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P215 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

Components of Renal System

A

kidneys, ureters, urinary bladder, urethra

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2
Q

Function of Renal System

A
  1. regulation of ECF volume (BP by maintaining blood volume)
  2. regulation of electrolytes (electropotentials)
  3. regulation of waste products (picking and choosing which waste products are kept)
  4. regulation of blood pH
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3
Q

Renal Cortex

A

outer kidney layer

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4
Q

Renal Medulla

A

inner kidney layer

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5
Q

Minor Calyx

A

urine begins here

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6
Q

Major Calyz

A

…

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7
Q

Renal Pelvis

A

…

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8
Q

Ureter

A

smooth muscle, contracts to squeeze fluid down to bladder

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9
Q

How many nephron are in a kidney?

A

1 million

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10
Q

Afferent Arteriole

A

towards the capillary bed (glomerulus)

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11
Q

Glomerulus

A

network of capillaries, transition point

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12
Q

Glomerular Capsule

A

cannot secrete anything

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13
Q

Efferent Arteriole

A

away from glomerulus

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14
Q

PCT

A

300 mOsm, in cortex

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15
Q

Descending Limb of the Loop of Henle

A

into medulla

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16
Q

DCT

A

secretion for final balance, in cortex

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17
Q

Collecting Duct

A

medulla, make chemical changes to fluid

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18
Q

Peritubular Capillaries

A

surrounds nephron, can go around collecting duct

  • arteriole -> capillary bed -> arteriole -> capillary bed -> venule
  • *can change resistance via precapillary sphincters
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19
Q

Filtration

A

movement of H2O out of the capillary

**passive

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20
Q

Filtration Mechanism

A

60 mmHg = increase in filtration (arteriole)
more pores = increase movement
**no formed elements can cross

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21
Q

Ascending Limb of the Loop of Henle

A

up into the cortex

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22
Q

Filtration Result

A

lots of small particles through fast

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23
Q

Glomerular Filtration Rate (GFR)

A

total volume of fluid filtered from the plasma per minute (in the kidneys)

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24
Q

How much of plasma that enters the glomerulus is filtered into the nephron tubules?

A

20%
= 4 oz of filtrate produced / minute
= 45 G (180 L) / day

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25
Q

Autoregulation of GFR

A

intrinsic in the nephron, triggered by changes in systemic BP

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26
Q

Goal of GFR

A

keep filtration rate constant b/c of fast filtration

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27
Q

What would happen to GFR if Arterial BLood Pressure rises and no corrections (autoregulations) are made

A

increase BP = increase glomerular pressure = increase filtration rate (increase GFR)
more likely to lose things that should’ve been reabsorbed (glucose, electrolytes)

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28
Q

How will GFR be controlled instrinsically (Autoregulated) if BP Lowers?

A
  • precapillary sphincters will dilate to regulate pressure of capillaries
  • afferent: vasoconstrict to resist high BP (90% of autoregulation)
  • efferent: vasodilate to allow pressure out of capillary faster
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29
Q

Reabsorption

A

ISF -> capillaries

filtered fluids -> capillary

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30
Q

Reabsorption Regulation

A

peritubular capillaries -> body

-membrane transports

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31
Q

Reabsorption Result

A

absorbing from filtrate -> bloodstream through peritubular capillaries -> body

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32
Q

Secretion

A

capillary -> nephron

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33
Q

Secretion Mechanism

A
  • peritubular capillaries
  • active
  • get rid of something
  • reabsorb too much = need to secrete some out
  • balance electrolytes
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34
Q

Filtration of Glucose

A

small amount in the bloodstream, 20% entered in glomerular capsule

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35
Q

Glucose Reabsorption

A

where- PCT
how- secondary coactive transport (sodium)
why- want to keep energy source

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36
Q

Glucose Secretion

A

NONE

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37
Q

Final net result of glucose regulation

A

100% reabsorbed via secondary coactive transport

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38
Q

Why is glycosuria (glucose in urine) observed in untreated diabetes mellitus?

A
  • glucose staying in bloodstream and not in the cells
  • saturation of secondary coactive transport export channels (some glucose doesn’t get reabsorbed)
  • glucose > transporters
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39
Q

Where is K found in highest conc. and what role does it play?

A
  • intracellular fluid

- repolarization

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40
Q

how will GFR be controlled intrinsically (autoregulated) if BP lowers?

A
  • afferent: vasodilate to allow more pressure to enter
  • efferent: vasoconstrict to keep pressure in capillary longer
  • *more effective @ higher pressures
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41
Q

What would happen if high [K+] was found in extracellular fluid?

A

-electrical dysfunction in the heart (arrhythmia, heart attack)

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42
Q

K Filtration

A

small amount in bloodstream, 20% filtrated

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43
Q

K Reabsorption

A

where- PCT
how- Na/K primary active transport
why- because transporters are there

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44
Q

K Secretion

A

could reabsorb too much K, needs to maintain final and low balance

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45
Q

Final net result of K Regulation

A

reabsorption in PCT, secretion in DCT

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46
Q

Filtration of water and Na

A

lots in bloodstream, 20% filtered

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47
Q

Reabsorption of Na and H20 in PCT

A

how- move Na+ (via secondary active transport with glucose) first, which moves H20 via aquaporins
net result- 65% Na and H20 reabsorbed
**PCT reabsorption is always constant

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48
Q

IF water is allowed to freely follow sodium, then what is happening to the osmotic gradient between the tubular fluid and the blood plasma?

A

no change in gradient in PCT

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49
Q

Net result of Na and H20 in the loop of henle

A

reabsorb 27% of H20 and Na in the loop and the vertical conc. gradient is created

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50
Q

Reabsorption of Na and H20 in DCT

A
  • final 7-8% of Na is reabsorbed here
    ^related to the intake and aldosterone levels
    -Na is NOT secreted
    -H20 is not affected (much)
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51
Q

Effect of Dietary Sodium on Reabsorption

A

-body only wants to reabsorb our Na, not dietary
-reabsorption rate = amount absorbed / amount filtered (both body Na and dietary Na)
**1,500 g / day are filtered
7,500 g of total Na in body

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52
Q

NEt result of Na reabsorption in DCT

A

> 99% is reabsorbed

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53
Q

H20 reabsorption in the collecting duct

A

-adjusted here
-final 5-7% of H20 is reabsorbed here
^related to ADH levels and intake
**H20 is NOT secreted
-Na is not effected

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54
Q

Without ADH in the Collecting Duct

A

no more H20 is reabsorbed = very dilute urine (3-4G)

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55
Q

With ADH in Collecting Duct

A

aquaporins are inserted

= very concentrated urine, low quantity

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56
Q

Net result of water reabsorption in the collecting duct

A

97-99% o H20 is reabsorbed

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57
Q

Role of DCT in acid/base

A

-secretion of H+
-reabsorption of HCO3-
balancing keeps blood @ 7.4 pH

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58
Q

Metabolic Acidosis

A

< 7.35
increase acid production in the body (cancer)
decrease H+ secretion
**not related to the lungs

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59
Q

Metabolic Alkalosis

A 
> 7.45 pH
increase base production in the body (tumor in pancreas)
-increase H+ loss (vomitting)
too much HCO3- reabsorption
**not related to the lungs
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60
Q

Hormones play an important role in the regulation of __ by monitoring 3 major fluid characteristics

A

ECF volume

  1. ISF osmolarity (@ hypothalamus via mechanoreceptors)
  2. blood volume
  3. plasma Na concentration
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61
Q

ADH

A

-released when blood volume is low and ISF osmolarity is high (dehydration)

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62
Q

ADH Mechanism

A
  • use baroreceptors to signal hypothalamus

- osmoreceptors (in hypothalamus) -> posterior pituitary -> kidneys

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63
Q

ADH Effect

A

receptors on collecting duct bind to ADH and increase water reabsorption

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64
Q

Symptoms / Treatments of Diabetes Insipidus

A
  • large amount of dilute urine
  • take ADH / ADH agonist
  • drink LOTS of water
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65
Q

Symtpoms / Treatments of Syndrome of Inappropriate ADH (SIADH)

A
  • swelling, edema
  • small, concentrated urine output
  • increase BP
  • hyponatremia (low Na+)
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66
Q

Aldosterone

A

indirectly released when plasma Na+ is low

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67
Q

Juxtaglomerular Appartus (JGA)

A

where the afferent arteriole contacts the DCT

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68
Q

Mascula Densa

A

in JGA, senses plasma Na+

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69
Q

Granular Cells

A

secrete Renin if Na+ is low

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70
Q

Mechanism of Aldosterone Secretion

A
  1. mascula densa senses plasma Na+
  2. granular cells secrete Renin if Na+ is low
  3. renin converts angiotensinogen -> angiotensin 1
  4. angiotensin 1 -> angiotensin 2 by angiotensin converting enzyme (ACE)
  5. angiotensin 2 stimulates secretion of aldosterone from adrenal cortex
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71
Q

Effects of Aldosterone Secretion

A
  • 92% of Na+ is reabsorbed BEFORE DCT
  • remaining Na+ is reabsorbed in the DCT to meet the body’s needs
  • w/out aldosterone, another 7% of Na+ is reabsorbed
  • if aldosterone levels are too high, ALL 8% of remaining Na+ is reabsorbed
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72
Q

Urine Transport

A

filtrate -> minor calyx -> major calyx -> renal pelvis -> ureters

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73
Q

Ureters

A

conduct urine from kidneys -> bladder

-utilize peristaltic contraction

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74
Q

Bladders

A
  • storage of urine (1-2 L a day)

- distensible organ w/ smooth muscle walls

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75
Q

Urethra

A

conveys urine to outside

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76
Q

Sphincters

A
  • contraction prevents urine flow, relaxation allows urine flow
    internal: smooth muscle, involuntary
    external: skeletal muscle, voluntary
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77
Q

Micturition (Urination)

A
  1. distension of bladder w/ urine
  2. stimulates bladders stretch receptors
  3. sensory input to spinal cord
  4. autonomic motor control- reflex contraction of bladder smooth muscle and relaxation of internal sphincter
  5. voluntary relaxation of external sphincter
  6. urine flows and contents of bladder lost from the body
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78
Q

Main role of Respiratory System

A
  1. supply oxygen for oxidative phosphorylation

2. eliminate CO2 (biproduct of pyruvate catabolism and CAC)

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79
Q

Conducting Zone

A

anatomical “dead space”
-no gas exchange, just tubing
roles- warms and humidifies air, uses mucus and cilia to trap pathogens

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80
Q

REspiratory Zone

A

site of gas exchange

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81
Q

REspiratory Bronchioles

A

1st site of gas exchange

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82
Q

Type 1 Alveolar Cells

A

gas exchange

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83
Q

Type 2 Alveolar Cells

A

regulate Na+ and H20

-secrete surfacant to break surface tensions

84
Q

How much is a normal resting breath?

A

500 mL

85
Q

Thoracic Cavity

A

control volume

change in thoracic cavity = change of pressure in lungs

86
Q

Diaphragm

A
  • contracts down and away from thoracic cavity = increase thoracic cavity volume
  • relax = dome up
87
Q

Intercostal Muscles

A

pull ribs outwards = increase volume

88
Q

Pectoralis Minor

A

increase volume = inspiratory

89
Q

Abdominal Muscles in Lungs

A

pull ribcage down = decrease volume = respiratory

90
Q

Scalenes and Sternocleiomastoid

A

pull away from diaphram = increase volume = inspiratory

91
Q

External Respiration

A

ventilation - moving air into/ out of lungs

gas exchange - moving O2/CO2 across capillaries

92
Q

Internal Respiration

A

cellular breathing

  • use of oxygen
  • production of CO2
  • goal = make ATP
93
Q

Intrapulmonary Pressure

A

within lungs, pressure INSIDE of lungs

  • should follow thoracic cavity pressure changes
  • always smaller than all other pressures
94
Q

Air Pressure Gradients

A

air from high -> low

need gradient!

95
Q

Boyle’s Law

A

increase volume = decrease pressure

96
Q

Mechanics of Inspiration @ Rest (Active)

A

goal - move air into lungs
needs- decrease pressure in thoracic cavity relative to atmospheric pressure (3 mmHg)
mechanics- use diaphram to contract = increase thoracic cavity volume = decrease pressure = gradient

97
Q

Mechanics of Expiration @ Rest (Passive)

A

goal- move air out
needs- increase thoracic cavity pressure
mechanics- relax diaphram = decrease thoracic volume = increase pressure = gradient

98
Q

How does the mechanics of expiration and inspiration change during exercise?

A

increase CO2 = decrease pH = increase breathing rate
want to increase gradient
-start using ALL muscles

99
Q

Intrapleural Pressure

A

goal - prevent lung collapse
needs- pin lungs to thoracic cavity lung
mechanics - 2 thin membranes and H20

100
Q

Parietal Pleura

A

thin membrane lining ribcage

101
Q

Visceral Pleura

A

thin membrane surrounding lungs

102
Q

Intrapleural Space

A
  • space b/w parietal and visceral pleura
  • filled with H20
  • *we want surface tension!
103
Q

WHat would happen to intrapleural pressure if something punctures the pleura

A

break surface tension = lung collapse

-lose pressure

104
Q

Pneumothorax

A

damage to a pleura

  • lung effected collapses
  • lung not punctured is uneffected
  • ribs bounce out of punctured side
105
Q

Pulmonary Compliance

A

how easy it is to expand the lung

= change of volume (lung) / change of pressure (thoracic)

106
Q

Elasticity

A

elastic force due to elastin fibers

  • not contributing to exhalation
  • return of lung to neutral size
  • elastic tension increases during inspiration and decreases during expiration
107
Q

Surface Tension

A

attraction of polar molecules (H20 to one another)

  • alveoli and bronchioles are lined by a thin film of H20
  • surface tension creates a “collapsing force”
  • if surface tension is too strong, alveoli will collapse
  • increase surface tension = decrease compliance = decrease gas exchange
108
Q

Pulmonary Surfacant

A

phospholipid detergent

  • secreted by type 2 alveoli during deep inhalation
  • breaks up surface tension in alveolis (NOT intrapleural space)
  • helps prevent alveolar collapse
109
Q

What happens if pathogens pass the conducting zone and reach alveoli

A

high replication rate, destroy lung tissue -> inflammation

110
Q

Why is inflammation bad in the lungs?

A

water is drawn b/c of osmotic gradient = increase surface tension = decrease compliance = decrease gas exchange

111
Q

If gas exchange and compliance decrease, what must happen?

A

breath more air in via accessory muscles

112
Q

If muscle activity increases, what happens to O2 demand in those cells?

A

increase O2 demand by breathing deeper = increase muscle action = increase O2 = more breathing

113
Q

WHy is pneumonia fatal

A

can’t keep up with O2 demand, wear muscles out

- can’t get enough CO2 out = respiratory acidosis

114
Q

Pressure

A

comes from gas molecules “pushing” against a container wall

115
Q

Partial Pressure

A

force generated by a single gas w/in a mix of gas

= % gas * atmospheric pressure

116
Q

Dalton’s Law

A

P (total) = P (A) + P (B)

117
Q

Effect on the Conducting Zone on inspired Air

A
  • atmospheric air has high O2 conc. and low CO2 conc.

- levels change a lot as air is inspired due to “stale air” mixing (CO2)

118
Q

Air entering lungs from outside air

A

Po2- 160

PCO2 - .3

119
Q

PO2 and PVO2 conducting zone levels

A

PO2- 105
PCO2- 40
due to mixing w/ stale air and adding water vapor

120
Q

PO2 and PCO2 Values in the Pulmonary Artery

A

PO2- 40
PCO2- 46
due to cellular respiration
**anything that changes metabolic rate changes these

121
Q

PO2 and PCO2 levels in Alveolar Capillaries

A

PO2- 100

PCO2- 40

122
Q

PO2 and PCO2 levels entering a Venule

A

PO2- 40

PCO2- 46

123
Q

PO2 and PCO2 levels entering capillaries

A 
PO2- 100
PCO2- 40
**hyperventilation = increase CO2 output
emphysema = not enough oxygen in and CO2 out
blood doping- increases O2 value
anemia- decreases O2 value
124
Q

Is it physically more difficult to ventilate the lungs at higher altitudes

A

no- only takes muscles to ventilate the lung

125
Q

What effect does hgih altitude have on breathing

A

decrease pressure = decrease O2 levels = decrease conc gradient
**denver, mount everest

126
Q

How is deep water diving breathing different than breathing at high altitude?

A

-increase depth = increase pressure

@ 10 m underwater, P ATM = 1520 mmHg

127
Q

Effects of depth on blood gases

A
  • nitrogen is dissolved from the sea -> body

- acts as a depressant (alcohol)

128
Q

Nitrogen Narcosis

A

“martini effect”

  • want to replace nitrogen w/ Helium b/c it does not dissolve when compressed
  • caused by descending deep under water
129
Q

Decompression Sickness

A

“bends / Caisson” disease

  • nitrogen bubbles out of the blood stream are too large and forming too rapidly
  • caused by a rapid ascent from depth
  • symptoms: joint pain, skin irritation, headache/dizziness, seizure, embolism, paralysis
130
Q

Bohr Effect

A

H2O + CO2 -> H2CO3 -> H + HCO3-

**respiration is adjusted to keep pace with metabolic rate

131
Q

REspiratory Acidosis

A

pH < 7.35

  • hypoventilation (symptom of concussion)
  • *respiratory gives quick changes, renal gives long term change
132
Q

Respiratory Alkalosis

A

pH> 7.45

  • hyperventilation
  • *respiratory gives quick changes, renal gives long term change
133
Q

Chemoreceptors in REspiratory System

A

detect changes in pH and PO2 (indirectly) in the blood

134
Q

Central Chemoreceptors

A
  • located in medulla oblongata
  • monitor pH of cerebral spinal fluid
  • have the STRONGEST effect on breathing rate
135
Q

Peripheral CHemoreceptors

A
  • in aortic arch and carotid artery
  • sense pH and PO2 levels in the blood
  • send feedback to the medulla oblongata
136
Q

Why sin’t PO2 and important contributor to control respiration

A

-oxygen levels do not change pH
-CO2 is coming from OUR metabolic processes
-PO2 changes lots but it still gives us 60 mmHg
-decrease blood PO2 ONLY increase chemoreceptor sensitivity to PCO2
^arterial blood PO2 must fall 50% before this effect occurs

137
Q

Medulla OBlongata

A

site of rhythmicity center (like SA node)

  • inspiratory- cause contraction of diaphram (can modulate depth)
  • expiration- inhibit inspiratory
138
Q

Pons

A

help modulate breathing rate, results in change of pH

139
Q

Apneustic Center

A

modulates depth of breathing

140
Q

Cerebral Cortex

A

breathing is “semi voluntary”

  • frontal lobe can send voluntary commands to respiratory muscles
  • overrides the rhythmicity center
141
Q

Tidal Volume (TV)

A

volume of air entering or leaving lungs during one breath

142
Q

Residual Volume (RV)

A

amount of air remaining in the lungs after max expiration

-need some for intrapleural pressure

143
Q

Vital Capacity (VC)

A

max amount of air that can be exhaled after max inspiration

= IRV + TV + ERV

144
Q

Minute Ventilation (VE)

A

= TV * respiratory rate

  • how much air can get into/out of the lungs in a minute
  • air moved thru entire respiratory system
145
Q

Alveolar Minute VEntilation (VA)

A

(TV - dead space) * respiratory rate

-how much air gets down to alveoli for gas exchange

146
Q

Forced Expiratory Volume in 1 Second (FEV1)

A

amount of air that can be exhaled rapidly

147
Q

Relative FEV1

A

= FEV1 / VC
-similar to ejection fraction
70-80% is normal

148
Q

Restrictive Disorders

A

leads to inspiratory difficulty
-decrease vital capacity
pulmonary fibrosis, pregnancy, pneumonia

149
Q

Obstructive Disorders

A

leads to expiratory difficulty
-decrease FEV1
asthma, bronchitis, emphysema

150
Q

What part of respiratory system is affected with asthma

A

conducting zone- decrease airflow due to resistance

151
Q

Sympathetic of Respiratory System

A

bronchodilation and inhibits mucous production ( via B2)

152
Q

Parasympathetic of Respiratory System

A

bronchoconstriction and stimulates mucous production (via muscarinic (odd #s) receptors)

153
Q

Why does a B2 adrengeric agonist make it easier to breathe after a few seconds?

A

relaxes the receptors for a sympathetic response

154
Q

Main functions of digestive system

A
  1. motility through muscle contractions
  2. secretion of enzymes, signals
  3. digestion -> enzymes breaking up macromolecules
  4. absorption of nutrients
155
Q

3 Phases of digestion

A
  1. cephalic- when you’re hungry, sympathetic vs. parasympathetic via CNS, chewing, swallowing, **hunger regulation
  2. gastric- stomach (holding center)
  3. intestinal- small and large
156
Q

Feed Forward

A

chemical signal (hormone/NT) that is sent to an upcoming part of the tract

  • secretions are ready
  • preparation
157
Q

Feed back

A

sends a stop signal backward in tract so a previous part (section) responds
-shut down

158
Q

Ghrelin SEcretion

A
  • secreted from lining of stomach
  • as stomach stretches, ghrelin signals stop
  • ghrelin receptors in hypothalamus sense ghrelin levels in stomach (more ghrelin = hungry)
  • *feed forward
159
Q

Extrinsic (Autonomic Control) of digestive system

A
  • parasympathetic: rest and digest
  • sympathetic: cessation of GI tract activity
  • longitudinal muscle: “pushing” muscle
  • myenteric and submucosal plexus: “squeezing” muscle
160
Q

Intrinsic Control of digestive system - ENS

A

-mechanism: sensory and motor neurons (where the food is via stretches)
-stretch receptors -> smooth muscle activity
role: establishes AUTOMATIC GI motility
=perastalsis is controlled by ENS via chemical signals

161
Q

Mechanical breakdown in mouth

A

teeth, not digestion

162
Q

Secretion in mouth

A
  • salivary amylase (7 pH) to digest carbs

- lingual lipase @ low pH in adults to digest lipids

163
Q

Carb digestion in mouth

A

digestion begins in mouth

164
Q

Proteins and lipids digestion in mouth

A

no digestion occurs in mouth

165
Q

Absorption in mouth

A

none

166
Q

Motility in the mouth

A

tongue moves food to pharynx

167
Q

Esophagus

A

neutral pH, connects mouth to stomach

  • peristalsis assisted by gravity (usually)
  • lower esophageal sphincter (LES): always tightly closed until food is present
168
Q

Heartburn (GERD)

A
  • symptoms: chest pain, burning sensation in sternum, nausea, vomiting, increase of salvation
  • cause: LES is not constantly closed when food is in the stomach
  • treatments: pills that neutralize acid, reduce acid production/kill proton pumps which leads to pathogens entering the body
169
Q

Stomach

A
  • distensible pouch b/w esophagus and SI, enclosed by LES and pyloric sphincter
  • stomach wall: rugae to shear food apart, gastric glands
170
Q

Mucous

A

protect stomach lining

171
Q

Pepsinogen

A
  • from chief cells

- converted to pepsin @ low pH to digest proteins

172
Q

HCl

A
  • from parietal cells
  • denature proteins
  • activate enzymes
173
Q

Gastrin

A
  • stimulates parietal cells -> HCl
  • stimulates chief cells -> pepsinogen
  • *not feed forward / backward
174
Q

Histamine

A
  • stimulates parietal cells

- increase by spicy foods

175
Q

Carb digestion in stomach

A

none, no enzyme to do so because it was denatured

176
Q

Protein digestion ins tomach

A

partially digested by pepsin

177
Q

Lipid digestion in stomach

A

-lingual lipase (from mouth) is activated by low pH

10-30% of fat digestion is due to lingual lipase “pooling” in the stomach from the mouth

178
Q

Absorption in the stomach

A
  • carbs, proteins, and fats are not absorbed

- water, alcohol, and aspirin are absorbed

179
Q

Motility in the stomach

A
  • storage: holds food until digestion proceeds and intestines ready to receive it
  • mixing: waves of contraction churn food w/ HCl, lingual lipase, and pepsin
  • gastric emptying: squirts liquefied food into the SI
180
Q

Peptic Ulcers

A

commonly found in duodenum

  • symptoms: pain, vomiting, blood in vomit and stool
  • causes: H. pylori, ibuprofen, alcohol, stress (lowers immune system)
  • treatments: antibiotics, antacid to stop proton pumps
181
Q

How does H. Pylori survive in the stomach?

A

lives in mucus layer, creates an individual bicarb layer

182
Q

Structure of SI Walls

A
  • plicae circulares
  • villi
  • microvilli (largest factor of increase of surface area for a better chance of absorption)
183
Q

Brush Border Enzymes

A
  • microvilli

- some SI enzymes are tethered to the microvilli

184
Q

CCK

A
  • responds to protein and fats
  • stimulates gall bladder and endocrine pancreas
  • inhibits stomach motility (via feedback)
185
Q

Secretin

A
  • responds to H in the duodenum
  • stimulates pancreas to release bicarb
  • inhibits parietal cells (feedback)
186
Q

Gastic Inhibitory Peptide (GIP)

A
  • stimulates the release of insulin (feed forward)

- inhibits parietal cells (feedback)

187
Q

Liver

A

produces and secretes bile

188
Q

Bile

A
  • goes down common bile duct
  • fat is nonpolar and forms fat droplets
  • bile increases SA for fat digestion by breaking down fat droplets into micelles
  • this increases SA for lipases to digest fat
  • *not digesting fat
189
Q

Gall Bladder

A
  • stores and concentrates bile

- ejects bile in response to CCK

190
Q

Bicarb Ions

A

part of “pancreatic juice” from pancreas
-released by secretin
pH of 8

191
Q

Pancreatic Amylase

A

part of “pancreatic juice” from pancreas

-digests carbs

192
Q

TRypsin

A

part of “pancreatic juice” from pancreas

  • digests proteins
  • takes over for pepsin
193
Q

PAncreatic Lipase

A

part of “pancreatic juice” from pancreas

-digests fats

194
Q

Digestion in small intenstine

A

carbs -> monosaccharides
proteins -> amino acids
lipids -> monoglycerides and fatty acids
(increases diffusion rates of lipids across membranes)

195
Q

Peristalsis in SI

A
  • weak and slow

- stretch receptors are not being activated because it’s all liquid in the SI

196
Q

Segmentation

A
  • circular muscles squashing down on liquid

- main contractile activity in SI

197
Q

Absorption of monosaccharides and AAs in the SI

A

-absorbed by secondary coactive transport with Na

198
Q

ABsorption of lipids in SI

A
  • packages fats into chylomicrons

- chylomicrons are absorbed into the lymphatic system thru lacteals

199
Q

Lactose intolerance causes

A

-decrease in secretion of lactase

200
Q

Cause of symptoms in lactose intolerance

A
  • bloating and gas: bacteria digest lactose in the LI and produce gas
  • cramps: gas builds up, stretched GI tract, stretch receptors are signaled, and peristalsis begins
  • diarrhea: lactose attracts water
201
Q

how is lactose intolerance different than an allergy to milk?

A

allergy: allergic to an antigen on a milk protein (immune system)

202
Q

Why do only some people have a lactose intolerance?

A
  • hereditary

- geographical

203
Q

Secretion and digestion in LI

A
  • secretion: mucus and sometimes water

- digestion: little by remaining enzymes, most by bacteria

204
Q

FIber

A
  • soluble: dissolves in water (fruit), partially digested by bacteria, bacteria make vitamin K and folic acid
  • insoluble: remains mostly undigested, osmotically active = water drawn to it
205
Q

Absorption in LI

A
  • NO absorption of carbs, fat, or protein
  • mostly water and electrolytes
  • vitamin K and folic acid
206
Q

LI structure of walls

A

No Villi

207
Q

Quizlet

A

https://quizlet.com/136185598/iu-p215-physiology-exam-4-respiratory-physiology-flash-cards/

P215 (3 decks)

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