Phys Exam 3 Flashcards
(440 cards)
1
Q
what are receptors
A
proteins or glycoproteins that bind different chemical signals
2
Q
where can you find receptors
A
cells’ plasma membrane or within the cytoplasm or nuclear membrane
3
Q
what are ligands
A
molecules like hormones, NT, and drugs that bind to a receptor
4
Q
can some NT act as hormones?
A
yes!
5
Q
some hormones can have what properties?
some growth factors can have what properties?
A
hormones can have GF like properties and visversa
6
Q
are hormones released at low or high concentrations?
A
LOW! they are super potent
act on target cells’ receptor
nanomolar and lower
7
Q
what is a trophic hormone
A
controls the secretion of another hormone
8
Q
what are exogenous chemicals
A
man-made
9
Q
what do exogenous chemicals do in terms of binding
A
can bind to hormone receptors (sex hormones) and exert hormone-like effects –> endocrine disrupters
10
Q
what are growth factors
A
control growth, development. activate physiological responses at LOW CONCENTRATIONS
11
Q
where do GF act
A
locally and SHORT distances
12
Q
what are cytokines
A
communication peptides produced immune system cells. produce many other non-immune system cell types
13
Q
where do cytokines act
A
locally at short distances
14
Q
what are chemokines
A
small proteins which form gradients to attract immune cells out of capillaries INTO tissue as needed, usually during inflam.
15
Q
where do chemokines act
A
locally at short distances
16
Q
what type of receptor does epi and norepi bind to
A
GCPR families -> alpha 1 and 2. Beta1-3
17
Q
what does epi do
A
released into blood. increases HR and enhances strength and physical performance
18
Q
what does norepi do
A
produced in response to low BP. promotes vasoconstriction and increases BP
19
Q
what effects can a hormone have (5)
A
PM permeability
protein synthesis
enzymatic activity -> P or de-P
induced secretion (if tropic)
stimulation of cell division/growth –> gene expression
20
Q
what type of gland is the anterior pituitary (AP)
A
endocrine
21
Q
what hormones does the AP secrete (6)
A
prolactin
GH
TSH
ACTH
LH/FSH
22
Q
what controls the release of hormones from the anterior pituitary hormones?
A
neurohormones from the hypothalamus
23
Q
what carries the trophic neurohormones to the AP
A
portal veins (portal system)
24
Q
endocrine means what
A
secreted directly into blood. disseminates WIDELY through body to affect distant target tissue receptors in an entire organ or subset of cells within that organ OR may target most bodily cells
25
what is paracrine
that cell's hormone/GF secretion affects ONLY NEARBY cells (neighboring)
26
what is autocrine
when the hormone or GF produced by a cell can also regulate ITSELF
27
what are ectohormones
released into the environment --> pheromones (detected by olfaction)
28
endocrine pathway sequence of events
stimulus
input
integration
output
target
response -> feedback action
29
what is neg. feedback
the system's product feeds back and INHIBITS its secretion
30
3 types of stimuli that control initiation/stimulation of hormone synthesis and release
1. hormonal control
2. humoral control
3. neural control
31
what is hormonal control
hypothalamus produces releasing and inhibiting hormones/factors
32
what is humoral control
changing blood levels of factors that regulate its release
33
what is neural control
ex. stress causing catecholamine release
34
what are ligands
molecules that bind to a R on a PM, cytoplasm, or nuclear membrane
anything that binds to a receptor
35
what can a ligand do
activate or inhibit a R.
activation may increase OR decrease a function
each ligand may interact with many R subtypes
36
what do activated R do
directly or indirectly regulate cellular biochemical processes
37
extend of cell activation depends on (4)
the # of R for that hormone expressed by the cell
R affinity for that hormone (how tightly it binds)
hormone blood levels/local concentration
changes in receptor response by disease states (can alter # of R or Rs' function)
38
what is desensitization
SHORT TERM decreased cell R responsiveness due to repeated or chronic exposure to agonist. ex. prolonged exposure to agonist/ high doses
involves signal transduction changes
39
what is an agonist
ligand that causes a response in cell after binding to receptor
40
what is an antagonist
sits on receptor (binds) doesn't do anything. blocks receptor!
41
what is downregulation
prolonged exposure to or too high of hormone. causes cells to pull R off the PM via endocytosis.
reduced sensitivity to hormone, decreases cellular response
42
what is upregulation
increased sensitivity to hormone, increases cellular response
43
many hormones acting on a single cell/different cells can play _______________________
different roles than when acting alone
44
3 types of hormone interaction
synergism (+ interaction)
permissiveness (exposure needed first to make the target cell responsive to another hormone)
antagonism (- interaction). glucagon/insulin
45
what is synergism
+ interaction
when 2 or more hormones work together to produce an effect of larger magnitude than each hormone alone
46
what is permissive
when a hormone needs the cell to be exposed to another hormone to be able to exert its full effect on the target cell
47
what is antagonism
- interaction
when the actions of a hormone are opposite to the actions of another hormone and so cancels out or weakens the action of the other hormone
48
what are the 2 major mechs of action for hormones
1st messengers
2nd messengers
49
what is a 1st messenger
those that communication b/w cells
NON-lipid hormones cannot cross PM
must bind to a PM R -> use 2nd messengers to relay their instructions in the inside of the cell
50
what are 2nd messengers
small diffusible molecules (Ca2+, cAMP, IP3)
51
how are hormones terminated
they must be terminated since theyre so strong
rapidly degraded locally or by liver
52
what are the 3 categories of hormones
AA derived
peptide
steroid
differ by synthesis, storage/release, transport in blood, cellular/subcellular R location and by cellular response mechs
53
what are the majority of hormones
peptides or proteins
use a PM R and signal transduction
54
how do lipid-soluble steroid hormones get into cell
diffuse EASILY across PM
1. bind to cytoplasmic or nuclear R
2. activated R-H complex interacts w/ DNA to regulate gene transcription
3. transcribed mRNAs direct the synthesis of other proteins/enzymes
55
what can tyrosine turn into (2)
catecholamines --> NT
thyroid hormones (T3/T4)
56
where are steroids made
adrenal glands and gonads
57
are steroid hormones stored?
NO! made as needed since theyre lipophilic so they can easily cross cell membranes so dont want a bunch floating around
58
are steroids H2O soluble?
NO! MUST bind to carrier protein in blood due to low blood solubility
largely albumin, CBG, SHBG
59
when does a steroid hormone become activation?
NOT when it is hound to carrier protein.
carrier protein must release hormone to cell bc only free hormone is active!!
60
where are classical steroid Rs
in cytoplasm or nuc -> genomic effects to activate/repress genes
SOME PM R also exist -> mediate faster NON-genomic responses
61
what do AP hormones control
control growth, metabolism, and reproduction
62
posterior pituitary is an extension of what
neural tissue
63
AP is a
true endocrine gland of epithelial origin
64
what is the hypothalamus's job
maintain homeostasis
65
what do the 1st set of cells in the hypothalamus do
send the H they produce down through the pituitary stalk to the post. lobe of the pit. gland. these H are then released directly into the bloodstream
66
what do the 2nd set of cells in the hypothalamus do
produces stimulating and inhbiting H that reach the anterior lobe of the pituitary gland via a network of BV (portal system) that run down through the pituitary stalk. these factors regulate the production of 6 hormones (FSH, LH,TR, ACTH, GH, PRL)
67
FSH
follicle-stimulating H
68
LH
luteinizing H
69
TRH
thyrotropin releasing hormone - master regulator of thyroid gland growth and function
70
ACTH
adrenocorticotropin
71
GH
growth H
72
PRL
prolactin
73
what does a tropic hormone control
the secretion of another hormone
74
what are the 3 integrating centers on the hypoothalamic-hypophyseal (pituitary) portal system
1. hypothalamic stimulation -> from CNS
2. AP stimulation -> from hypothalamic tropic hormones
3. endocrine gland stimulation -> from AP tropic hormones (except PRL) cortisol
75
what does pineal gland make
melatonin
76
what does AP secrete
GH and somatotropin
77
what does adrenal gland CORTEX and MEDULLA secrete
CORTEX: aldosterone, cortisol, androgens
MEDULLA: epi and norepi
78
what does thyroid secrete
T3 T4 and calcitonin
79
what does parathyroid secrete
PTH
80
what does kidney/skin secrete
erythropoietin and vit. D3
81
what does pancreas secrete
insulin and glucagon
82
what does melatonin do and where is it made
made by pineal gland. plays a role in sleep-wake cycle. circadian internal clock
anti-nociceptive, potent antioxidant, anti-inflam, memory, osteoblast regulator
low during day (sees light)
83
what is the biosynthesis route of melatonin
Trp --> serotonin --> melatonin
LIPID SOLUBLE
84
where place melatonin is found and what does it do
oral cavity! secreted from acinar cells
anti-inflam and antioxidant
85
what does GHRH do and where is it from
from hypothalamus. regulates the secretion of GH (somatoTROPIN from the AP)
86
what antagonizes GHRH release
somatoSTATIN (from the anterior periventricular nucleus of the hypothalamus)
87
how and when is GH released
in a pulsatile manner, mostly overnight. prevents desensitization!
88
what does GH bind to and what does it do
binds to GHR, inducing direct or initiating the production of insulin-like GF (IGF-I) which is the most important mediator of GH effects!!!
89
what does GH promote
longitudinal growth and also has many important metabolic functions throughout adult life
90
what does IGF (insulin-growth factor) mediate
actions of GH in adulthood
includes regulation of glucose and AA metabolism
91
What stores, makes, and releases TSH
pituitary gland
TSH secretion causes the thyroid gland to release more T3 and T4
92
what does a HIGH level of TSH mean
there isnt enough thyroid hormone
93
what does a LOW level of TSH mean
there is too much thyroid hormone
94
what are considered master regulators of the body
thyroid hormones
95
what do thyroid hormones control
metabolism, slow/speed up HR, regulated body temp, regulate digestion, contribute to regulating muscle strength, control body tissue turnover
96
is T3 or T4 more activated?
T3!
97
what do thyroid hormones bind to
hormone response elements in DNA either as monomers, heterodimers. dimerizing with different nuclear receptors leads to the regulation of different genes
THR commonly interacts with retinoid X receptor = Vit A
98
can T3/T4 diffuse on own?
NO! needs transporter (T3 transporter)
99
what are the genomic and non-genomic effects of thyroid hormone
genomic: signaling pathway directly influences gene transcription and translation
non-genomic: pathway involves more rapid, cellular changes, some of which also regulate gene expression
100
what happens when we have low levels of T3/T4 in blood
hypothalamus releases TRH --> TSH released by the pituitary
this triggers release of T3/T4 by thyroid follicle cells
the release of T3/T4 causes increased basal metabolic rate of body cells and rise in body temp. really effects the mito!!
^ causes neg. feedback and inhibits release of TRH and TSH
101
what happens when we have high levels of T3/T4 in blood
hypothalamus stops TRH release and AP stops TSH release
102
what makes calcitonin
it is a type of thyroid hormone
made by parafollicular cells of the thyroid gland
103
What does calcitonin do
regulates Ca2+ blood levels by DECREASES it
104
calcitonin opposes what
the actions of PTH which INCREASE blood Ca2+ levels
105
what increases Ca2+ levels in blood and what decreases it
calcitriol INCREASES
calciTONIN Decreases
antagonist to each other
106
how does calcitonin work
blocks activity of osteoclasts and it can decrease amt of Ca2+ that your kidney reabsorbs
Lowers blood calcium “tones down”
107
what is the most important influence on Ca2+ levels?
PTH
secreted by epithelial chief cells of the 4 small parathyroid glands
108
what does PTH do
main action is control of Ca2+ levels but also helps control the levels of phosphorus and Vit d (calcitriol) in blood/bones
109
is vit d a hormone?
YES!
110
what are the 2 forms of vit D and where do they enter
from the blood D2 and D3 enter the liver and kidneys where they are hydroxylated to form
25-(OH)vitamin D
1,25(OH)2 vitamin D
111
which is the storage form?
25-(OH)vitamin D
1,25(OH)2 vitamin D
25-(OH)vitamin D
112
which is HIGHLY active? what does it do
25-(OH)vitamin D
1,25(OH)2 vitamin D
1,25(OH)2 vitamin D
levels are tightly controlled. has many critical metabolic functions, including bone health and immune regulation
113
what does vit d do in our body
regulates mineral and skeletal homeostasis but tons of other roles too
114
what causes rickets (kids) osteomalacia (adults)
vit d deficiency. decreased bone mass and mineralization
115
with a vit d deficiency, what percentage of dietary Ca2+ can be utilized for building new bone
only 10-15%
116
what form of vit d do they measure: 25-(OH)vitamin D
1,25(OH)2 vitamin D?
25-(OH)vitamin D -> storage form
117
what vit d receptor is a member of what
steroid hormones
118
what level of issue is vit d deficiency
global health issue
can cause caries and perio and implant failure!!!
vit d is also an anti-inflam agent
119
steroid hormones MOA
lipid soluble SO cross the PM into the cell cytosol and bind with their nuclear Rs in the cytosol or on the nuclear envelope
HR complex binds to its DNA binding domain where the steroid-response elements are
the HR/SRE recruit transcription factors and effect the rate of mRNA production --> mRNAs direct new protein synthesis THEN cellular responses/action occur
120
what two places do adrenal glands make hormones
cortex and medulla
121
what 3 things are made in the cortex and what type of H are they
STEROIDS
1. mineralocorticoids
2. glucocorticoids
3. androgens
122
what is the starting substrate for ALL steroid hormones
cholesterol
123
what are mineralocorticoids
aldosterone. it is essential for Na+ conservation in kidney, salivary and sweat glands, and colon. plays central role in homeostatic BP regulation and maintaining plasma Na+ and K+ levels. does so primarily by acting on the mineralocorticoid receptors in the kidney
124
what are glucocorticoids
cortisol. regulates fat, protein, and carbs used by body. homesostatically regulates BP, suppresses inflam. increases blood sugar and can also decrease bone formation. EXTRA is released under stress to raise blood sugar and sharpen survival responses. (brain needs glucose)
125
what are androgens
weak ones are DHEA and DHEA-S. transformed locally into potent androgens like testosterone or dihydrotestosterone.
Females: further converted in ovaries into estrogens
Males: remains as T or can becomes estrogens (E3 or E2)
126
what does the medulla release
catecholamines (NT) NE / E
127
what are examples of catecholamines
noradrenaline and adrenaline (norepi and epi)
128
what does the release of epi/norepi do
increase HR and force of contractility, increase brain and muscle blood flow, relax smooth muscles and enhance glucose utilization. vasoconstrictors!! local -> helps pain signals be blocked longer
129
stress response pathway HPA axis
stress is sense --> to brain
brain sends signal to hypothalamus
hypo releases CRH
CRH -> pituitary gland
pituitary gland releases ACTH -> goes to adrenal cortex
adrenal gland releases cortisol and DHEA (secreted into saliva)
130
what is erythropoetin
produced and released in kidney. carried to bone marrow and spleen to enhance proliferation and survival of erythroid progenitors (increase RBCs) corrects hypoxic conditions and returns to normal
131
what cells produce insulin
B cells of pancreas
132
what pathways is insulin involved in
INCREASES: glucose uptake, glycogen synthesis, protein synthesis, gene expression, DNA synthesis
DECREASES: gluconeogenesis and lipolysis
133
what processes is insulin involved in
anabolism, glucose homeostasis, lipid metabolism, protein metabolism, growth/mitogenesis, reproduction, lifespan, cognition
134
what cells produce glucagon
alpha cells of the pancreas
135
what does glucagon do
OPPOSES the actions of insulin. (insulin and glucagon are counter-balancing regulatory hormones)
136
when is glucagon secreted
when blood levels are LOW
137
what is hypersecretion and what can cause it
excess hormone production
caused by tumors or exogenous iatrogenic treatment
neg feedback may lead to atrophy of gland
thus ABSENCE of neg feedback leads to overproduction of tropic hormones
138
what is hyposecretion and what can cause it
too low of hormone production
caused by decrease synthesis or gland atrophy
139
what is graves disease
autoimmune -> body produces antibodies to the TSHR on thyroid cells. causes hyperthyroidism
140
primary pathology due to issues with
last endocrine gland in pathway
141
secondary pathology due to
pituitary gland
142
tertiary pathology due to
hypothalamus
143
Type I diabetes
lack of insulin. life threatening.
144
type II diabetes
receptors dont response to insulin.
high insulin and high glucose
145
all oral cells have R for what 3 hormones
estrogen, progesterone and testosterone
146
ovary produces 2 hormones
estrogen and progesterone
147
pathway of estrogens
binds to 2 nuclear receptors: ERalpha and ERbeta
these R mediate GENOMIC actions of E
the PM GPCR (GPER): E binding to GPER plays a central role in regulating vascular tone, cell growth and lipid and glucose homeostasis. NON GENOMIC
148
what does progesterone bind to
intracellular PR
149
what mediates the NON-genomic actions of estrogen
GPERs
150
what is GPERs do in non-reproductive tissues in females
adapt her body for pregnancy by immune suppression, strengthening of bone structures and behavioral changes
151
GPER can affect the endocrine system leading to
obesity, diabetes
152
what does the adrenal gland secrete small amounts of
androgenic steroids (andro = male)
153
what do androgenic steroids do in F and M
F: regulate libido
M: development and maintenance of male characteristics (T regulates libido in M)
154
what triggers puberity
increased pulsatile secretion of GnRH
155
hypothalamus has a _____ generator and what does it release
pulse generator
releases gonadotropin releasing hormone in a PULSATILE fashion (controlled by NTs, CRH, PRL, stress and gonadal hormones) not continuous
156
what induces gonadal production of steroids (E2, P, T) and peptide hormones (inhibin and activin)
the pattern of LH and FSH
157
MALE REPRODUCTION:
what do sertoli cells do
make the peptide inhibin and androgen binding protein
158
MALE REPRODUCTION:
what do leydig cells do
take T and convert some T to E2
159
MALE REPRODUCTION:
what produces T
testis
160
MALE REPRODUCTION:
what converts T to E2
aromatase. E2 acts on ERs to mediate some of the effects attributed to T
161
MALE REPRODUCTION:
prostate gland does what
nutrient fluids for sperm
162
MALE REPRODUCTION:
seminal vesicle does what
above glands' secretions make up the fluid and sperm from seminiferous tubules = semen
163
MALE REPRODUCTION:
testes:
epididymis:
Vas deferens:
sperm production
sperm maturation
passageway into abdomen and delivery to the urethra
164
MALE REPRODUCTION:
what does inhibin do
released when sperm is too high. inhibits the release of GnRH and FSH
165
what can inhibit the secretion of GnRH and LH/FSH
T and inhibin
166
androgenic steroids have pronounced _______ effects
T- like
often used illegally by athletes (anabolic steroids)
167
what are metabolic effects of androgen R activation in males
decrease in adipogenesis and decrease in visceral fat
increase insulin sensitivity in skeletal muscle
why men can eat so much
168
what does a sustained high estrogen level do in terms of feedback and gonadotropin level
POST feedback and INCREASES gonadotropin levels
169
hormones from where stimulate the ovaries
the hypothalamus and AP
170
what do the ovaries release
E and P in pre-set patterns during each cycle
E and P prepare uterus for possible pregnancy
171
LH binds to what type of cell in ovaries
THECA (like Leydig)
172
FSH binds to what type of cell in ovaries
Granulosa (like sertoli)
173
Testosterone can cause negative feedback on (2)
Hypothalamus and AP
174
in men, what is libido regulated by
T
175
what does a pulsatile manner mean?
NOT continuously releases
176
what cells are known as the nursemaids in male?
sertoli cells
177
inhibin can cause negative feedback on the
AP
178
LH goes with what type of cell
Leydig cells (LL)
Theca
179
FSH goes with what type of cell
Sertoli cells (SS)
Granulosa
180
what converts T into estrogen?
aromatase
181
what converts T into DHT?
5alpha reductase
182
when there are sustained HIGH levels of estrogen, what type of feedback loop happens
POSITIVE!!!
this is the weird one. REMEMBER ON EXAM***
183
what type of cell receptors are found on Theca and Granulosa cells?
ER, AR, and PR
184
what do theca cells produce
T
185
what do granulosa cells produce
estradiol
186
what arteries are found in the endometrium
spiral arteries
what sheds every month
187
what is the definition of the follicular phase
a certain follicle is selected to grow.
188
what is the definition of the luteal phase
ruptured follicle develops into corpus luteum
189
what H dominates the first half of the cycle (follicular phase)
Estrogen
190
what phase is progesterone super high
luteal phase
prepares uterus lining for implantation
191
the LH surge happens at
ovulation
192
what happens to the corpus luteum is not implantation occurs
apoptosis!
193
lack of what H causes the endometrium to die
P
194
If NO implantation occurs, do FSH and LH secretion resume?
YES!
195
during what days of cycle does the endometrium shed with bleeding
days 1-7 (follicular) = menses
196
what is happening during the proliferative phase?
the endometrium grows and thickens in preparation for pregnancy
(due to high levels of E)
197
how do we want the cervical mucus to be for max sperm survival?
viscosity -> THIN
quantity -> MANY
198
high E triggers the LH surge -- what type of feedback is this?
POSITIVE!! ***Weird one
199
what causes cramping? and how do they do it?
Prostaglandins
produce STRONG vasoconstriction of the spiral arteries and contraction of the myometrium
200
why does the stratum functionalis (part of endometrium) slough off
the prostaglandins effects leads to loss of nutrients and hypoxia
201
what is the actual layer of tissue called that sloughs off during period
stratum functionalis
202
what hormone does an ovulation test test for
LH
the LH surge = ovulation
203
what hormone does a pregnancy test test for
hcG (human chorionic gonadotropin)
204
what two ways is hcG secreted (assume implantation has occured)
1. by the implanting embryo first
2. the placenta layer will secrete
205
what 2 hormones are CRITICAL for supporting and maintaining the endometrial lining (assume implantation has occured)
P and E
super important to maintain pregnancy!!
206
what structure secretes P and E?
corpus luteum
(if implantation has occurred, hcG supports the corpus luteum so it doesn't become the corpus albicans)
207
what hormone is secreted during labor to induce contractions? type of feedback?
oxytocin from posterior pituitary
POS feedback
208
what hormone regulates breast milk/lactation
oxytocin
209
how does a baby initially get its FIRST antibodies
from the mother IN UTERO. has antibodies BEFORE birth
210
why is breastfeeding so important right after birth?
the first breast milk (colostrum) is a huge source of antibodies
super watery. contains tons of proteins
211
an infant's gut epi. cells have receptors that transport what?
intact maternal antibodies into the fetal circulation
212
what causes menopause
complete loss of ovarian responsiveness to gonadotropins --> leads to erratic cycles = perimenopause
213
menopause:
tissue hormonal withdrawal is equivalent to
drug withdrawal
214
what are the 3 types of estrogens?
1. Estrone (E1)
2. estradiol (E2)
3. estriol (E3)
215
rank potency of estrogens --> most to least (3 types)
Estradiol>estrone>estroil
E2>E1>E3
216
what estrogen dominates reproductive years?
estradiol/E2
217
what estrogen is produced during pregnancy?
Estriol/E3
218
what estrogen is produced during menopause?
estrone/E1
219
what is estrone/E1
it is produced during menopause by FAT TISSUE
220
types of HRT delivery methods
1: systemic: pills, gels, creams, etc
2: vaginal products
**a lot of doctors start with bisphosphonates to prevent osteoporosis due to menopause
221
what is the difference between bio-identical and conventional HRT?
bio-identical: EXACTLY the same chemical structure.
conventional: NOT the same chemical structure. "Similar" but not really. Comes from horse estrus cycle --> polyestrous
222
method of HRT administration:
2 ways
oral delivery
transdermal drug delivery
223
method of HRT administration:
significance of oral delivery
it has UNDESIRABLE PHYSIOLOGIC EFFECTS!!!
it increases the risk of blood clots do to stimulating blood clotting. passes through liver and GI metabolism by microbiota
224
method of HRT administration:
advantages of transdermal drug delivery
bypasses hepatic and GI metabolism
-goes directly into bloodstream
-can administer a lower dose compared to oral delivery
-minimal stimulation of hepatic protein production
-many ways to administer
225
do males produce T all their lives?
YES! but slowly declines with age
226
can F sex hormones influence microbiota?
yes! especially in the mouth and gut! (perio and osteoporosis)
227
4 ways sex hormones are thought to act by
1. strengthening the epi barrier to resist bacterial invasion
2. modulating immunity to oral bac
3. + affecting maintenance and repair of collagen
4. BONE. E inhibits bone breakdown
228
what are endocrine disruptors?
there are natural or man-made chemicals the interfere with the body's endocrine system.
found in many everyday products! ACCUMULATE IN FAT (highly lipophilic)
when absorbed, it can decrease or increase normal H levels. BAD! disrupts body's chemistry
229
Sum of ALL estrogen refers to what
ALL endogenous AND environmental exposure to E and E like compounds
230
what is the most common endocrine disorder in the US
diabetes
231
what is type 1 diabetes caused by and what do patients rely on to maintain normal blood glucose levels
autoimmune destruction of insulin producing pancreatic beta cells
these patients rely on insulin injections
232
what represents a majority of cases - type 1 or 2 diabetes
type 2
233
what is type 2 diabetes caused by
tissue resistance to insulin (due to weight, age, not active)
234
what is gestational diabetes and what is it caused by
it occurs in the second half of pregnancy
caused by placental hormones -> results in insulin resistance and deficiency
235
what does HbA1c measure
the irreversible binding of glucose to Hb
test provides an approximate gauge of the blood glucose level over 3 months
236
lifespan of RBC
120 days
237
4 classes of drugs used to treat diabetes
Sulfonylureas
Biguanides
Alphaglucosidase inhibitors
Insulin
238
normal HbA1c numbers:
PREdiabetes:
Diabetes:
<5.7%
5.7-6.4%
>6.5%
239
target blood sugar levels BEFORE meals
80-130mg/dL
240
target blood sugar levels 2 hours after meals
180mg/dL
241
7 medical complications of diabetes
heart disease
stroke
kidney disease
blindness
neuropathy
retinopathy
amputation
242
what are oral manifestations of diabetes
increased risk of dental caries, gingivitis and perio, xerostomia, delayed wound healing, oral candidiasis, lichen planus
243
steps to use a glucometer
clean site
insert lancet into device
adjust depth setting and insert test strip into meter
poke finger and put blood drop onto test strip
244
what should you do if your patient glucometer results show ketoacidosis
ER or call doctor
245
what should you do if your patient glucometer results show hyperglycemia
lifestyle changes and medications
246
what should you do if your patient glucometer results show HYPOglycemia
give carb (juice, honey, glucose tablet)
247
3 ways dentistry is affected by bone quality
osteoporosis (implants)
wound healing (implants/surgery)
perio
248
what elements does bone contain a lot of
Ca2+, Mg+, P+
249
bone formation depends on
biomechanical loading
250
what is Piezo1
ion channel embedded in the osteoblasts and osteocytes PM that responds to mechanical loading on bone
251
bone is ________ and needs this stimulation to form new bone
piezoelectric (Piezo1)
252
activation of what stimulates the formation of new bone via OB
activation of Piezo1
253
what is the major signaling metabolic factor secreted by osteocytes
prostaglandin E2 (PGE2)
254
bone homeostasis is a perpetual cycle of
destruction and formation -> undergoes daily wear and tear and micro-factors
255
what 2 consecutive cellular events do we need for bone remodeling
resorption via osteoCLASTS
formation of new bone via osteoBLASTS
256
what types of factors is bone under the influence of?
LOCAL factors
257
what cell senses microfractures in the bone
osteoCYTES (which then signal to osteoclasts for bone RESORPTION --> osteoblasts drop new bone)
258
what produces osteocalcin
osteoBLASTS
259
RANKL in the presence of MCSs is primarily responsible for
activation of osteoclasts leading to bone loss
260
what is a decoy receptor for RANKL
OPG (osteoprotegerin)
261
osteoblasts produce OPG (osteoprotegerin) which
inhibits bone loss by inhibiting osteoclastogenesis
262
explain what RANK and RANKL are
OB produce RANK and osteoclasts have receptors for this ligand (RANKL).
After RANKL binds to RANK, osteoclast precursors proliferate, merge into multicellular structures and differentiate into mature osteoclasts
263
what plays an important role in osteoclast differentiation
cytokines
264
decrease in RANKL and increase in OPG does what
suppresses osteoclast differentiation
265
what can be detected in urine that shows bone resorption activity/marker
collagen telopeptides
266
what are collagen telopeptides
during resorption, osteoclasts release small collagen fragments containing (OH)proline = collagen telopeptides
267
what are the 4 steps of bone remodeling
activation, resorption, reversal and formation
268
activation of osteoclasts is controlled through what pathway
RANK/RANKL/OPG pathway
269
what positively regulates bone formation
androgens, mechanical load, PTH, B-blockers
270
what blocks bone formation
B-adrenergic stimulation (via leptin), immobilization, aging
271
what + regulates bone resorption
estrogen deficiency, immobilization, low Ca2+ (PTH)
272
what blocks bone resorption
estrogen, SERMs, Bisphosphonates, Calcitonin, Ca2+/Vit D
273
is calcidiol or calcitriol the active form
calciTRIOL
274
what is osteoporosis
metabolic disease characterized by a decrease in bone strength and bone mineral density and altered bone quality
women are way more affected
275
what is osteopenia
loss of bone mass but not bad enough to be osteoporosis (kinda like pre-osteoporosis)
276
is estrogen anabolic or catabolic
ANAbolic -> builds up!
277
what does bisphosphonates do
bind to bone mineral and are taken up by osteoclasts, causing them to undergo apoptosis or have reduced resorptive capacity
278
what is teriparatide
a recombinant fragment of PTH, stimulates bone formation by increasing osteoblast activity and to a less extent, inhibiting osteoclast recruitment
279
what H does bone release
osteokines
osteocalcin -> interacts with muscle H and fat H to regulate homeostasis, metabolism, learning memory and depression
**bone is an endocrine organ!
280
what produces osteocalcin
Osteoblasts. Need Vit K2 also
281
Vit K1 is found where and is good for what
good for blood clotting
found in green leafy vegetables
282
Vit K2 is found where
fermented foods like cheese, egg yolk, beef liver
283
Vit K3 is
toxic to humans
284
Vit K2 can inhibit ______ and promote __________________
inhibit vascular calcification
promote bone mineralization
285
what drug blocks all forms of Vit K
Coumadin (warfarin) -> anti-coagulants
286
cOCN/GlaOCN contains what types of residues
Y-carboxyglutamic acid
287
Y-carboxyglutamic acid production depends on
Vit K2 and is stimulated by 1,25 (OH)2 Vit D
288
what is the major NONcollagenous protein in bone ECM
osteocalcin -> osteoblast secreted and vit K2 dependent protein!
289
what 2 forms does osteocalcin exist in
undercarboxylated (ucOCN) and carboxylated osteocalcin (GlaOCN)
290
between ucOCN and GlaOCN, which has greatest affinity for hydroxyapatite in bone matrix
GlaOCN!
becomes trapped in the bone matrix after secretion from the OBs
291
characteristics of ucOCN
acts as a H by being secreted into the circulation during bone formation
helps regulates glucose tolerance and energy metabolism by helping to regulate both insulin secretion and insulin sensitivity
serves as a clinical biomarker to monitor bone turnover and formation
292
what is analogous to OCN
MGP (matrix-gla protein)
293
what makes MGP
chondrocytes and vascular smooth muscle cells (MGP is analogous to OCN)
294
what does MGP need to be in its active form
Vit K2
295
what is a KEY inhibitor of vascular calcification
MPG
the absence of it leads to excessive calcification of vasculature
296
what does the active form of MPG do
binds to calcification crystals in blood vessels (prevents it)
directly prevents calcium phosphate precipitation
prevents the trans-differentiation of vascular smooth muscle cells into an osteogenic (calcifying) phenotype
297
hallmark of cardiac vascular calcifications
presence of atherosclerotic plaques in arterial walls
298
muscles secrete what H
myokines -> endocrine organ
^ prevent bone and muscle loss
299
adipocytes secrete what H
adipokines
300
adiponectin
good! controls glucose and fatty acid metabolism and food intake
301
leptin
signals being full via adipose tissue
302
resistin
high resistin levels are associated with an impaired glucose tolerance test
in obesity, macrophages that infiltrate and live in WAT produce resistin
303
do skeletal muscle, fat and bone talk to each other?
YES! organ cross-talk
304
obesity and T2D and osteoporosis are considered what level of disease
global epidemic
all have high fat mass as a known risk factor
305
what does high glucose levels do to osteoclasts
inhibit OC viability and differentiation
inhibit OC resorption function
306
what are some examples of diseases that disrupt the activity of salivary gland secretion
inflammatory, infectious and neoplastic diseases
307
3 salivary gland names
parotid
submandibular
sublingual
308
what are the 2 main components of saliva
serous and mucous
309
what are the tonicity changes seen in saliva
is isotonic in gland but once in oral cavity -> HYPOtonic
310
what is the main differences b/w submand. and parotid salivary glands
they have different gene expression profiles (different mRNAs) and these properties have a genetic basis
both have tumor and transport associated genes
311
saliva pH and osmolarity
slightly acidic -> pH of 6-7
HYPOosmotic
312
what are the organic and inorganic components of saliva
orgo: proteins and NON-proteins
in-orgo: electrolytes
313
components of whole mouth saliva
99% water
1% inorgo and orgo components
314
main jobs of saliva
acts as a lubricant, demineralization inhibitor, promotes remineralization, aids digestion, provides antibacterial and antiviral protection AND promotes the natural beneficial relationship b/w oral microbiota and the host!!!
315
what 2 ions are present in a supersaturated form in saliva
Ca2+ and Phosphorus
316
what are things saliva can dissolve
chemicals, odorants and taste sensation when those two are combined
317
MALT significance to salivary glands
MALT is in direct contact with environment which is good because our mucosa is constantly exposed to viruses, toxins, etc
***MALT is lymphoid tissue -> immune defense. can also function independently of the internal immune system
318
where is the 1st line of defense in our body
oropharynx mucosa
319
what does the oropharynx secrete as an immune response
IgA-secreting cells -- these then redistribute to other remote sites to help fight infection
320
where is a good pace to do an analysis of immune response
SALIVA!! NOT BLOOD. Saliva shows a general picture of body's mucosal immunity
321
what do a lot of prescription drugs affect
salivary flow
322
what meds are commonly associated with xerostomia
ones with anticholinegeric or sympathomimetic effects and long-term opioids
323
5 NON-specific macromolecules found in saliva
histatins
lysozyme
carbonic anhydrase
amylase enzyme
mucins
324
what are histatins
NON- specific macromolecule in saliva. buffering, mineralization, antimicrobial activity against a broad spectrum of bac and fungi
325
what are lysozymes
NON- specific macromolecule in saliva.
attacks and degrades bac cell walls
326
what are carbonic anhydrases
NON- specific macromolecule in saliva.
enzyme -> buffering --> makes HCO3-
327
what are amylase enzymes
NON- specific macromolecule in saliva.
CHO digestion and some antimicrobial activity
328
what are mucins
NON- specific macromolecule in saliva.
lubrication and anti bac/viral
329
what are the 4 SPECIFIC salivary macromolecules
Growth factors --> EGF and NGF
Regulatory Peptides
Cytokines
Secretory IgA
330
what are growth factors in saliva
SPECIFIC salivary macromolecules
have 2:
Epidermal growth factor (EGF): present in mucosal lining of esophagus and attach to EFGR to promote mucosal cell growth
Nerve growth factor (NGF): contributes to the oral wound healing process: cellular proliferation, inflammation, angiogenesis and tissue remodeling
331
what are regulatory peptides in saliva
SPECIFIC salivary macromolecules
332
what are cytokines in saliva
SPECIFIC salivary macromolecules
immune-regulatory peptides
333
what is IgA in saliva
SPECIFIC salivary macromolecules
secreted for protecting mucosal surfaces
334
characteristics of IgA in saliva
produced by plasma cells
in serum, IgA is in MONOmeric form
salivary ducts cells produce R (secretory component) for POLYmeric IgA
335
what is the secretory component for IgA regulated by
H! male and female H, glucocorticoids, thyroid H
secretion of POLYmeric IgA onto mucosal surface depends on availability of secretory component
336
what type of control is saliva secretion under
under NT and hormonal control
337
what types of R do acinar cells have
adrenergic (E,NE)
muscarinic (ACh, GPCR)
substance P
prostaglandin
peptide H R
338
what does B-adrenergic R stimulation from acinar cells in the salivary glands result in
LOW volume of saliva but protein and mucin RICH
339
what does mACh R stimulation from acinar cells in the salivary glands result in
+ regulates fluid transport
food stimulates chemo, presso-receptors -> so get a SEROUS enzyme-rich saliva (TONS!) with SOME mucins
340
saliva serous secretion depends mainly on what
activations GPCRs (mAChRs)
**protein secretion is controlled mainly by B-adrenergic stimulation
341
if hormonal imbalances exists, what does this mean for our saliva
salivary immunity CHANGES
342
what types of steroids are found in saliva
biologically active, FREE forms
343
most important daily job of saliva is to
provide mucous so food can be bound in bolus
344
where can you find HCl, pepsin, gastric lipase
stomach! very acidic here
mechanical and enzymatic processing of ingested bolus
345
where can you find pancreatic juice, bile, NaHCO3
small intestine
breaking down of macromolecules and absorption of nutrients
346
where does microbial fermentation of undigested food and water reabsorption happen
colon
347
what are the 2 accessory organs in the GI
pancreas and liver
348
the large intestine consists of (2)
colon and rectum
349
5 main activities of digestion
ingestion -> mechanical digestion -> chemical digestion -> absorption -> excretion
350
when is food considered a bolus
once chewed and moistened (when it leaves the mouth)
351
how does the bolus travel
through peristalsis
352
Does the CNS control the enteric nervous system?
NO! it functions independently
the CNS can speed it up or slow down. Does not activate it though
353
which part of the esophagus is responsible for voluntary swallowing (voluntary phase)
upper 1/3
mostly striated muscle
once a swallow is initiated, everything else is in-vol (smooth muscle). You don't have to think about pushing your food down your esophagus
354
where does tonic contractions happen and what is its job (GI)
these are SUSTAINED
occurs in smooth muscle sphincters
keeps bolus from moving backwards
355
what are phasic contractions (GI)
they last only a few seconds
peristalsis moves bolus forward
segmentation mixes
squeezes bolus through so once bolus has passed, that specific section of muscle relaxes
356
digestive enzymes are secreted into (3)
mouth, stomach and small intestine
357
what produces mucous (GI)
mucus cells in stomach and goblet cells in intestine
358
bile is SECRETED where
liver
***STORED in gallbladder
359
what is an example of a long reflex in digestive system
smell food and starting to salivate
360
does ACh or epi/norepi slow the digestive system down
epi/norepi
**dont want to be stressed while eating!
ACh = rest and digest
361
what are short reflex patterns (GI)
contained within the ENS
peristalsis, secretion, mixing contractions, local inhibitory effects
362
what are long reflex patterns (GI)
travel OUTSIDE of the ENS - 2 kinds ->
Long: involve the CNS. ex -> vomiting
Short: ex -> gastrocolic = stomach stretching from food causes increase peristalsis
363
what is the hunger hormone
Ghrelin
FEED ME!! "gremlin"
364
rank order of meals digested the slowest (slowest first):
carbs, high fat, high protein
high fat > high protein > carbs
carbs digested the fastest
365
how do we get pepsin
gastric juices contain pepsinogen which gets activated by H+ from parietal cells --> pepsin
366
what is role of bile
emulsifying dietary fats into small droplets
367
which parts of the small intestine are involved in the most nutrients, vit and mineral absorption
jejunum and ileum
368
where are bile salts reabsorbed
ileum and recycling to the bile via enterohepatic circulation
369
what is incretin
stimulates secretion of insulin via GLP-1 Hormone
incretin mimetic drugs -> T2D patients
370
pancreas exocrine secretions
secretes pancreatic juices and NaHCO3 to neutralize the acidity of the stomach-derived chyme
Acinar cells secrete digestive enzymes that further break down proteins, CHOs and lipids
371
what secretes NaHCO3 in the pancreas
duct cells
372
what is cystic fibrosis
CFTR is a membrane protein that is an Cl- channel. This channel is messed up in CF patients. VERY bad. Can get bad infections
373
in small intestine: enzymes stored? released? when?
they are stored until needed then released
many not fully released -> stay attached to the apical membranes of intestinal cells aka the brush border enzymes
374
what is the brush border
it is on the microvilli on epithelium in the small intestine
enzymes are located here
375
what is absorbed into lacteals
fats
376
capillaries dump nutrients to
liver
377
lymphatic vessels (containing absorbed fats) dump into
bloodstream
378
if you don't eat/drink a lot of lactose things, you lose which enzyme
lactase -> lactose intolerance. Throws off tonicity
379
glucose enters with what ion in the small intestine cells
enters the cell with Na+
380
where do proteins get digested and absorbed
in small intestine
381
pathway that causes the gallbladder to release bile
secretin causes the pancreas to produce HCO3 to neutralize H+ in the chyme. Secretin acts with CCK. CCK stimulates gallbladder to release bile.
382
what cells secrete bile
hepatocytes
383
what is bile
bile salts + bile pigments
384
what are bile salts
steroid bile acids combined with amino acids
385
what is the cause of super infections we leanred about
drugs affecting the microflora of our GI
386
Most important daily job of saliva
to provide mucous so food can be bound in bolus
387
digestion in mouth is
chewing and mixing with saliva
388
digestion in stomach is
mechanical and enzymatic processing of ingested bolus
389
digestion in small intestine is
breaking down of macromolecules and absorption of nutrients
390
digestion in colon is
microbial fermentation of undigested food and water reabsorption
391
what do fatty acids get broken down into and what breaks them down
bile breaks them down
fatty acids -> monoglycerides -> micelles -> trigylcerides -> chylomicrons
392
what do chylomicrons enter
lacteal
393
what do the collecting lymphatics pass through
the lymph nodes and converge into main lymph duct. eventually reach the systemic circulation through the subclavian vein
394
3 endocrine functions in the liver
1. in response to GH, it secretes insulin-like growth factors-1 (IGF-1) which promotes growth --> forms T3 from T4 / activates vit D /. secretes angiotensiongen
2. metabolizes hormones
3. secretes cytokines involved in immune defenses
395
what breaks down drugs in the liver
P450 system
converts compounds to glucuronide which makes them more water soluble.
396
how are water soluble vitamins absorbed and digested
mediated transport --> vit b12 is complexed to IF and absorbed in small intestine
397
how are nucleic acids digested
digested into their basic units
398
how are minerals digested
actively transported through channels
399
T/F do all microbiomes affect each other
TRUE! for example, gut microbiome affects oral microbiome!
400
when does bacterial colonization start?
at birth
401
what is the significance of a c-section
babies pick up microbes when they are born vaginally vs when they are born c-section. can get sicker easier
402
the CNS and the gut microbiota interact with each other in a___________
what regulates it
bidirectional way
via endocrine, immune and neural pathways
regulated at intestinal epi and blood brain barrier
403
what types of patients are at high risk for tooth erosion
GERD, bulimia
404
what are NSAIDs
non-steroidal anti-inflam. drugs like aspirin, ibuprofen
for pain and inflammation
405
cons of NSAIDS
affect GI tract homeostasis
406
what H is the opposite of somatostatin
GH
407
what does somatostatin inhibit
ghrelin release and parietal cell H+ secretion and histamine secretion
AND
secretion of gastrin and pepsinogen from chief cells
408
T/F parietal cells make IF
true
409
gastrin stimulates ____ secretion from parietal cells
H+
410
what does H2R antagonists block
block parietal cells to produce acids in the stomach so there is a decrease in acid in stomach and therefore less pepsinogen is getting activated to pepsin = less protein digestion
411
3 main stimulants of H+ secretion at level of parietal cells
histamine, ACh, and gastrin
when all there are present = MAX H+ secretion!!
412
do parietal cells contain proton pumps
yes
413
protein pump inhibitors (Prilosec) form what type of bond to H+ and why is. this important
covalent. IRREVERSIBLE!!
enables prolong inhibition of H+ secretion even after the drug concentration in blood has gone way down
414
what is a problem with prolong PPI drugs
lowering the H+ long term can cause bacterial overgrowth = dysbiosis
415
how is vit B12 absorbed
2 step process
1. HCl acid in the stomach separates vit B12 from the protein that its attached to
2. the freed vit B12 combines with an IF and the body absorbs them together
416
what H tells us when we are full
leptin
417
what are NSAIDS
diverse group of compounds that are mainly used to reduce pain, inflam, and fever
418
what are the two groups pain drugs belong to
non-narcotic analgesics = NSAIDS and acetaminophen
Opioids (narcotics)
decrease synthesis of PG which is bad bc they help regulate homeostasis and inflam
419
MOA of NSAIDs
non-selectively blocking the enzymes that make PGs. inhibition of COX1 is also mostly responsible for GI side effects like bleeding
420
what is point of people taking baby asprin daily
bc it is a low dose, it inhibits platelet COX1 and decreases platelet aggregation and preventing heart attacks and strokes
***not suggested to do this anymore though
421
what does mucus do in stomach
acts as a lubricant to reduce physical damage to the epi from the H+.
stomach would be shredded by the H+ without mucus
**also traps microbes
422
what controls stomach mucus secretion
mainly PG (PGE2)
423
how does the stomach mucosal layer neutralize H+
it secretes bicarb and HCO3 + H+ -> H2O + CO2
424
NSAIDs block COX1, this causes
decrease in mucus secretion, bicarb secretion, and blood flow.
this all leads to ulcers in stomach
425
NSAIDS increase/decrease gastric homeostatic PGE2 production
DECREASES
426
how does our circadian timing system work
when it gets dark --> body produces melatonin
when it is light out --> no more production of melatonin
427
circadian rhythms are key regulators of
metabolism, thermogenesis, immune function, and reproduction
428
shift workers circadian system
chronodisruption: decrease-protective factors (PGE2) --> decrease melatonin
***lack of sleep = more ghrelin = overweight and T2D RISK factor
429
Ghrelin appetite regulation
released by stomach and stimulates food intake. Ghrelin allows the hypothalamus to sense stomach fullness
430
Leptin appetite regulation
released by adipocytes and signals the extent of fat stores to the hypothalamus. Involved in regulation of appetite (suppression) and energy expenditure
431
T/F: if you don't get enough sleep, it can make you hungier
TRUE. INCREASES ghrelin secretion
432
stimulators of ghrelin secretion
fasting, being lean/underweight, T, GHRH
433
inhibitors of ghrelin secretion
feeding/obesity
insulin
GH
leptin
somatostatin
TH
CCK
434
Major GI Functions Affected by circadian rhythms (2)
H+ secretion
maintenance and repair of stomach protective mucus barrier
435
humans in developed countries have 3 ways in which we messed up our gut --> chronodisruption
we can have light 24/7 -> decreases melatonin secretion
24h tv and communications
24h food availability
436
decrease in leptin and increase in ghrelin increases/decreases appetite
INCREASES appetite
437
gastroparesis
stomach muscles work poorly or not at all. delays digestion.
throwing up, heartburn, stomach spasms
in T1D and T2D this is caused by poorly controlled high blood glucose levels which long-term damage the vagus nerve
****when taking med history, super important to ask if they have this condition in order to plan correct treatment
438
how common is gastroparesis
1 in 4 people
439
gastroparesis can be from these 2 drug classes
ALL opioids
certain anti-diabetic medications and GLP-1 agonists used to treat T2D
440
how can a dentist see diabetes in the mouth
if we are seeing gingivitis/perio could be due to the increase blood sugar --> increase glucose in saliva
