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Physiology > Phys Exam 3 > Flashcards

Phys Exam 3 Flashcards

1
Q

what are receptors

A

proteins or glycoproteins that bind different chemical signals

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2
Q

where can you find receptors

A

cells’ plasma membrane or within the cytoplasm or nuclear membrane

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3
Q

what are ligands

A

molecules like hormones, NT, and drugs that bind to a receptor

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4
Q

can some NT act as hormones?

A

yes!

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5
Q

some hormones can have what properties?

some growth factors can have what properties?

A

hormones can have GF like properties and visversa

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6
Q

are hormones released at low or high concentrations?

A

LOW! they are super potent

act on target cells’ receptor

nanomolar and lower

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7
Q

what is a trophic hormone

A

controls the secretion of another hormone

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8
Q

what are exogenous chemicals

A

man-made

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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

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10
Q

what are growth factors

A

control growth, development. activate physiological responses at LOW CONCENTRATIONS

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11
Q

where do GF act

A

locally and SHORT distances

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12
Q

what are cytokines

A

communication peptides produced immune system cells. produce many other non-immune system cell types

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13
Q

where do cytokines act

A

locally at short distances

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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.

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15
Q

where do chemokines act

A

locally at short distances

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16
Q

what type of receptor does epi and norepi bind to

A

GCPR families -> alpha 1 and 2. Beta1-3

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17
Q

what does epi do

A

released into blood. increases HR and enhances strength and physical performance

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18
Q

what does norepi do

A

produced in response to low BP. promotes vasoconstriction and increases BP

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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

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20
Q

what type of gland is the anterior pituitary (AP)

A

endocrine

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21
Q

what hormones does the AP secrete (6)

A

prolactin
GH
TSH
ACTH
LH/FSH

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22
Q

what controls the release of hormones from the anterior pituitary hormones?

A

neurohormones from the hypothalamus

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23
Q

what carries the trophic neurohormones to the AP

A

portal veins (portal system)

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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

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25
Q

what is paracrine

A

that cell’s hormone/GF secretion affects ONLY NEARBY cells (neighboring)

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26
Q

what is autocrine

A

when the hormone or GF produced by a cell can also regulate ITSELF

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27
Q

what are ectohormones

A

released into the environment –> pheromones (detected by olfaction)

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28
Q

endocrine pathway sequence of events

A

stimulus
input
integration
output
target
response -> feedback action

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29
Q

what is neg. feedback

A

the system’s product feeds back and INHIBITS its secretion

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30
Q

3 types of stimuli that control initiation/stimulation of hormone synthesis and release

A
  1. hormonal control
  2. humoral control
  3. neural control
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31
Q

what is hormonal control

A

hypothalamus produces releasing and inhibiting hormones/factors

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32
Q

what is humoral control

A

changing blood levels of factors that regulate its release

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33
Q

what is neural control

A

ex. stress causing catecholamine release

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34
Q

what are ligands

A

molecules that bind to a R on a PM, cytoplasm, or nuclear membrane

anything that binds to a receptor

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35
Q

what can a ligand do

A

activate or inhibit a R.

activation may increase OR decrease a function

each ligand may interact with many R subtypes

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36
Q

what do activated R do

A

directly or indirectly regulate cellular biochemical processes

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37
Q

extend of cell activation depends on (4)

A

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)

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38
Q

what is desensitization

A

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

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39
Q

what is an agonist

A

ligand that causes a response in cell after binding to receptor

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40
Q

what is an antagonist

A

sits on receptor (binds) doesn’t do anything. blocks receptor!

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41
Q

what is downregulation

A

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

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42
Q

what is upregulation

A

increased sensitivity to hormone, increases cellular response

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43
Q

many hormones acting on a single cell/different cells can play _______________________

A

different roles than when acting alone

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44
Q

3 types of hormone interaction

A

synergism (+ interaction)
permissiveness (exposure needed first to make the target cell responsive to another hormone)
antagonism (- interaction). glucagon/insulin

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45
Q

what is synergism

A

+ interaction

when 2 or more hormones work together to produce an effect of larger magnitude than each hormone alone

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46
Q

what is permissive

A

when a hormone needs the cell to be exposed to another hormone to be able to exert its full effect on the target cell

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47
Q

what is antagonism

A
  • 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

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48
Q

what are the 2 major mechs of action for hormones

A

1st messengers
2nd messengers

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49
Q

what is a 1st messenger

A

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

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50
Q

what are 2nd messengers

A

small diffusible molecules (Ca2+, cAMP, IP3)

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51
Q

how are hormones terminated

A

they must be terminated since theyre so strong

rapidly degraded locally or by liver

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52
Q

what are the 3 categories of hormones

A

AA derived
peptide
steroid

differ by synthesis, storage/release, transport in blood, cellular/subcellular R location and by cellular response mechs

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53
Q

what are the majority of hormones

A

peptides or proteins

use a PM R and signal transduction

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54
Q

how do lipid-soluble steroid hormones get into cell

A

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
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55
Q

what can tyrosine turn into (2)

A

catecholamines –> NT
thyroid hormones (T3/T4)

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56
Q

where are steroids made

A

adrenal glands and gonads

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57
Q

are steroid hormones stored?

A

NO! made as needed since theyre lipophilic so they can easily cross cell membranes so dont want a bunch floating around

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58
Q

are steroids H2O soluble?

A

NO! MUST bind to carrier protein in blood due to low blood solubility

largely albumin, CBG, SHBG

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59
Q

when does a steroid hormone become activation?

A

NOT when it is hound to carrier protein.

carrier protein must release hormone to cell bc only free hormone is active!!

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60
Q

where are classical steroid Rs

A

in cytoplasm or nuc -> genomic effects to activate/repress genes

SOME PM R also exist -> mediate faster NON-genomic responses

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61
Q

what do AP hormones control

A

control growth, metabolism, and reproduction

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62
Q

posterior pituitary is an extension of what

A

neural tissue

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63
Q

AP is a

A

true endocrine gland of epithelial origin

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64
Q

what is the hypothalamus’s job

A

maintain homeostasis

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65
Q

what do the 1st set of cells in the hypothalamus do

A

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

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66
Q

what do the 2nd set of cells in the hypothalamus do

A

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)

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67
Q

FSH

A

follicle-stimulating H

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68
Q

LH

A

luteinizing H

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69
Q

TRH

A

thyrotropin releasing hormone - master regulator of thyroid gland growth and function

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70
Q

ACTH

A

adrenocorticotropin

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71
Q

GH

A

growth H

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72
Q

PRL

A

prolactin

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73
Q

what does a tropic hormone control

A

the secretion of another hormone

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74
Q

what are the 3 integrating centers on the hypoothalamic-hypophyseal (pituitary) portal system

A
  1. hypothalamic stimulation -> from CNS
  2. AP stimulation -> from hypothalamic tropic hormones
  3. endocrine gland stimulation -> from AP tropic hormones (except PRL) cortisol
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75
Q

what does pineal gland make

A

melatonin

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76
Q

what does AP secrete

A

GH and somatotropin

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77
Q

what does adrenal gland CORTEX and MEDULLA secrete

A

CORTEX: aldosterone, cortisol, androgens
MEDULLA: epi and norepi

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78
Q

what does thyroid secrete

A

T3 T4 and calcitonin

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79
Q

what does parathyroid secrete

A

PTH

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80
Q

what does kidney/skin secrete

A

erythropoietin and vit. D3

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81
Q

what does pancreas secrete

A

insulin and glucagon

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82
Q

what does melatonin do and where is it made

A

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)

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83
Q

what is the biosynthesis route of melatonin

A

Trp –> serotonin –> melatonin

LIPID SOLUBLE

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84
Q

where place melatonin is found and what does it do

A

oral cavity! secreted from acinar cells

anti-inflam and antioxidant

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85
Q

what does GHRH do and where is it from

A

from hypothalamus. regulates the secretion of GH (somatoTROPIN from the AP)

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86
Q

what antagonizes GHRH release

A

somatoSTATIN (from the anterior periventricular nucleus of the hypothalamus)

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87
Q

how and when is GH released

A

in a pulsatile manner, mostly overnight. prevents desensitization!

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88
Q

what does GH bind to and what does it do

A

binds to GHR, inducing direct or initiating the production of insulin-like GF (IGF-I) which is the most important mediator of GH effects!!!

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89
Q

what does GH promote

A

longitudinal growth and also has many important metabolic functions throughout adult life

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90
Q

what does IGF (insulin-growth factor) mediate

A

actions of GH in adulthood

includes regulation of glucose and AA metabolism

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91
Q

What stores, makes, and releases TSH

A

pituitary gland

TSH secretion causes the thyroid gland to release more T3 and T4

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92
Q

what does a HIGH level of TSH mean

A

there isnt enough thyroid hormone

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93
Q

what does a LOW level of TSH mean

A

there is too much thyroid hormone

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94
Q

what are considered master regulators of the body

A

thyroid hormones

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95
Q

what do thyroid hormones control

A

metabolism, slow/speed up HR, regulated body temp, regulate digestion, contribute to regulating muscle strength, control body tissue turnover

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96
Q

is T3 or T4 more activated?

A

T3!

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97
Q

what do thyroid hormones bind to

A

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

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98
Q

can T3/T4 diffuse on own?

A

NO! needs transporter (T3 transporter)

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99
Q

what are the genomic and non-genomic effects of thyroid hormone

A

genomic: signaling pathway directly influences gene transcription and translation

non-genomic: pathway involves more rapid, cellular changes, some of which also regulate gene expression

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100
Q

what happens when we have low levels of T3/T4 in blood

A

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

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101
Q

what happens when we have high levels of T3/T4 in blood

A

hypothalamus stops TRH release and AP stops TSH release

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102
Q

what makes calcitonin

A

it is a type of thyroid hormone

made by parafollicular cells of the thyroid gland

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103
Q

What does calcitonin do

A

regulates Ca2+ blood levels by DECREASES it

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104
Q

calcitonin opposes what

A

the actions of PTH which INCREASE blood Ca2+ levels

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105
Q

what increases Ca2+ levels in blood and what decreases it

A

calcitriol INCREASES

calciTONIN Decreases

antagonist to each other

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106
Q

how does calcitonin work

A

blocks activity of osteoclasts and it can decrease amt of Ca2+ that your kidney reabsorbs

Lowers blood calcium “tones down”

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107
Q

what is the most important influence on Ca2+ levels?

A

PTH

secreted by epithelial chief cells of the 4 small parathyroid glands

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108
Q

what does PTH do

A

main action is control of Ca2+ levels but also helps control the levels of phosphorus and Vit d (calcitriol) in blood/bones

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109
Q

is vit d a hormone?

A

YES!

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110
Q

what are the 2 forms of vit D and where do they enter

A

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

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111
Q

which is the storage form?
25-(OH)vitamin D
1,25(OH)2 vitamin D

A

25-(OH)vitamin D

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112
Q

which is HIGHLY active? what does it do
25-(OH)vitamin D
1,25(OH)2 vitamin D

A

1,25(OH)2 vitamin D

levels are tightly controlled. has many critical metabolic functions, including bone health and immune regulation

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113
Q

what does vit d do in our body

A

regulates mineral and skeletal homeostasis but tons of other roles too

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114
Q

what causes rickets (kids) osteomalacia (adults)

A

vit d deficiency. decreased bone mass and mineralization

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115
Q

with a vit d deficiency, what percentage of dietary Ca2+ can be utilized for building new bone

A

only 10-15%

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116
Q

what form of vit d do they measure: 25-(OH)vitamin D
1,25(OH)2 vitamin D?

A

25-(OH)vitamin D -> storage form

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117
Q

what vit d receptor is a member of what

A

steroid hormones

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118
Q

what level of issue is vit d deficiency

A

global health issue

can cause caries and perio and implant failure!!!

vit d is also an anti-inflam agent

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119
Q

steroid hormones MOA

A

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

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120
Q

what two places do adrenal glands make hormones

A

cortex and medulla

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121
Q

what 3 things are made in the cortex and what type of H are they

A

STEROIDS

  1. mineralocorticoids
  2. glucocorticoids
  3. androgens
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122
Q

what is the starting substrate for ALL steroid hormones

A

cholesterol

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123
Q

what are mineralocorticoids

A

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

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124
Q

what are glucocorticoids

A

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)

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125
Q

what are androgens

A

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)

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126
Q

what does the medulla release

A

catecholamines (NT) NE / E

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127
Q

what are examples of catecholamines

A

noradrenaline and adrenaline (norepi and epi)

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128
Q

what does the release of epi/norepi do

A

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

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129
Q

stress response pathway HPA axis

A

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)

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130
Q

what is erythropoetin

A

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

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131
Q

what cells produce insulin

A

B cells of pancreas

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132
Q

what pathways is insulin involved in

A

INCREASES: glucose uptake, glycogen synthesis, protein synthesis, gene expression, DNA synthesis

DECREASES: gluconeogenesis and lipolysis

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133
Q

what processes is insulin involved in

A

anabolism, glucose homeostasis, lipid metabolism, protein metabolism, growth/mitogenesis, reproduction, lifespan, cognition

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134
Q

what cells produce glucagon

A

alpha cells of the pancreas

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135
Q

what does glucagon do

A

OPPOSES the actions of insulin. (insulin and glucagon are counter-balancing regulatory hormones)

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136
Q

when is glucagon secreted

A

when blood levels are LOW

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137
Q

what is hypersecretion and what can cause it

A

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

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138
Q

what is hyposecretion and what can cause it

A

too low of hormone production

caused by decrease synthesis or gland atrophy

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139
Q

what is graves disease

A

autoimmune -> body produces antibodies to the TSHR on thyroid cells. causes hyperthyroidism

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140
Q

primary pathology due to issues with

A

last endocrine gland in pathway

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141
Q

secondary pathology due to

A

pituitary gland

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142
Q

tertiary pathology due to

A

hypothalamus

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143
Q

Type I diabetes

A

lack of insulin. life threatening.

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144
Q

type II diabetes

A

receptors dont response to insulin.

high insulin and high glucose

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145
Q

all oral cells have R for what 3 hormones

A

estrogen, progesterone and testosterone

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146
Q

ovary produces 2 hormones

A

estrogen and progesterone

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147
Q

pathway of estrogens

A

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

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148
Q

what does progesterone bind to

A

intracellular PR

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149
Q

what mediates the NON-genomic actions of estrogen

A

GPERs

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150
Q

what is GPERs do in non-reproductive tissues in females

A

adapt her body for pregnancy by immune suppression, strengthening of bone structures and behavioral changes

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151
Q

GPER can affect the endocrine system leading to

A

obesity, diabetes

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152
Q

what does the adrenal gland secrete small amounts of

A

androgenic steroids (andro = male)

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153
Q

what do androgenic steroids do in F and M

A

F: regulate libido
M: development and maintenance of male characteristics (T regulates libido in M)

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154
Q

what triggers puberity

A

increased pulsatile secretion of GnRH

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155
Q

hypothalamus has a _____ generator and what does it release

A

pulse generator

releases gonadotropin releasing hormone in a PULSATILE fashion (controlled by NTs, CRH, PRL, stress and gonadal hormones) not continuous

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156
Q

what induces gonadal production of steroids (E2, P, T) and peptide hormones (inhibin and activin)

A

the pattern of LH and FSH

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157
Q

MALE REPRODUCTION:

what do sertoli cells do

A

make the peptide inhibin and androgen binding protein

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158
Q

MALE REPRODUCTION:

what do leydig cells do

A

take T and convert some T to E2

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159
Q

MALE REPRODUCTION:

what produces T

A

testis

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160
Q

MALE REPRODUCTION:

what converts T to E2

A

aromatase. E2 acts on ERs to mediate some of the effects attributed to T

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161
Q

MALE REPRODUCTION:

prostate gland does what

A

nutrient fluids for sperm

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162
Q

MALE REPRODUCTION:

seminal vesicle does what

A

above glands’ secretions make up the fluid and sperm from seminiferous tubules = semen

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163
Q

MALE REPRODUCTION:

testes:
epididymis:
Vas deferens:

A

sperm production
sperm maturation
passageway into abdomen and delivery to the urethra

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164
Q

MALE REPRODUCTION:
what does inhibin do

A

released when sperm is too high. inhibits the release of GnRH and FSH

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165
Q

what can inhibit the secretion of GnRH and LH/FSH

A

T and inhibin

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166
Q

androgenic steroids have pronounced _______ effects

A

T- like

often used illegally by athletes (anabolic steroids)

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167
Q

what are metabolic effects of androgen R activation in males

A

decrease in adipogenesis and decrease in visceral fat
increase insulin sensitivity in skeletal muscle

why men can eat so much

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168
Q

what does a sustained high estrogen level do in terms of feedback and gonadotropin level

A

POST feedback and INCREASES gonadotropin levels

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169
Q

hormones from where stimulate the ovaries

A

the hypothalamus and AP

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170
Q

what do the ovaries release

A

E and P in pre-set patterns during each cycle

E and P prepare uterus for possible pregnancy

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171
Q

LH binds to what type of cell in ovaries

A

THECA (like Leydig)

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172
Q

FSH binds to what type of cell in ovaries

A

Granulosa (like sertoli)

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173
Q

Testosterone can cause negative feedback on (2)

A

Hypothalamus and AP

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174
Q

in men, what is libido regulated by

A

T

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175
Q

what does a pulsatile manner mean?

A

NOT continuously releases

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176
Q

what cells are known as the nursemaids in male?

A

sertoli cells

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177
Q

inhibin can cause negative feedback on the

A

AP

178
Q

LH goes with what type of cell

A

Leydig cells (LL)
Theca

179
Q

FSH goes with what type of cell

A

Sertoli cells (SS)
Granulosa

180
Q

what converts T into estrogen?

A

aromatase

181
Q

what converts T into DHT?

A

5alpha reductase

182
Q

when there are sustained HIGH levels of estrogen, what type of feedback loop happens

A

POSITIVE!!!

this is the weird one. REMEMBER ON EXAM***

183
Q

what type of cell receptors are found on Theca and Granulosa cells?

A

ER, AR, and PR

184
Q

what do theca cells produce

A

T

185
Q

what do granulosa cells produce

A

estradiol

186
Q

what arteries are found in the endometrium

A

spiral arteries

what sheds every month

187
Q

what is the definition of the follicular phase

A

a certain follicle is selected to grow.

188
Q

what is the definition of the luteal phase

A

ruptured follicle develops into corpus luteum

189
Q

what H dominates the first half of the cycle (follicular phase)

A

Estrogen

190
Q

what phase is progesterone super high

A

luteal phase

prepares uterus lining for implantation

191
Q

the LH surge happens at

A

ovulation

192
Q

what happens to the corpus luteum is not implantation occurs

A

apoptosis!

193
Q

lack of what H causes the endometrium to die

A

P

194
Q

If NO implantation occurs, do FSH and LH secretion resume?

A

YES!

195
Q

during what days of cycle does the endometrium shed with bleeding

A

days 1-7 (follicular) = menses

196
Q

what is happening during the proliferative phase?

A

the endometrium grows and thickens in preparation for pregnancy

(due to high levels of E)

197
Q

how do we want the cervical mucus to be for max sperm survival?

A

viscosity -> THIN
quantity -> MANY

198
Q

high E triggers the LH surge – what type of feedback is this?

A

POSITIVE!! ***Weird one

199
Q

what causes cramping? and how do they do it?

A

Prostaglandins

produce STRONG vasoconstriction of the spiral arteries and contraction of the myometrium

200
Q

why does the stratum functionalis (part of endometrium) slough off

A

the prostaglandins effects leads to loss of nutrients and hypoxia

201
Q

what is the actual layer of tissue called that sloughs off during period

A

stratum functionalis

202
Q

what hormone does an ovulation test test for

A

LH

the LH surge = ovulation

203
Q

what hormone does a pregnancy test test for

A

hcG (human chorionic gonadotropin)

204
Q

what two ways is hcG secreted (assume implantation has occured)

A
  1. by the implanting embryo first
  2. the placenta layer will secrete
205
Q

what 2 hormones are CRITICAL for supporting and maintaining the endometrial lining (assume implantation has occured)

A

P and E

super important to maintain pregnancy!!

206
Q

what structure secretes P and E?

A

corpus luteum

(if implantation has occurred, hcG supports the corpus luteum so it doesn’t become the corpus albicans)

207
Q

what hormone is secreted during labor to induce contractions? type of feedback?

A

oxytocin from posterior pituitary

POS feedback

208
Q

what hormone regulates breast milk/lactation

A

oxytocin

209
Q

how does a baby initially get its FIRST antibodies

A

from the mother IN UTERO. has antibodies BEFORE birth

210
Q

why is breastfeeding so important right after birth?

A

the first breast milk (colostrum) is a huge source of antibodies

super watery. contains tons of proteins

211
Q

an infant’s gut epi. cells have receptors that transport what?

A

intact maternal antibodies into the fetal circulation

212
Q

what causes menopause

A

complete loss of ovarian responsiveness to gonadotropins –> leads to erratic cycles = perimenopause

213
Q

menopause:

tissue hormonal withdrawal is equivalent to

A

drug withdrawal

214
Q

what are the 3 types of estrogens?

A
  1. Estrone (E1)
  2. estradiol (E2)
  3. estriol (E3)
215
Q

rank potency of estrogens –> most to least (3 types)

A

Estradiol>estrone>estroil
E2>E1>E3

216
Q

what estrogen dominates reproductive years?

A

estradiol/E2

217
Q

what estrogen is produced during pregnancy?

A

Estriol/E3

218
Q

what estrogen is produced during menopause?

A

estrone/E1

219
Q

what is estrone/E1

A

it is produced during menopause by FAT TISSUE

220
Q

types of HRT delivery methods

A

1: systemic: pills, gels, creams, etc
2: vaginal products

**a lot of doctors start with bisphosphonates to prevent osteoporosis due to menopause

221
Q

what is the difference between bio-identical and conventional HRT?

A

bio-identical: EXACTLY the same chemical structure.

conventional: NOT the same chemical structure. “Similar” but not really. Comes from horse estrus cycle –> polyestrous

222
Q

method of HRT administration:

2 ways

A

oral delivery

transdermal drug delivery

223
Q

method of HRT administration:

significance of oral delivery

A

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
Q

method of HRT administration:

advantages of transdermal drug delivery

A

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
Q

do males produce T all their lives?

A

YES! but slowly declines with age

226
Q

can F sex hormones influence microbiota?

A

yes! especially in the mouth and gut! (perio and osteoporosis)

227
Q

4 ways sex hormones are thought to act by

A
  1. strengthening the epi barrier to resist bacterial invasion
  2. modulating immunity to oral bac
    • affecting maintenance and repair of collagen
  4. BONE. E inhibits bone breakdown
228
Q

what are endocrine disruptors?

A

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
Q

Sum of ALL estrogen refers to what

A

ALL endogenous AND environmental exposure to E and E like compounds

230
Q

what is the most common endocrine disorder in the US

A

diabetes

231
Q

what is type 1 diabetes caused by and what do patients rely on to maintain normal blood glucose levels

A

autoimmune destruction of insulin producing pancreatic beta cells

these patients rely on insulin injections

232
Q

what represents a majority of cases - type 1 or 2 diabetes

A

type 2

233
Q

what is type 2 diabetes caused by

A

tissue resistance to insulin (due to weight, age, not active)

234
Q

what is gestational diabetes and what is it caused by

A

it occurs in the second half of pregnancy

caused by placental hormones -> results in insulin resistance and deficiency

235
Q

what does HbA1c measure

A

the irreversible binding of glucose to Hb

test provides an approximate gauge of the blood glucose level over 3 months

236
Q

lifespan of RBC

A

120 days

237
Q

4 classes of drugs used to treat diabetes

A

Sulfonylureas
Biguanides
Alphaglucosidase inhibitors
Insulin

238
Q

normal HbA1c numbers:
PREdiabetes:
Diabetes:

A

<5.7%
5.7-6.4%
>6.5%

239
Q

target blood sugar levels BEFORE meals

A

80-130mg/dL

240
Q

target blood sugar levels 2 hours after meals

A

180mg/dL

241
Q

7 medical complications of diabetes

A

heart disease
stroke
kidney disease
blindness
neuropathy
retinopathy
amputation

242
Q

what are oral manifestations of diabetes

A

increased risk of dental caries, gingivitis and perio, xerostomia, delayed wound healing, oral candidiasis, lichen planus

243
Q

steps to use a glucometer

A

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
Q

what should you do if your patient glucometer results show ketoacidosis

A

ER or call doctor

245
Q

what should you do if your patient glucometer results show hyperglycemia

A

lifestyle changes and medications

246
Q

what should you do if your patient glucometer results show HYPOglycemia

A

give carb (juice, honey, glucose tablet)

247
Q

3 ways dentistry is affected by bone quality

A

osteoporosis (implants)
wound healing (implants/surgery)
perio

248
Q

what elements does bone contain a lot of

A

Ca2+, Mg+, P+

249
Q

bone formation depends on

A

biomechanical loading

250
Q

what is Piezo1

A

ion channel embedded in the osteoblasts and osteocytes PM that responds to mechanical loading on bone

251
Q

bone is ________ and needs this stimulation to form new bone

A

piezoelectric (Piezo1)

252
Q

activation of what stimulates the formation of new bone via OB

A

activation of Piezo1

253
Q

what is the major signaling metabolic factor secreted by osteocytes

A

prostaglandin E2 (PGE2)

254
Q

bone homeostasis is a perpetual cycle of

A

destruction and formation -> undergoes daily wear and tear and micro-factors

255
Q

what 2 consecutive cellular events do we need for bone remodeling

A

resorption via osteoCLASTS
formation of new bone via osteoBLASTS

256
Q

what types of factors is bone under the influence of?

A

LOCAL factors

257
Q

what cell senses microfractures in the bone

A

osteoCYTES (which then signal to osteoclasts for bone RESORPTION –> osteoblasts drop new bone)

258
Q

what produces osteocalcin

A

osteoBLASTS

259
Q

RANKL in the presence of MCSs is primarily responsible for

A

activation of osteoclasts leading to bone loss

260
Q

what is a decoy receptor for RANKL

A

OPG (osteoprotegerin)

261
Q

osteoblasts produce OPG (osteoprotegerin) which

A

inhibits bone loss by inhibiting osteoclastogenesis

262
Q

explain what RANK and RANKL are

A

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
Q

what plays an important role in osteoclast differentiation

A

cytokines

264
Q

decrease in RANKL and increase in OPG does what

A

suppresses osteoclast differentiation

265
Q

what can be detected in urine that shows bone resorption activity/marker

A

collagen telopeptides

266
Q

what are collagen telopeptides

A

during resorption, osteoclasts release small collagen fragments containing (OH)proline = collagen telopeptides

267
Q

what are the 4 steps of bone remodeling

A

activation, resorption, reversal and formation

268
Q

activation of osteoclasts is controlled through what pathway

A

RANK/RANKL/OPG pathway

269
Q

what positively regulates bone formation

A

androgens, mechanical load, PTH, B-blockers

270
Q

what blocks bone formation

A

B-adrenergic stimulation (via leptin), immobilization, aging

271
Q

what + regulates bone resorption

A

estrogen deficiency, immobilization, low Ca2+ (PTH)

272
Q

what blocks bone resorption

A

estrogen, SERMs, Bisphosphonates, Calcitonin, Ca2+/Vit D

273
Q

is calcidiol or calcitriol the active form

A

calciTRIOL

274
Q

what is osteoporosis

A

metabolic disease characterized by a decrease in bone strength and bone mineral density and altered bone quality

women are way more affected

275
Q

what is osteopenia

A

loss of bone mass but not bad enough to be osteoporosis (kinda like pre-osteoporosis)

276
Q

is estrogen anabolic or catabolic

A

ANAbolic -> builds up!

277
Q

what does bisphosphonates do

A

bind to bone mineral and are taken up by osteoclasts, causing them to undergo apoptosis or have reduced resorptive capacity

278
Q

what is teriparatide

A

a recombinant fragment of PTH, stimulates bone formation by increasing osteoblast activity and to a less extent, inhibiting osteoclast recruitment

279
Q

what H does bone release

A

osteokines
osteocalcin -> interacts with muscle H and fat H to regulate homeostasis, metabolism, learning memory and depression

**bone is an endocrine organ!

280
Q

what produces osteocalcin

A

Osteoblasts. Need Vit K2 also

281
Q

Vit K1 is found where and is good for what

A

good for blood clotting
found in green leafy vegetables

282
Q

Vit K2 is found where

A

fermented foods like cheese, egg yolk, beef liver

283
Q

Vit K3 is

A

toxic to humans

284
Q

Vit K2 can inhibit ______ and promote __________________

A

inhibit vascular calcification

promote bone mineralization

285
Q

what drug blocks all forms of Vit K

A

Coumadin (warfarin) -> anti-coagulants

286
Q

cOCN/GlaOCN contains what types of residues

A

Y-carboxyglutamic acid

287
Q

Y-carboxyglutamic acid production depends on

A

Vit K2 and is stimulated by 1,25 (OH)2 Vit D

288
Q

what is the major NONcollagenous protein in bone ECM

A

osteocalcin -> osteoblast secreted and vit K2 dependent protein!

289
Q

what 2 forms does osteocalcin exist in

A

undercarboxylated (ucOCN) and carboxylated osteocalcin (GlaOCN)

290
Q

between ucOCN and GlaOCN, which has greatest affinity for hydroxyapatite in bone matrix

A

GlaOCN!

becomes trapped in the bone matrix after secretion from the OBs

291
Q

characteristics of ucOCN

A

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
Q

what is analogous to OCN

A

MGP (matrix-gla protein)

293
Q

what makes MGP

A

chondrocytes and vascular smooth muscle cells (MGP is analogous to OCN)

294
Q

what does MGP need to be in its active form

A

Vit K2

295
Q

what is a KEY inhibitor of vascular calcification

A

MPG

the absence of it leads to excessive calcification of vasculature

296
Q

what does the active form of MPG do

A

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
Q

hallmark of cardiac vascular calcifications

A

presence of atherosclerotic plaques in arterial walls

298
Q

muscles secrete what H

A

myokines -> endocrine organ

^ prevent bone and muscle loss

299
Q

adipocytes secrete what H

A

adipokines

300
Q

adiponectin

A

good! controls glucose and fatty acid metabolism and food intake

301
Q

leptin

A

signals being full via adipose tissue

302
Q

resistin

A

high resistin levels are associated with an impaired glucose tolerance test

in obesity, macrophages that infiltrate and live in WAT produce resistin

303
Q

do skeletal muscle, fat and bone talk to each other?

A

YES! organ cross-talk

304
Q

obesity and T2D and osteoporosis are considered what level of disease

A

global epidemic

all have high fat mass as a known risk factor

305
Q

what does high glucose levels do to osteoclasts

A

inhibit OC viability and differentiation
inhibit OC resorption function

306
Q

what are some examples of diseases that disrupt the activity of salivary gland secretion

A

inflammatory, infectious and neoplastic diseases

307
Q

3 salivary gland names

A

parotid
submandibular
sublingual

308
Q

what are the 2 main components of saliva

A

serous and mucous

309
Q

what are the tonicity changes seen in saliva

A

is isotonic in gland but once in oral cavity -> HYPOtonic

310
Q

what is the main differences b/w submand. and parotid salivary glands

A

they have different gene expression profiles (different mRNAs) and these properties have a genetic basis

both have tumor and transport associated genes

311
Q

saliva pH and osmolarity

A

slightly acidic -> pH of 6-7

HYPOosmotic

312
Q

what are the organic and inorganic components of saliva

A

orgo: proteins and NON-proteins
in-orgo: electrolytes

313
Q

components of whole mouth saliva

A

99% water
1% inorgo and orgo components

314
Q

main jobs of saliva

A

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
Q

what 2 ions are present in a supersaturated form in saliva

A

Ca2+ and Phosphorus

316
Q

what are things saliva can dissolve

A

chemicals, odorants and taste sensation when those two are combined

317
Q

MALT significance to salivary glands

A

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
Q

where is the 1st line of defense in our body

A

oropharynx mucosa

319
Q

what does the oropharynx secrete as an immune response

A

IgA-secreting cells – these then redistribute to other remote sites to help fight infection

320
Q

where is a good pace to do an analysis of immune response

A

SALIVA!! NOT BLOOD. Saliva shows a general picture of body’s mucosal immunity

321
Q

what do a lot of prescription drugs affect

A

salivary flow

322
Q

what meds are commonly associated with xerostomia

A

ones with anticholinegeric or sympathomimetic effects and long-term opioids

323
Q

5 NON-specific macromolecules found in saliva

A

histatins
lysozyme
carbonic anhydrase
amylase enzyme
mucins

324
Q

what are histatins

A

NON- specific macromolecule in saliva. buffering, mineralization, antimicrobial activity against a broad spectrum of bac and fungi

325
Q

what are lysozymes

A

NON- specific macromolecule in saliva.

attacks and degrades bac cell walls

326
Q

what are carbonic anhydrases

A

NON- specific macromolecule in saliva.

enzyme -> buffering –> makes HCO3-

327
Q

what are amylase enzymes

A

NON- specific macromolecule in saliva.

CHO digestion and some antimicrobial activity

328
Q

what are mucins

A

NON- specific macromolecule in saliva.

lubrication and anti bac/viral

329
Q

what are the 4 SPECIFIC salivary macromolecules

A

Growth factors –> EGF and NGF
Regulatory Peptides
Cytokines
Secretory IgA

330
Q

what are growth factors in saliva

A

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
Q

what are regulatory peptides in saliva

A

SPECIFIC salivary macromolecules

332
Q

what are cytokines in saliva

A

SPECIFIC salivary macromolecules

immune-regulatory peptides

333
Q

what is IgA in saliva

A

SPECIFIC salivary macromolecules

secreted for protecting mucosal surfaces

334
Q

characteristics of IgA in saliva

A

produced by plasma cells

in serum, IgA is in MONOmeric form

salivary ducts cells produce R (secretory component) for POLYmeric IgA

335
Q

what is the secretory component for IgA regulated by

A

H! male and female H, glucocorticoids, thyroid H

secretion of POLYmeric IgA onto mucosal surface depends on availability of secretory component

336
Q

what type of control is saliva secretion under

A

under NT and hormonal control

337
Q

what types of R do acinar cells have

A

adrenergic (E,NE)
muscarinic (ACh, GPCR)
substance P
prostaglandin
peptide H R

338
Q

what does B-adrenergic R stimulation from acinar cells in the salivary glands result in

A

LOW volume of saliva but protein and mucin RICH

339
Q

what does mACh R stimulation from acinar cells in the salivary glands result in

A

+ regulates fluid transport

food stimulates chemo, presso-receptors -> so get a SEROUS enzyme-rich saliva (TONS!) with SOME mucins

340
Q

saliva serous secretion depends mainly on what

A

activations GPCRs (mAChRs)

**protein secretion is controlled mainly by B-adrenergic stimulation

341
Q

if hormonal imbalances exists, what does this mean for our saliva

A

salivary immunity CHANGES

342
Q

what types of steroids are found in saliva

A

biologically active, FREE forms

343
Q

most important daily job of saliva is to

A

provide mucous so food can be bound in bolus

344
Q

where can you find HCl, pepsin, gastric lipase

A

stomach! very acidic here

mechanical and enzymatic processing of ingested bolus

345
Q

where can you find pancreatic juice, bile, NaHCO3

A

small intestine

breaking down of macromolecules and absorption of nutrients

346
Q

where does microbial fermentation of undigested food and water reabsorption happen

A

colon

347
Q

what are the 2 accessory organs in the GI

A

pancreas and liver

348
Q

the large intestine consists of (2)

A

colon and rectum

349
Q

5 main activities of digestion

A

ingestion -> mechanical digestion -> chemical digestion -> absorption -> excretion

350
Q

when is food considered a bolus

A

once chewed and moistened (when it leaves the mouth)

351
Q

how does the bolus travel

A

through peristalsis

352
Q

Does the CNS control the enteric nervous system?

A

NO! it functions independently

the CNS can speed it up or slow down. Does not activate it though

353
Q

which part of the esophagus is responsible for voluntary swallowing (voluntary phase)

A

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
Q

where does tonic contractions happen and what is its job (GI)

A

these are SUSTAINED

occurs in smooth muscle sphincters

keeps bolus from moving backwards

355
Q

what are phasic contractions (GI)

A

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
Q

digestive enzymes are secreted into (3)

A

mouth, stomach and small intestine

357
Q

what produces mucous (GI)

A

mucus cells in stomach and goblet cells in intestine

358
Q

bile is SECRETED where

A

liver

***STORED in gallbladder

359
Q

what is an example of a long reflex in digestive system

A

smell food and starting to salivate

360
Q

does ACh or epi/norepi slow the digestive system down

A

epi/norepi

**dont want to be stressed while eating!

ACh = rest and digest

361
Q

what are short reflex patterns (GI)

A

contained within the ENS

peristalsis, secretion, mixing contractions, local inhibitory effects

362
Q

what are long reflex patterns (GI)

A

travel OUTSIDE of the ENS - 2 kinds ->

Long: involve the CNS. ex -> vomiting

Short: ex -> gastrocolic = stomach stretching from food causes increase peristalsis

363
Q

what is the hunger hormone

A

Ghrelin

FEED ME!! “gremlin”

364
Q

rank order of meals digested the slowest (slowest first):

carbs, high fat, high protein

A

high fat > high protein > carbs

carbs digested the fastest

365
Q

how do we get pepsin

A

gastric juices contain pepsinogen which gets activated by H+ from parietal cells –> pepsin

366
Q

what is role of bile

A

emulsifying dietary fats into small droplets

367
Q

which parts of the small intestine are involved in the most nutrients, vit and mineral absorption

A

jejunum and ileum

368
Q

where are bile salts reabsorbed

A

ileum and recycling to the bile via enterohepatic circulation

369
Q

what is incretin

A

stimulates secretion of insulin via GLP-1 Hormone

incretin mimetic drugs -> T2D patients

370
Q

pancreas exocrine secretions

A

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
Q

what secretes NaHCO3 in the pancreas

A

duct cells

372
Q

what is cystic fibrosis

A

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
Q

in small intestine: enzymes stored? released? when?

A

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
Q

what is the brush border

A

it is on the microvilli on epithelium in the small intestine

enzymes are located here

375
Q

what is absorbed into lacteals

A

fats

376
Q

capillaries dump nutrients to

A

liver

377
Q

lymphatic vessels (containing absorbed fats) dump into

A

bloodstream

378
Q

if you don’t eat/drink a lot of lactose things, you lose which enzyme

A

lactase -> lactose intolerance. Throws off tonicity

379
Q

glucose enters with what ion in the small intestine cells

A

enters the cell with Na+

380
Q

where do proteins get digested and absorbed

A

in small intestine

381
Q

pathway that causes the gallbladder to release bile

A

secretin causes the pancreas to produce HCO3 to neutralize H+ in the chyme. Secretin acts with CCK. CCK stimulates gallbladder to release bile.

382
Q

what cells secrete bile

A

hepatocytes

383
Q

what is bile

A

bile salts + bile pigments

384
Q

what are bile salts

A

steroid bile acids combined with amino acids

385
Q

what is the cause of super infections we leanred about

A

drugs affecting the microflora of our GI

386
Q

Most important daily job of saliva

A

to provide mucous so food can be bound in bolus

387
Q

digestion in mouth is

A

chewing and mixing with saliva

388
Q

digestion in stomach is

A

mechanical and enzymatic processing of ingested bolus

389
Q

digestion in small intestine is

A

breaking down of macromolecules and absorption of nutrients

390
Q

digestion in colon is

A

microbial fermentation of undigested food and water reabsorption

391
Q

what do fatty acids get broken down into and what breaks them down

A

bile breaks them down

fatty acids -> monoglycerides -> micelles -> trigylcerides -> chylomicrons

392
Q

what do chylomicrons enter

A

lacteal

393
Q

what do the collecting lymphatics pass through

A

the lymph nodes and converge into main lymph duct. eventually reach the systemic circulation through the subclavian vein

394
Q

3 endocrine functions in the liver

A
  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
Q

what breaks down drugs in the liver

A

P450 system

converts compounds to glucuronide which makes them more water soluble.

396
Q

how are water soluble vitamins absorbed and digested

A

mediated transport –> vit b12 is complexed to IF and absorbed in small intestine

397
Q

how are nucleic acids digested

A

digested into their basic units

398
Q

how are minerals digested

A

actively transported through channels

399
Q

T/F do all microbiomes affect each other

A

TRUE! for example, gut microbiome affects oral microbiome!

400
Q

when does bacterial colonization start?

A

at birth

401
Q

what is the significance of a c-section

A

babies pick up microbes when they are born vaginally vs when they are born c-section. can get sicker easier

402
Q

the CNS and the gut microbiota interact with each other in a___________

what regulates it

A

bidirectional way

via endocrine, immune and neural pathways

regulated at intestinal epi and blood brain barrier

403
Q

what types of patients are at high risk for tooth erosion

A

GERD, bulimia

404
Q

what are NSAIDs

A

non-steroidal anti-inflam. drugs like aspirin, ibuprofen

for pain and inflammation

405
Q

cons of NSAIDS

A

affect GI tract homeostasis

406
Q

what H is the opposite of somatostatin

A

GH

407
Q

what does somatostatin inhibit

A

ghrelin release and parietal cell H+ secretion and histamine secretion

AND

secretion of gastrin and pepsinogen from chief cells

408
Q

T/F parietal cells make IF

A

true

409
Q

gastrin stimulates ____ secretion from parietal cells

A

H+

410
Q

what does H2R antagonists block

A

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
Q

3 main stimulants of H+ secretion at level of parietal cells

A

histamine, ACh, and gastrin

when all there are present = MAX H+ secretion!!

412
Q

do parietal cells contain proton pumps

A

yes

413
Q

protein pump inhibitors (Prilosec) form what type of bond to H+ and why is. this important

A

covalent. IRREVERSIBLE!!

enables prolong inhibition of H+ secretion even after the drug concentration in blood has gone way down

414
Q

what is a problem with prolong PPI drugs

A

lowering the H+ long term can cause bacterial overgrowth = dysbiosis

415
Q

how is vit B12 absorbed

A

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
Q

what H tells us when we are full

A

leptin

417
Q

what are NSAIDS

A

diverse group of compounds that are mainly used to reduce pain, inflam, and fever

418
Q

what are the two groups pain drugs belong to

A

non-narcotic analgesics = NSAIDS and acetaminophen

Opioids (narcotics)

decrease synthesis of PG which is bad bc they help regulate homeostasis and inflam

419
Q

MOA of NSAIDs

A

non-selectively blocking the enzymes that make PGs. inhibition of COX1 is also mostly responsible for GI side effects like bleeding

420
Q

what is point of people taking baby asprin daily

A

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
Q

what does mucus do in stomach

A

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
Q

what controls stomach mucus secretion

A

mainly PG (PGE2)

423
Q

how does the stomach mucosal layer neutralize H+

A

it secretes bicarb and HCO3 + H+ -> H2O + CO2

424
Q

NSAIDs block COX1, this causes

A

decrease in mucus secretion, bicarb secretion, and blood flow.

this all leads to ulcers in stomach

425
Q

NSAIDS increase/decrease gastric homeostatic PGE2 production

A

DECREASES

426
Q

how does our circadian timing system work

A

when it gets dark –> body produces melatonin

when it is light out –> no more production of melatonin

427
Q

circadian rhythms are key regulators of

A

metabolism, thermogenesis, immune function, and reproduction

428
Q

shift workers circadian system

A

chronodisruption: decrease-protective factors (PGE2) –> decrease melatonin

***lack of sleep = more ghrelin = overweight and T2D RISK factor

429
Q

Ghrelin appetite regulation

A

released by stomach and stimulates food intake. Ghrelin allows the hypothalamus to sense stomach fullness

430
Q

Leptin appetite regulation

A

released by adipocytes and signals the extent of fat stores to the hypothalamus. Involved in regulation of appetite (suppression) and energy expenditure

431
Q

T/F: if you don’t get enough sleep, it can make you hungier

A

TRUE. INCREASES ghrelin secretion

432
Q

stimulators of ghrelin secretion

A

fasting, being lean/underweight, T, GHRH

433
Q

inhibitors of ghrelin secretion

A

feeding/obesity
insulin
GH
leptin
somatostatin
TH
CCK

434
Q

Major GI Functions Affected by circadian rhythms (2)

A

H+ secretion
maintenance and repair of stomach protective mucus barrier

435
Q

humans in developed countries have 3 ways in which we messed up our gut –> chronodisruption

A

we can have light 24/7 -> decreases melatonin secretion
24h tv and communications
24h food availability

436
Q

decrease in leptin and increase in ghrelin increases/decreases appetite

A

INCREASES appetite

437
Q

gastroparesis

A

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
Q

how common is gastroparesis

A

1 in 4 people

439
Q

gastroparesis can be from these 2 drug classes

A

ALL opioids
certain anti-diabetic medications and GLP-1 agonists used to treat T2D

440
Q

how can a dentist see diabetes in the mouth

A

if we are seeing gingivitis/perio could be due to the increase blood sugar –> increase glucose in saliva

Physiology (4 decks)

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