytosis to increase absorption when insulin is detected (insulin-dependent)
166
why does exercise help with managing diabetes
it can mimic activity of insulin & absorb all the extra glucose
167
insulin control of beta cells for high vs low glucose
high: activates beta cells = release insulin
low: inhibits beta cells = no insulin release
168
glucagon has ( ) effects of insulin
opposite
169
glucagon control on alpha cells for high vs low blood glucose
high: inhibits alpha cells = no glucagon secretion
low: activates alpha cells = glucagon secretion
170
diabetes mellitus
elevated blood glucose levels
171
type 1 vs 2 diabetes
1) insulin dependent
- no insulin produced
- genetic
2) insulin independent
- insulin produced but cells stop responding
- mature onset
172
chances of getting diabetes increases after the age of
40
173
long term effects of diabetes
blindness & leg pain
174
prevention of diabetes
avoid sugar spikes, work out, lose weight
175
how can fiber diets help with preventing diabetes
can slow down rate your body produces sugar
176
what is one of the most tightly controlled variable
calcium
177
short vs long term calcium homeostasis
short: neuromuscular excitability, blood clotting cascade
long: structural support in bones & teeth, milk production, egg laying
178
where is 99% of Ca found
bones & teeth
179
bone fluid
liquid layer around hard layer so need to decrystalize it to get ions
180
2 timescales of Ca regulation
short- give ions of Ca to bones
long- control how much Ca to keep & excrete
181
primary scale of short term vs long term calcium regulation
short: rapid exchange between bone & ECF and via urine
long: diet & reabsorption
182
parathyroid gland function & secretion
control Ca regulation & release parathyroid hormone (PTH)
183
effect of PTH
increase Ca in plasma
184
what happens if you have no PTH
asphyxia
185
how do Ca pumps work
parathyroid gland detects low Ca, PTH goes to Ca pump & the pump grabs Ca from bone & pumps it out to plasma
186
fast vs slow exchange of Ca from bone fluid
fast: Ca pump takes Ca from bone fluid & into plasma
slow: bone must be dissolved by osteoclasts= Ca produced for bone fluid to store
187
osteoblasts are derived from ( ) once trapped inside bone they become ( )
stroma cells, osteocytes
188
osteoclasts are derived from ( )
macrophages
189
bone spurs
natural bone growth in response to tension & creates a bump
190
estrogen increases ( ) apoptosis
osteoclast
191
T or F: adults cannot deposit Ca into bones anymore, just strengthen the outside layer
T
192
osteoporosis
taking all Ca away from bone
193
<6 vs >6 phosphorus levels & bone
<6= liquid form
>6= crystalizes
194
if phosphate increass = plasma calcium ( )
decreases
195
hypocalcemia
try lower plasma phosphate & increase plasma calcium concentrations
196
T or F: you need P & Ca to make bones
T
197
calcitonin
produced by C cells in the thyroid, decreases Ca plasma concentration
198
short vs long term calcitonin
short- decreased Ca movement into plasma
long- inhibits osteoclasts
199
T or F: vitamin D is an essential nutrient
T
200
2 ways vitamin D gets activated
sunlight or diet
201
3 steps to activate vitamin D
1) sunlight
2) liver (add HO group)
3) kidney (add another HO group)
202
vitamin d3 requires two ( ) groups to be activated
hydroxyl
203
calbindin
transporter for Ca
204
3 functions of vitamin D
1) Ca absorption
2) phosphate absorption
3) bone responsiveness to PTH
205
overall function of vitamin D
long term calcium balance
206
hyperparathyroidism
- what is it
- cause
- symptoms
excess secretion of PTH
low Ca & vitamin D diets or tumor of parathryoid gland
kidney stones, weak bones
207
vitamin D deficiency
- cause
- symptoms
not enough sun exposure or low diet supplementation
- low absorption of Ca
- rickets
208
rickets
soft bones that bend under pressure of body weight = arched legs
209
milk fever & treatment
hypocalcemia
IV or sub-q calcium
210
milk fever prevention
high Ca diets to trigger calcitonin pathway
