Test 3 Flashcards

1
Q

How do we find the rate of air flow

A

Difference in pressure between atmosphere and intra-alveolar pressure
divided by the resistance of airways

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2
Q

What causes air to move into the lungs

A

when the pressure in the lungs is less than the pressure of the atmosphere

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3
Q

How does the diaphragm cause inspiration

A

the diaphragm contracts decreasing pressure in the thorax, causes the lungs to expand, which causes the pressure to go down, and air rushes in

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4
Q

How does the diaphragm affect inspiration

A

it relaxes, increasing pressure in the thorax, which causes the lungs to shrink, increasing pressure, forcing air out

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5
Q

What is boyles law

A

p1v1 = p2v2
The greater the pressure the less the volume
the less the volume the greater the pressure
less pressure = more volume
more volume = less pressure

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6
Q

How do the intercostals affect breathing

A

contraction leads to increased rib cage = increase volume of lungs = decrease pressure = inspiration

relaxation = decreased rib cage size = less volume in lungs = more pressure = expiration

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7
Q

contraction of the abdominals does what to inspiration and expiration

A

contraction leads to expiration, relaxation leads to inspiration.

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8
Q

What is pneumothorax, what happens

A

when air gets into the plural cavity, it gets rid of the negative intrapleural pressure in the pleural sac. so the increase in pressure there causes the lung to collapse

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9
Q

what is the primary way to regulate air flow into the lungs

A

the radius of the conducting airway

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10
Q

what controls the radius of the conducting airway

A

the autonomic nervous system
sympathetic - relaxation of smooth muscle = bronchodialation
parasympathetic = contraction of smooth muscle = bronchoconstriction

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11
Q

What is compliance

A

distensability - the ease with which lungs expand under pressure
(The lungs must be compliant for inspiration)

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12
Q

What is elasticity

A

Tendancy to return to size after being stretched

lungs must be elastic for expiration

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13
Q

What is it that makes the lungs elastic

A

the high content of elastin in the lungs

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14
Q

how often are the lungs under elastic tension

A

constantly, it increases with inspiration and decreases with expiration but it never goes away

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15
Q

what happens as lungs become less compliant

A

they become harder to expand and therefor it requires more work to inflate them

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16
Q

What is surfactant

A

A fluid secreted by the lungs that decreases the surface tension within the alveoli

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17
Q

Where does surfactant come from

A

type II alveolar cells

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18
Q

What is the result of surfactant decreasing the surface tension within the alveoli

A

it leads to increased compliance and decreased tendency to recoil

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19
Q

Why is it bad to not have surfactat

A

the lungs become really hard to inflate because of low compliance, the lungs will often collapse

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20
Q

What is respiratory distress syndrome

A

surfactant is produced late in fetal developpment, so often premature infants don’t have enough surfactant and thier lungs are hard to inflate and often collapse

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21
Q

What is a spirogram

A

The thing that measures lung volumes, inspiration and expiration

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22
Q

What is tidal volume TV

A

the amount of air inspired and expired during normal breathing (Middle portion on spirogram)

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23
Q

What is inspiratory reserve volume IRV

A

how much more you could breath in more than how much you normally do ( big peak )

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24
Q

What is expiratory reserve volume ERV

A

how much more you could breath out than you normally do. (big dip)

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25
Q

What is residual volume (RV)

A

the difference between 0 volume in the lungs and how much you have when you do a maximal expiration. (between bottom of graph and low dip)

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26
Q

What is Inspiratory capacity IC

A

how much you can breath in, includes tidal volume and max inspiratory volume (IRV + TV)

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27
Q

What is Vital capacity VC

A

the maximum amount of air that can be inhaled and exhaled ( tidal volume + IRV + ERV)

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28
Q

What is functional reserve capacity FRC

A

the difference between no volume in the lungs to the bottom of tidal volume ( ERV + RV)

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29
Q

what is total lung capacity

A

the total amount of air the lungs can hold, from 0 to top of max inspiration (IRV + TV + ERV + RV)

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30
Q

What is FEV1

A

Forced expiratory volume

the maximum amount of air that can be expired in one second after max inspiration

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31
Q

What is anatomical dead space

A

the air passageways (150 ml)

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32
Q

what is minute respiratory volume

and how do you find it

A

the amount of air inhaled or exhaled during one minute of breathing
MRV = TV * Rate of breathing

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33
Q

what is minute alveolar ventilation

A

the amount of new air entering the alveoli per minute

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34
Q

how do you find minute alveolar ventilation

A

MAV = Rate * (TV - Dead space)

rate is # of breaths per minute

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35
Q

what happens to minute alveolar ventilation after exercise

A

it increases

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36
Q

What is obstructive lung disease

A

an increase in resistance in air pathways

causes dificulty in expiration

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37
Q

What are two types of obstructive lung diseases

A

Asthma

Chronic Obstructive pulmanory disease (COPD)

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38
Q

What is asthma

A

airway obstruction due to inflammation, mucous secretion, brachoconstriction

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39
Q

what can cause asthma

A

allergic reaction
exercise
infection

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40
Q

What are the two main types of COPD

A

Emphysema

Chronic Bromchitis

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41
Q

what is emphysema

A

desctuction of alveoli = larger but fewer alveoli
this leads to decreased area for gas exchange and can lead to the bronchiolies collapsing

(caused by smoking)

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42
Q

What is chronic bronchitis

A

lower airways are chronically inflammed
airways swell, thicken and produce mucus. the mucus doesn’t move because the cillia are damaged

(Caused by smoking, pollution, and allergins)

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43
Q

what does obstructive lung diseases do to the spirometer

A

it decreases FEV1, and just ERV

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44
Q

What do restrictive lung diseases do to the spirometer

A

they decrease IRV, FEV1 is normal

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45
Q

what do restrictive lung diseases do

A

they decrease compliance and make inspiration dificult

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46
Q

What is an example of a restrictive lung disease

A

Pulmonary fibrosis

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47
Q

what is pulmonary fibrosis

A

it’s caused by inhaling smoke, pollution, and irritants and it causes scar tissue to build up in the lungs. this decreases compliance and diffusion of gasses

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48
Q

how much of our energy expenditure is used for quiet breathing

A

3%

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49
Q

When is energy expenditure for breathing increased

A

when pulmonary compliance is decreased (NRDS)
When resistance is increased (COPD)
When elastic recoil decreases (EMPHYSEMA)
when more ventilation is needed (exercise)

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50
Q

What is partial pressure

A

the amount of pressure each substance is contributing to the whole pressure

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51
Q

how to calculate partial pressure

A

take the percentage .05 and times it by the total pressure

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52
Q

What does the dorsal respiration group do

A

it stimulates the phrenic to incite breathing

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53
Q

what does the ventral respiration group do

A

it helps in breathing when its heavy

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54
Q

What does the central pattern generator do

A

it helps build the breathing rythym

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55
Q

what does the pontine respiratory group do

A

helps transistion between inspiration and expiration

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56
Q

what receptors are the most important in regulating breathing rate

A

chemoreceptors

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57
Q

what are the chemicals that are the most important in signaling to help regulate breathing rate

A

CO2 and H+

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58
Q

What are pulmonary receptors for

A

detect irritants - leads to caughing

to prevent excessive stretching

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59
Q

during normal expiration what fraction of lung volume is exchanged

A

1/7

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60
Q

what are the two ways to transport O in the blood

A

It can bind to hemoglobin, or it can be dissolved in the blood

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61
Q

What is oxygen carrying capacity

A

how much O the blood can hold

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62
Q

how does Hemoglobin affect the oxygen carrying capacity

A

each molecule of hemoglobin can carry some Oxygen, more hemoglobin = more oxygen

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63
Q

how does the % satuation of HB change

A

the higher the pressure of O in the blood the higher the %saturation of HB

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64
Q

how do you calculate the oxygen content of blood

A

you find the oxygen carrying capacity (how much each molecule of HB can hold)
how much HB there is in the blood then figure out the %saturation of HB and multiply capacity by % saturation

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65
Q

What is the Bohr effect

A

it states that when the CO2 pressure increases ( or the H+) the HB will release % satureation of HB by oxygen.

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66
Q

What are the three types of CO2 transport in blood

A
  1. DIssolved in the blood (9%)
  2. as Bicarbonate (64%)
  3. as carbaminohemoglobin (27%)
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67
Q

what is the function of carbonic anhydrase and where is it locate

A

it’s located in the blood and it turns CO2 to Bicarbonate and the other carbaminohemoglobin and vice-verse to dissolve it in the blood or allow it to be realeased

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68
Q

what are the three factors in blood that are important in breathing regulation

A

H+
CO2
Low O2

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69
Q

where in the CNS is breathing controlled

A

medulla oblongata and pons

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70
Q

what is the hering Bruer reflex

A

it prevents the over inflation of the lungs

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71
Q

What is the functional unit of the kidney

A

the nephron

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72
Q

What is a juxtamedullary nephron

A

they have a long loop of henle,

important in urine concentration

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73
Q

what is a cortical nephron

A

has a short loop of henle

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74
Q

What are the 4 basic renal processes

A

Glomerular filtration
tubular reabsorption
tubular secretion
excretion

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75
Q

what happens to fluid filtered by the glomerulus

A

it passes through
the glomerular capillary wall
the basement membrane
inner layer of bowmans capsule

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76
Q

What is the glomerular capillary wall like

A

more permiable to water and solutes than anywhere in the body

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77
Q

What is the basement membrane like

A

gelatinous layer, acellular

78
Q

what is the inner layer of bowmans capsule like

A

has podocytes that encircle the glomerular capillaries and form slit pores

79
Q

what are the four forces that determine glomerular filtration pressure

A

bowmans capsule hydrostatic pressure
glomerular capillary hydrostatic pressure
and both have osmotic pressure

80
Q

What are the 3 factors that influence glomerular filtration rate

A

Glomerular Filtration pressure (GFP)

Renal plasma flow (RPF)

81
Q

what is renal plasma flow

A

how many ml of plasma go through the kidney

82
Q

how do you get the filtration fraction

A

GFR/RPF, how much is filtered over how much goes through

83
Q

how is GFR regulated

A

largely by GFP, most pressures can’t be changed, but glomerular capillary hydrostatic pressure can be

84
Q

how is the glomerular capillary hydrostatic pressure controlled

A

intrinsic and extrinsic factors

85
Q

What are the two types of intrinsic control of GFR

A

Myogenic regulation

tubeoglomerular feedback

86
Q

What is myogenic regulation as intrinsic conrtol of GFR

A

the muscles on the afferent artery squeeze down and don’t let as much blood to the glomerulus

87
Q

What is tubeoglomerular feedback as intrinsic control of GFR

A

the macula densa cells detect changes in GFR
high GFR leads the macula dense cells to release adenosine, which leads to constriction of the afferent arterioles = decreased blood flow = decreased GFR

88
Q

What is extrinsic control of GFR

A

its most important when MAP gets way off (dehydration, hemorrhage)
MAP increases to decrease urine output, which decreases blood through to the kidneys

89
Q

What is filtered load

A

the quantity of a solute that is filtered per unit of time. take concentration of substance in blood and times it by GFR

90
Q

what is tubular reapsorption

A

when the water and solutes filtered by the glomerulus enter back into the peritubular capillaries

91
Q

What are the two types of tubular reapsorption

A

Active = things are transported against their gradient back into the blood
(glucose, AA’s, NA+ proximal tubules) ( NA+ distal tubules)
Passive = things move down thier gradients back into the blood
(H2O, cl-, Urea proximal)(H20 distal)

92
Q

What is transport (tubular) maximun

A

it’s the max amount of a solute that can be reabsorbed, if the filtered load is greater that the transport maximum, some of the solute will be excreted

93
Q

how does it work when transport maximum is exceeded

A

all of the transporters are occupied so all of the solute can’t be reabsorbed

94
Q

What is tubular secretion

A

its the active transport of substances in the blood into the lumen of the kidney tubules

95
Q

What can be removed from the blood stream by tubular secretion

A

H+, K+, and drugs

96
Q

What is plasma clearance

A

measure of the rate at which substances are cleared from the plasma

97
Q

how is plasma clearance expressed

A

volume of plasma completely cleared of the substance per minute

98
Q

how is plasma clearance found

A

rate of urine formation * urine concentration / plasma concentration

99
Q

how can filtration fraction be determined by inulin and PAH clearance

A

Inulin clearance / PAH clearance

100
Q

How does the Renin-angiotensin system work

A

1) activated by a drop in blood pressure,
2) stimulates the JG cells to release renin.
3) renin turns angiotensinogen to angiotensin I
4) angiotensin converting enzyme turns Angiotensin I to Angiotensin II

101
Q

What does angiotensin II do

A
  1. it causes vasoconstriction = increase in TPR (increases BP)
  2. it stimulates the adrenal cortex to secrete aldosterone (holds sodium in blood, which because of osmotic pressure holds more water in blood) = increase in BP
    2.
102
Q

How does aldosterone increase Na in blood

A

it opens up the Na/K channels on the luminal membrane. so more Na is resorbed in the kidney

103
Q

What are the 4 ways that angiotensin II affects blood pressure

A
  1. Vasoconstriction of the systemic arterioles
  2. increase aldosterone in the adrenal cortex
  3. increase in ADH secretion from post. pituitary
  4. increase in thirst stimulation
104
Q

Why does the body need to modify urine concentration

A

because if you drank a lot of water and it didn’t modify concentration, then it would throw off plasma volume, blood pressure

105
Q

what are the steps involved in concentrating urine

A
  1. long loops of henle establish osmotic gradient
    (greater from cortex to medulla)
  2. Preservation of the gradient by vasa recta
  3. gradient dependent water absorption through the collecting ducts
106
Q

How is the osmotic gradient established

A

by countercurrent multiplication

107
Q

how does permiability of the loops of henle change

A

descending limb is permeable to water, not NaCl

Ascending limb is permeable to NaCl, not water

108
Q

what happens to water and Na concentration through the tubes

A

descending limb water leaves and the solute becomes more concentrated. then as it goes up the ascending limb the water can’t enter but the Na leaves until it gets low.

109
Q

What is the affect of ADH on urine concentration

A

it makes the collecting tubule permiable to water

110
Q

what happens to ADH during de hydration and too much water

A

dehydration stimulates ADH to be released, which causes water to leave the collecting tubule and urine to be very concentrated
too much water blocks ADH release so that water can’t leave collecting duct and the urine is very dilute

111
Q

what is vasopressin

A

ADH

112
Q

Where is ADH from

A

posterior pituitary

113
Q

What is aquaporin

A

they are water channels that are opened up by ADH

114
Q

What is micturition

A

urination/ emptying the bladder

115
Q

how is micturition controlled

A
  1. too much pee = walls expanding = sets off stretch receptors
  2. that leads to cause the opening of the internal urethral sphincter
    parasympathetic = contraction of detruser
    sympathetic = relaxation of internal sphincter
  3. then we control the external urethral sphincter
116
Q

What digestive processes happen in the mouth

A

Motility

Saliva Secretion

117
Q

What is motility in the mouth

A

chewing on food that breaks it down

118
Q

what are the functions of the saliva

A
moisten and lubricate the food
salivary amylase starts to break down starch
antibacterial action
solvent to allow for taste
buffers acid
119
Q

does any absorption take place in the mouth

A

no, except for some drugs

120
Q

what is the motility in the stomach

A

stores food, the contraction of smooth muscle mixes and grinds the food into chyme

121
Q

what is secreted in the stomach

A
mucus
pepsinogen
HCL
intrinsic factor
gastrin 
somatosatin
histamine
122
Q

What is the digestion that takes place in the stomache

A

salivary amylase continues to break down starch

pepsinogen breaks down proteins

123
Q

What is the absorption that takes place in the stomach

A

none, except some drugs

124
Q

how is gastric emptying regulated

A
  1. Stretching leads to increased gastric contractivity
  2. the fluidity of gastric contents become greater
  3. fat in the duodenum is the most potent inhibitor of gastric emptying
  4. acid in the duodenum, it has to be neutralized before it can empty more in
  5. Hypertonicity in the duodenum
  6. emotion and pain
  7. distention of duodenum inhibits motility
125
Q

what is the most potent inhibitor of gastric emptying

A

fat in the duodenum

126
Q

what do parietal cells do

A

Secrete HCL and intrinsic factor

127
Q

what do Chief cells do

A

secrete pepsinogen

128
Q

what is the function of HCL in the stomach

A

activates pepsinogen
breaks down connective tissue and food particles
denatures proteins
kills microorganisms

129
Q

what is the function of intrinsic factor

A

important in vitamin b12 absorption

130
Q

what is the function of pepsinogen

A

it is cleaved to pepsin by HCL
pepsin then cleaves more pepsinogen
breaks proteins down into peptide fragments

131
Q

What is the motility of the small intestine

A

segmentation = mixes and propels chyme

migrating motility complex = cleans between meals

132
Q

What is the secretion of the small intestine

A

juice of the intestine protects and lubricates intestine and water (needed by hydrolysis)
no digestive enzymes

133
Q

What is the digestion of the small intestine

A

major site of digestion

accompanied by pancreatic digestive enzymes, secretions, bile and brush border

134
Q

What is the absorption of the small intestine

A

the site of food absorption

135
Q

What does the pancrease secrete

A
  1. bicarbonate
  2. proteolytic enzymes
  3. pancreatic amylase
  4. pancreatic lypase
136
Q

what is the function of bicarbonate

A

neutralizes acidic chyme because:
acid inhibits pancreatic enzyme activity
protects the small intestine from damage

137
Q

what is the function of the proteoltic enzymes

A

they are secreted inactive, then converted to active forms by enterokinase and trypsin (trypsin is a converted proteolytic enzyme that goes and converts the others)

138
Q

what are the functions of pancreatic amylase

A

break down polysaccharides into maltose

139
Q

what is the function of pancreatic lipase

A

breaks down triglycerides into monoglycerides

140
Q

What happens when acid is in the duodenum

A

secretin is released from the duodenum which leads to release of bicarbonate, which neutralizes it

141
Q

What happens when there is fat in the doudenum

A

CCK is released from the duodenal mucosa, which causes the release of pancreatic enzymes which digest the fat

142
Q

what is the function of bile

A
  • excretion of bilirubin

- emulsification of fat (breaks down the fat globs)

143
Q

where is bile from

A

continuously made in the liver and stored in the gall bladder

144
Q

how is the hormonal release of bile controlled

A

Fat stimulates the secretion of CCK

CCK stimulates bile to be released from the GB

145
Q

what is the brush border

A

folds, villi, microvili all increase the surface area for absorption. but the brushborder is specifically made by the microvilli

146
Q

what does the brush border have in it

A

enterokinase, maltase, sucrase, lactase, aminopeptidases

147
Q

how is the digestion of carbs done (whole process)

A

Starches - polysaccharides in mouth
polysaccharides - disaccharides in doudenum
dissaccharides - monosaccharides on brush border

148
Q

Monosach absorption

A

(secondary active transport) into cell, facilitated diffusion into blood

149
Q

How are proteins digested (whole process)

A

broken down by pepsin and pancreatic enzymes into small amino acid chains
then broken down into individual amino acids by brush border and absorbed

150
Q

how are fats absorbed

A

monoglycerides are paired up with free fatty acids in the brush border cell, then they are exocytosed into the lymph

151
Q

what is the motility in the large intestine

A

haustral contractions mix feces, and mass movements propel the feces long distances

152
Q

what stimulates mass movements

A

the gastrocolic reflex, food entering the stomach

153
Q

what are the secretions of the large intestine

A

alkaline mucus that lubricates and facilitates the passage of feces, sodium bicarbonate neutralizes acid from bacteria

154
Q

What is the digestion of the large intestine

A

none

155
Q

what is the absorption of the large intestine

A

salt and water

156
Q

how does the defication reflex go

A

feces enters rectum and stretches it
that initiates defication reflex
internal anal sphincter relaxes, and muscle of rectum and sigmoid colon contract.
external anal sphincter is voluntarily controlled, when it opens we have defication

157
Q

what are the 3 main types of chemical messagers

A

autocrine/paracrine
neurotransmitters
hormones

158
Q

what is a paracrine/autocrine

A

messanger to its own cell, or to a neighbor cell

159
Q

What is a neurotransmitter

A

released from a neuron

160
Q

what is a hormone

A

released from endocrine glands into the blood
long distance signal
carried by blood to target cells where they regulate cell functions

161
Q

what are the three categories of hormones

A
  1. peptide hormone (most common)
  2. Amino acids, or modified amino acids
  3. steroids
162
Q

what are some peptide hormones

A

pituitary hormones
angiotensin
insulin
glucagon

163
Q

What are some amino acid hormones

A

epinephrine, thyroid hormones

164
Q

what are some steroid hormones

A

aldosterone, estradiol

165
Q

how are hormones transported

A

peptide - usually just in the blood

steroid and thyroid hormones - bound by a carrier protein

166
Q

how do steroid and thyroid hormones work

A

they bind nuclear receptors and those bind DNA, this causes altered protein expression which makes the desired response

167
Q

how do peptide and catecholamines work

A

they bind to cell surface receptors, these then send signals which activate and deactivate all sorts of things (enzymes, channels)

168
Q

What hormones are released from the posterior pituitary

A

vasopressin

oxytocin

169
Q

tell me about vasopressin

A

it is synthsized in the hypotalamus
secreted from the posterior pituitary
osmoreceptors stimulate its release
inhibited by blood vessel strech receptors

170
Q

what are the functions of vasopressin

A

vasoconstriction

increases water reapsorption

171
Q

What stimulates oxytocin release

A

mechanoreceptors at nipple and cervix
infants cry
stress inhibits

172
Q

what does oxytocin do

A

stimulates the contraction of the uterus during childbirth

stimulates milk ejection

173
Q

what hormones come from the hypothalamus

A
PRH
PIH
TRH
CRH
GHRH
GHIH
GNRH
174
Q

what do the hormones from the hypothalamus do

A

they stimulate or inhibit the release of the hormones from the anterior pituitary

175
Q

What are the hormones of the ANterior pituitary

A
prolactin
TSH
ACTH
GH
LH 
FSH
176
Q

Where is growth hormone from

A

the anterior pituitary

177
Q

what does GH target and what does it do there

A

targets most tissues
promotes protein synthesis and growth
promotes lipolysis
promotes increase of blood glucose

178
Q

how does GH work

A

it causes cell to differentiate and the liver to secrete IGF1

179
Q

What is dwarfism

A

hyposecretion of GH
small weak muscle
increased subcutaneous fat

180
Q

What is gigantism

A

hypersecretion of GH before growth plates close

181
Q

what is acromegaly

A

hyper secretion of GH after growth plates have closed

182
Q

What is TSH

A

its a hormone from the Ant pit

stimulates the secretion of thyroid hormones, and the growth of the thyroid

183
Q

How is TSH controlled

A

Stimulated by TRH and inhibited by thyroid hormones

184
Q

T4 vs t3

A

most of the thyroid hormone released is T4, but most in then converted to T3 because it’s more active

185
Q

what do t3/t4 do

A

increase metabolic rate and heat production

stimulates protein synthesis and growth

186
Q

t4 participates in negative feed back

A

yep

187
Q

what is hypothyroidism

A

thyroid gland failure due to no TRH or TSH, or iodine deficiency

188
Q

what is cretinism

A

hypothyroidism

low metabolic rate = growth and mental retardation, hypothermia

189
Q

What is Myxedema

A

hypothyroidism in adults
puffy eyes
low BMR
dry rough skin

190
Q

what happens with low iodine

A

endemic goiter because no T4 is made but TSH still tells the thyroid to grow, T4 can’t stop it

191
Q

What is hyperthyroidism

A

Excess TSH or TRH

causes a thyroid tumor

192
Q

what is graves disease

A
hyperthyroidism
TSI bind to TSH sites
goiter
bulging eyes
muscle weakness