Exam #4_Semester 2 Flashcards

1
Q

partial pressure - definition

A

amount of pressure that a gas exerts in a mix of other gases

  • fraction of barometric pressure
  • only gases that are in solution (not bound)
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2
Q

partial pressure - key values

A
Pb = 760mmHg (sea level)
PH20 = 47mmHg (constant)
PIO2 = 150
PICO2 = 0
PAO2 = 102
PACO2 = 40
PaO2 = 40 (pulm art)
PaCO2 = 46 (pulm art)
PvO2 = 102 / 95 (pulm vein)
PvCO2 = 40 (pulm vein)
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3
Q

respiratory quotient (R)

A

ratio of CO2 produced relative to O2 consumed

  • function of fuel being used (carbs=1, fats=0.7, mixed=0.8)
  • variable in alveolar gas equation
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4
Q

what is the driving force between the liquid/air interface at the alveolar/capillary border

A

diffusion - Ficke’s Law

flux = -DA (ΔC/ΔX)

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5
Q

cardiovascular and respiratory system interactions

A

ventilatory pump: musculature that drives ventilation changes in lung
- chemoreceptors (carotid body) detect changes in partial pressure of key gases (O2, CO2, and pH) and primarily effect this

circulatory pump: heart (pumps blood)
- baroreceptors (carotid sinus) detect pressure changes (MAP) and primarily effect this

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6
Q

chemo-receptors

A

detect changes in chemicals (pH, O2, CO2) in blood (key blood gases) and send signals to respiratory neural centers which influence activity of respiration
- carotid body

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7
Q

minute ventilation

A

volume of air moved in and out of the lungs per unit time (minute)

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8
Q

alveolar ventilation

A

volume of air at level of alveoli available to diffuse across alveolar/capillary interface
- fraction of minute ventilation

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9
Q

why is albuterol an effective rescue medication

A

target is specific to beta 2 adrenergic receptors of the SM surrounding the respiratory system (conducting portion and respiratory bronchioles of the gas exchange portion)
- albuterol binds beta 2 receptors, causing CA++ extrusion from SM cells and relaxation (inc. air flow)

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10
Q

why are isoproterenol and epi (in over the counter inhalers) not ideal

A

although there target is beta-2 adrenergic receipts, they are non-specific and also bind beta-1 and alpha-1 which can cause contraction of SM

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11
Q

pleurisy

A

painful pathologic rubbing of visceral lining of lung and parietal lining of inside of thoracic cavity
- normally pleural space between these 2 linings has fluid to reduce friction

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12
Q

pleural space

A

space between visceral lining of lung and parietal lining of thoracic cavity

  • pressure here is sub-atmospheric (key to maintain this negative pressure)
  • becomes even more negative when chest expands - draws air in
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13
Q

muscles of inspiration

A

diaphragm: passive breathing

external intercostals: active breathing

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14
Q

muscles of expiration

A

passive recoil of lungs: passive breathing

internal intercostals: active breathing

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15
Q

what happens to pleural pressure when you inhale / expand chest cavity

A

it becomes more negative - pulls air in

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16
Q

negative pressure breathing

A

during inhalation, pressure in alveoli becomes more negative (pressure at airway opening stays the same)
- increase in pressure difference causes air to flow into alveoli

note: positive pressure breathing occurs when on ventilator

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17
Q

hysteresis

A

prior state dictates what will occur

  • In lung: prior state will dictate pressure/volume relationship that is observed (esp. w.out surfactant)
  • lungs behave differently depending on state of inflation
  • In lung: surface tension varies with area of alveoli (ST increases as area (radius) increases)
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18
Q

compliance

A

change in volume that accompanies a change in pressure

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19
Q

surface tension

A

phenomenon of differences in attractive forces at the air/liquid interface (cells are filled with liquid and alveoli with air)

  • large attractant forces between adjacent molecules at air-liquid interface compared with molecules lower down in body of fluid
  • typically: surface tension increases as volume decreases - but not in lung b/c of surfactant!
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20
Q

surfactant

A

complexmixture of phospholipids and proteins that play key immunological and biophysical roles
- amphipathic (hydrophobic and hydrophilic ends)

causes surface tension to increase proportionately with radius of alveoli, keeping pressure constant (prevents collapse of smaller alveoli)

produced at 32-34 weeks in utero (septal cells) - why premature infants can have respiratory distress syndrome (hyaline membrane disease)

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21
Q

hyaline membrane disease of the newborn

A

infants born with insufficient surfactant in lungs; alveoli can collapse (atelectasis) since pressure b/t large and small alveoli is unequal and air moves to larger alveoli and small alveoli collapse

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22
Q

babies first breath

A

birth: very small alveoli with high surface tension (require huge negative pressure to combat surface tension and open alveoli)
- use substantial inspiratory muscles to expand thoracic cavity and create large negative pleural pressure
- this initial effort is same with of without surfactant

Second breath: surfactant coats alveoli (type 2 cells) and subsequent inhalations become easier due to decreases surface tension
- radius of alveoli doubles and effort is 1/4th that of first breath

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23
Q

pneumothorax

A

integrity of pleural space is disrupted (breached) ad lung and chest wall behave how they want to (seperately)

  • negative intrapleural pressure is wiped out (air from atmosphere rushes in), lung recoils, and chest wall expands out to 70% of TLC
  • chest tube is used to re-establish pressure - lung will naturally re-expand
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24
Q

transmural pressure

A

difference between pressure inside a vessel / conduit and that which exists outside
• As lung volume decreases, transmural pressure becomes negative (outside higher than inside), radius of the airway decreases, leading to an increase in resistance
• As lung volume increases, transmural pressure in the airway is positive (inside pressure greater than outside), radius of airway increases, leading to less resistance to flow

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25
Q

chemical / pharmacological factors causing SM contraction

A

Chemoreceptor mediated – irritants
Acetylcholine (muscarinic receptors)
Histamine (endogenous substance released by mast cells)

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26
Q

chemical / pharmacological factors causing SM relaxation

A

Epinephrine - receptors in SNS – beta 2 mediated effect
- physiological antagonist of acetylcholine

Isoproterenol: pure beta agonist, non-specific
- useful rescue medication

Beta 2 agonists (albuterol, terbutaline)
- selective beta-2 agonist (best rescue)

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27
Q

obstructive lung disease

A

problem is getting air out: asthma, chronic bronchitis, COPPD, emphysema

Lung recoil is not as strong / lungs loose elasticity (not able to push as much air out - RV increases)
Compliance (change in volume with pressure changes) actually increases

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28
Q

restrictive lung disease

A

problem is getting air in: pulmonary fibrosis

Lungs become very stiff - problem is getting the air in - reduction in TLC

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29
Q

respiratory gases - what we breath in

A

oxygen
carbon dioxide
water
nitrogen

Note: total pressure will always be 760mmHg, but components change (see table in notes)

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30
Q

hypoventilation

A

causes dropping PO2 levels within the system (at both level of alveoli and subsequently tissues)
- does not just mean breathing too slowly

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31
Q

why is PO2 leaving lungs (94-96mmHg - PaO2) not equal to PO2 in alveoli (102mmHg - PAO2)

A

PaO2 is a reflection of the cumulative input from every segment of the lung in terms of V/Q ratio (some high, some low, some zero - vary!!)
- anatomic venous shunts: areas in lung where blood flows but never interacts with alveolar surface

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32
Q

what happens when you hold your breath

A

alveolar ventilation decreases, PACO2 increases as does PaCO2
- increasing degree of acidosis

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33
Q

value to use for tidal volume

A

500 ml (0.5 liters)

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34
Q

value to use for anatomic dead space

A

150ml

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35
Q

anatomic dead space -air

A

air exists but no gas exchange occurs (approx. 150ml)

- note: this air has properties of inspired air (PO2=150mmHg, no CO2, water vapor present)

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36
Q

alveolar ventilation

A

rate at which gas exchange can occur

  • reflection of tidal volume adjusted for dead space
  • fraction of minute ventilation
  • two equations (simple and more precise - see notes)
  • exclusively about CO2!!
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37
Q

increase alveolar ventilation (hyperventilate)

A
decrease PACO2 ("blowing off CO2")
 - recall, PACO2 is a reflection of PaCO2
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38
Q

anatomic venous shunts - blood

A

areas in the lung where blood flows but never interacts with alveolar surface
• Blood in anatomic venous shunts will have a V/Q ratio of zero (blood is not re-oxygenated at all)

Note: blood will have partial pressures identical to when it entered lung (PO2=40 and PCO2=46mmHg)

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39
Q

three types of shunts

A

Anatomic: portion of CO bypasses the lung

Alveolar: perfusion passes through alveolar save with no ventilation

Physiologic: due to very low V/Q ratios in some areas of lung

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40
Q

anatomic shunt

A

portion of CO (cardiac output) bypasses lung
– Intracardiac right to left shunt (septal defect - pathologic condition)
• Mixing venous blood with arterial blood results in decreased PaO2
– Lung vasculature that doesn’t interface with alveoli – normal condition

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41
Q

alveolar shunt

A

perfusion that passes through an alveolar interface with no gas exchange
– Collapsed alveoli (atelectasis)
– Pus-filled or edematous alveoli (increase thickness or distance = reduction in flux)

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42
Q

physiologic

A

due to very low V/Q ratios of some areas in the lungs (essentially no gas exchange)
– Venous admixture (wasted blood flow)
– Clinically - most common cause is atelectasis (mucus, edema, tumor, foreign body)

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43
Q

V/Q ratio

A

ratio of air reaching the alveoli to the amount of blood reaching the alveoli

  • unites value
  • varies depending on lung location and body position (gravity has effect)
  • average for healthy lung = 0.84
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44
Q

oxygen content

A

total amount of oxygen in the blood

  • total dissolved oxygen plus oxygen associated with other molecules (Hgb)
  • ml oxygen / deciliter blood
  • normal: 19.5 ml O2 per 100 ml blood

note: very different than partial pressure which only included free O2 (not bound)

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45
Q

factors that determine oxygen content

A
  1. Amount of gas dissolved (PO2)
  2. Amount of Hgb and its saturation
  3. Amount of MetHgb
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46
Q

why is there only 6mmHg difference b/t PaO2 (40mmHg) and PaCO2 (46mmHg) in pulmonary artery

A

this small difference in partial pressure corresponds to a large difference in the volume of these two gases in the blood of the pulmonary artery (CO2 high O2 low)
- CO2 is WAY more soluble that O2 in liquid

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47
Q

goal of oxygen therapy

A

elevate PO2 and drive Hgb to 100% saturation

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48
Q

key roles of Hgb

A

Oxygen transport to tissues (through binding with ferrous iron – Fe+2)

Buffing capability – Bohr effect

CO2 transport molecule – key for transport from periphery (loading it up) to the lungs (offloading it)

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49
Q

Bohr effect

A

Hgb gains a proton (acts as weak base) when oxygen dissociates from Hgb

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50
Q

form of CO2 in blood

A

Large amount as HCO3- (HCO3- is a transport mechanism for CO2)

Small amount is dissolved

Small amount is carbamino (bound to proteins, such as Hgb)

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51
Q

forms of O2 in blood

A

Bound to Hgb = 98.6% - reversibly associated with Hgb

Dissolved O2 (PO2) = 1.4%

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52
Q

what determines the volume of a gas in a liquid (2 factors)

A
  1. partial pressure of the gas
  2. solubility coefficient (O2=0.024, CO2=0.57)

Note: CO2 is WAY more soluble than O2 in liquid
- small changes in partial pressure result in large volume of CO2 leaving blood into alveoli

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53
Q

3 factors that determine amount of O2 bound to Hgb

A
  • amount of Hgb in system
  • capacity of O2 to be bound to Hgb (determined by existence of methemoglobin - iron in ferric form, 3+)
  • degree to which Hgb is saturated (can bind 1-4 molecules) - determined by PO2
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54
Q

difference in amount of O2 Hgb can bind v. capacity of O2 to bind Hgb

A

Hgb binds 1.39 ml O2 / gram Hgb

1.34 grams O2 will combine with 1 gram Hgb

Note: 0.05 ml difference is due to presence of ferric iron (oxidized iron) and methemoglobin - exists to a small degree under normal conditions

Note: ferrous iron (Fe2+) is required for heme to reversible associate with oxygen

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55
Q

4 factors that effect Hgb’s affinity for oxygen

i.e. what make Hgb an effective transport molecule for oxygen / factors that decrease its affinity for oxygen

A

Partial pressure of CO2: increasing CO2

Proton concentration (H+): increasing proton conc. (decreasing pH – more acidic)

Temperature: increase in temperature

2,3-BPG (same as 2,3-BPG): increase in metabolic activity→inc. in 2,3 BPG (BPG is a reflection of overall glycolytic activity in RBCs)

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56
Q

PulseOx

A

provides degree of saturation of hemoglobin (percentage reading)

Clinically: indirect window to PaO2

Recall: tells us nothing about amount of Hgb in system (can have very anemic person with normal PulseOx)

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57
Q

extraction ratio

A

difference in oxygen conc. (vol./dL blood) between venous and arterial blood; how much oxygen is extracted by certain tissues

  • Kidneys - 10% (small percentage since the blood flow is so massive to kidneys)
  • Heart - 60-65% (peak extractor of O2 on continuous basis)
  • Exercising muscle - 90% (huge ER) ; muscle at rest is about 30%
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58
Q

oxygen saturation of Hgb effects CO2 concentration for any given PCO2 (since Hgb is also a CO2 carrier)

A

Deoxy-hgb: reacts to a greater degree with CO2 (binds more CO2)

  • periphery: PO2 40mmHg - deoxygenated Hgb is carrying more CO2 (picking it up – more effective “sink” for CO2)
  • capillary-alveolar interface: PO2 is 100mmHg (more oxygenated / more fully saturated Hgb, Hgb does not carry as much CO2)
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59
Q

carboxyhemoglobin (HbCO)

A

Hgb bound to carbon monoxide

  • Hgb has wickedly high affinity for CO – over 300 times greater than its affinity for O2
  • heme group of Hgb binds CO at O2 binding site – reduces total O2 binding
  • HbCO has greater affinity for O2 than does Hg (will hold onto O2 in periphery and starve tissues of O2)
60
Q

goal of respiratory system

A

maintain constancy in face of exercise or other stressors

  • maintain PaO2, PCO2, pH
  • keep PO2 in pulmonary vein (and thus systemic PaO2) at 95mmHg
61
Q

causes of respiratory acidosis

A

Too much CO2 in system

lung disease, sedatives, neuromuscular disorders brain damage

62
Q

causes of metabolic acidosis

A

adds acid: DM, uremia, lactic acidosis

loses base: diarrhea

63
Q

causes of respiratory alkalosis

A

too little CO2

hyper-ventilation, fever, anxiety, brain disorders

64
Q

causes of metabolic alkalosis

A

adds base: alkali ingestion

loses acid: diuretics, vomiting, gastric suction

65
Q

hypercapnic state

A

excess CO2 in blood (usually due to decrease in ventilation)
- hypoxia (low PO2): system is even more sensitive to changes in PCO2

Note: PCO2 is principle regulator og respiratory system

66
Q

alveolar-arterial PO2 difference

A

difference in alveolar PO2 and arterial PO2 (normal “defect” in gas transfer)
varies normally with age and PIO2 (partial pressure of inspired air)

oxygen therapy: increase PAO2 results in inc. in PaO2

If P(A-a) O2 is increased above normal, there is a defect of gas transfer within the lungs (likely due to V-Q imbalance)

67
Q

diffusing capacity of the lung

A

diffusion of CO is used as means of assessing DL (since CO is poorly soluble in plasma but avidly binds Hgb –> equilibrium b/t PACO and PaCO doesn’t occur across alveolar-capillary interface during transit, but constant diffusion does)

Diffusional capacity of the lungs for gases increases with exercise

68
Q

why does CO2 make us acidic

A

CO2 is the regulated variable b/c it is quite soluble in our plasma and it quickly creates carbonic acid (H2CO3)

Carbonic acid quickly dissociates and lets go of its proton because our system has a pH of 7.4

So, CO2 makes us acidic – it is a volatile acid

CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

69
Q

muscles of respiration and innervation of these muscles

A

inhalation: diaphragm and external intercostals
- phrenic nerve APs synchronized with external intercostals

exhalation: internal intercostals

70
Q

normal levels for PCO2 and PO2

A
PCO2 = 40 mmHg
PO2 = 95mmHg
71
Q

systemic vs. pulmonary circulatory pressures

A

pressures are much lower in pulmonary circulation (versus systemic circulation)

72
Q

starling forces in pulmonary capillaries vs. systemic capillaries

A

k (permeability factor) is higher: lungs are more permeable

HPcap is much less: hydrostatic pressure in lung capillaries is lower

π ISF is greater: higher oncotic pressure in interstitial fluid of lungs

HPISF is negative: evaporation of water from ISF into air of alveoli
- helps to keep alveoli relatively “dry” (along with surfactant)

Note: all factors lead to minimal NFP (still positive, but very low)

73
Q

what keeps hydrostatic pressure and oncotic pressure low in capillaries

A

lymphatic system

74
Q

left sided heart failure: what effects will we see in the lungs (given greater permeability and low capillary HP of pulmonary capillaries)

A

Inadequacy of left ventricle to adequately generate pressure to move blood into circulation

  • fluid accumulation in lungs due to inc. in capillary HP due to “back-up” of pressure (fluid) in lungs
  • increase fluid in the lungs à hypoxic state/rales/SOB (seen in later stages of heart failure)
75
Q

causes of hypoxemia (low level of O2 in arterial blood) - 4 things on ddx

A

1Hypoventilation → inadequacy of alveolar ventilation (doesn’t necessary mean low ventilation rate)
- ex. mushroom lady

Diffusion → impairment of ability of gases to diffuse freely in accordance with concentration differences and partial pressure at capillary/alveolar interface (fluid accumulation - edema, atelectasis)

Shunt → blood that is not reaching alveoli to participate in gas exchange (anatomic, physiologic)
- ex. septal defect (pathologic)

Ventilation/Perfusion Mismatch → V/Q ratios vary depending on location in lung or activity level; need to have proper ventilation with proper perfusion based on scenario
- most common cause

76
Q

driver of increased respiratory rate with exercise

A

increase in protein conc (H+ - decreased pH)

77
Q

driver of increased respiratory effort at altitude

A

chemoreceptors detect drop in PO2 and slight elevation in PCO2 drives inc. in RR

78
Q

effect of altitude on blood gases and respiration

A

Barometric pressure is 622 vs. 720 mmHg

  • PO2 of inspired air is low
  • alveolar PO2 is decreased (90 to 65 mmHg)
  • Hgb saturation low
  • all tissues are slightly hypoxic

Drive for inc. respiratory rate is chemoreceptors: sense low PO2 high PCO2 and increase firing rate to inc. respiration

79
Q

GI tract - basic info

A

largest endocrine organ of body (secretes huge # of hormones)

site of all nutrient absorption into our systems (excluded O2)

autonomous: can function without external stimulation (via enteric NS)
- however. modified by PNS and SNS

80
Q

4 main processes of GI tract

A

motility
digestion
secretion
absorption

81
Q

exception to trans-celluylar absorption in GI tract

A

fats - enter vasculature by way of lymphatic system

82
Q

segmentation

A

characteristic of GI system motility

  • circular constriction that mixes intestinal contents (chyme)
  • isolated, closely spaced contractions of circular smooth muscle of GI tract
  • most frequent type of contractile activity (random in frequency and in pressure change)
83
Q

peristalsis

A

successive (consecutive) contractions of circular smooth muscle

  • stimulated by local distention which triggers the contraction/relaxation reflex
  • provides a 1-4cm movement per contraction
84
Q

chyme

A

liquid contents of GI tract

Note: composition has large influence over activity of GI tract

85
Q

unstirred layer

A

layer in lumen of gut right above epithelial cells (adjacent and linked to brush border) where microvilli of epithelial cells enter GI lumen
- slow moving layer that allows for transport and diffusion to occur so nutrients can be absorbed by epithelial cells

86
Q

is digestion an active or passive process

A

passive process: dependent entirely on concentrations of enzymes and substrates
- process of secretion provides enzymes needed for digestion

87
Q

atropine

A

drug that blocks Ach receptors (muscarinic receptor blocker) - blocks PNS activity on GI tract

Effective anti-diarrheal medication

88
Q

secretin family of hormones

A

Secretin, VIP, GIP, glucagon, GLP-1 (AA sequence homology)
• Glucagon is a pancreatic hormone – part of endocrine portion of pancreas
• Glucagon-like polypeptide 1 (GLP-1 - also part of this group)

Due to similar make-up, these substances bring about similar effects

89
Q

incretins

A

hormones that stimulate insulin release

- secretins, especially GIP and GLP-1

90
Q

3 phases of digestion

A

Cephalic: site, smell, taste, anticipation
- contributes 30% of total vol. of secretory activity

Gastric: chyme in stomach
- contributes 50% of total vol. of secretory activity

Intestinal: chyme in intestine

Note: all of these phases are integrated (but unique)

91
Q

3 salivary glands

A

parotid: 25% vol., watery
submandibular: 70% vol., watery
sublingual: 5% vol, mucousy

Note: salivary glands secrete 2 liters/day

92
Q

salivary enzymes

A

digestion begins in mouth:

mucin: mucous released to lubricate food

alpha-amalase: hydrolyze starches (CHO digestion begins); amylase also secreted by pancreas

lingual lipase: hydrolyzes triglycerides

lysozyme and lactoferrin: protective mechanisms (dec. bacteria)

93
Q

properties of saliva

A

hypo-osmotic, slightly alkaline

94
Q

autonomic innervation of salivary glands

A

both PNS and SNS are stimulatory

- PNS (cholinergic receptors) play main role (anticholinergic meds have side effect of dry mouth)

95
Q

salivary composition - changes with flow rate

A

low flow: K+

High flow: Na+, HCO3-, Cl- (hypo-osmotic, slightly alkaline)

96
Q

receptive relaxation

A

relaxation of adjacent structures (dec. in pressure) to prevent back flow through GI tract

  • pressure in fundus diminishes with reducing LES pressure (relaxation of LES (lower esophageal sphincter)
  • prevents back flow when sphincter opens
  • breathing is temporarily halted during relaxation
97
Q

causes of reflux esophagitis (heartburn)

A

inadequate closure (or maintenance of pressure) of LES - chyme from stomach goes into esophagus and can cause cell damage due to acidity

98
Q

achalasia

A

insufficient LES relaxation - hard time swallowing

99
Q

cells of gastric glands (stomach) and anthem of stomach

A

surface epithelium (protected by mucous)

mucous cells

parietal cells - secrete H+ (HCL) and intrinsic factor

chief cells: pepsinogen (enzyme that initiates protein digestion)

G cells: secrete gastrin (stimulated by GRP and Ach)

100
Q

where does digestion begin for carbohydrates, fats, and proteins?

A

carbohydrates: mouth (a-amylase)
fats: mouth (lingual lipase)
proteins: stomach (pepsinogen)

101
Q

key gastric juice components

A
Hydrogen ions (HCL key for acidic nature of lumen of gut)
 - parietal cells
Intrinsic factor (binds and transports vit. B12)
 - parietal cells

Pepsin (proteolytic enzyme that begins protein digestion)
- chief cells

Mucus (protects stomach from corrosive environment)
- goblet cells

Overall: complex mix of ions, mucin, and pepsin

102
Q

what two things protect the epithelial cells of the stomach from corrosive environment

A

mucous layer

HCO3- secretion from epithelial cells (buffering capacity)

103
Q

parietal cell ionic contributions to gastric juice

A

mainly H+, Cl- and some K+

Also, intrinsic factor!

104
Q

nonpareil cell contributions to gastric juice

A

Na+, Cl-, and HCO3-

105
Q

gastric juice composition - changes with flow rate

A

Slow flow: NaCl

Fast flow: H+ increases, Na+ decreases (K+ reamins
- HCL rich solution with K+

106
Q

alkaline tide

A

system (ECF) becomes more basic (alkalytic) following consumption of a meal

  • food entering stomach acts like a buffer (pH increases)
  • pH stimulates parietal cells to release H+
  • H+ moves out into lumen while HCO3-moves back into ECF
107
Q

cephalic phase of digestion - triggers

A

Anticipation, sound, sight, and smell – contribute to collective neural efferent activity (vagus nerve)

Conditioned reflexes (time of day, auditory signal), chewing, swallowing

Hypoglycemia (chemical inducer): through natural or stimulated drop in blood sugar

108
Q

cephalic phase - sequence of events during anticipation of meal

A

vagus nerve stimulates release of Ach, which mediates activity in stomach though 2 routes:

Direct: stimulation of post-ganglionic fibers in gut (enteric NS), release Ach and directly stimulate parietal cells of stomach

Indirect: stimulation of post-ganglionic fibers in gut (enteric NS), release GRP, GRP stimulates G cells to release gastrin, gastrin circulates through system and binds parietal cells

109
Q

gastric phase of digestion - triggers

A

chemical: composition of chyme (AAs and peptides act as secretagogues)

pH: local pH in lumen effects secretion

  • high pH: inc. parietal cell activity
  • low pH: dec. parietal cell activity

distention: mechanoreceptors sense physical distention and release Ach, which stimulates G cells to release gastrin, leads to stimulation of parietal cells

110
Q

secretagogues

A

general term for chemical substances that stimulate secretory activity
ex. amino acids in stomach - stimulates parietal cells to release H+ (HCL)

111
Q

enterogastrones

A

chemical substances that are inhibitory for gastric activity

- generated by cells of the intestine, circulate in ECF, ultimately impact what occurs in stomach

112
Q

intestinal phase of digestion

A

Duodenal chemical contents impact gastric activity: what occurs in intestine effects what goes on in stomach

Secretin, GIP, and CCK: reduce gastric motility and secretion (enterogastrones)

Peptides (AA): stimulate gastrin release and HCL secretion (secretagogues)

Duodenal pH will influence what happens in stomach

113
Q

why is having an acidic (HCL) lumen in the gut important

A

helps with protein digestion - proteins denature in low pH

114
Q

intrinsic factor

A

protein secreted from parietal cells of stomach; key in assimilation of vitamin B12

  • no role in digestion
  • helps B12 to be transported to ilium where it is absorbed
  • Vit. B12 key to heme synthesis and RBC production
115
Q

effects of defected parietal cell release of intrinsic factor or nutritional deficiency in vitamin B12

A

pernicious anemia as a result of reduced heme synthesis

116
Q

what happens with prolonged vomiting (empty contents of stomach)

A

hypokalemic state and metabolic acidosis

  • K+ conc. is high in stomach lumen
  • H+ conc is high in stomach lumen; parietal cells will work to replace H+ in lumen (restore pH) and, subsequently pump HCO3- into ECF
117
Q

pepsinogen secretion and activation

A

pepsinogen: inactive form of pepsin (begins protein digestion)
- secreted from chief cells in stomach (rate-limiting step)
- pH of stomach is main stimulator of conversion to pepsin

118
Q

pepsin

A

enzyme that has great proteolytic actions in stomach (active form of pepsinogen)

  • key in protein digestion
  • operates optimally at low pH (around 2) - unique
119
Q

pepsinogen - regulation of release

A

vagal stimulation

gastrin release from G cells of stomach - stimulates

secretin release from s cells of duodenum - stimulates

main regulators: Ach secretion (vagus nerve), activation of chief cells, and protein population in stomach

120
Q

importance of mucin secretion - key roles of mucous layer in stomach

A

Provides protective layer for epithelial cells of stomach

Lubricates food

Sets up diffusional (pH) gradient

Creates neutral pH at epithelial cell surface (stimulate non-parietal cells to secrete HCO3-)

121
Q

what happens with breach in mucosal barrier of stomach

A

chemical erosion of epithelial cells = ulcer

122
Q

pyloric sphincter

A

gateway between stomach and duodenum - enlargement of mainly circular muscle

under control of enteric nervous system - drives relaxation of sphincter so food can move through

pressure differences cause chyme to move through sphincter into duodenum

123
Q

ghrelin

A

hormone found in stomach, pancreas, and hypothalamus

produced during fasting between meals; drops with food consumption

124
Q

ghrelin - effects

A

effects metabolic rate and food intake - effects across multiple organ systems

stimulates GH (growth hormone) release - GH raises blood glucose levels, reduces glucose use, mobilizes fat stores, reduces protein catabolism

increases hunger, food intake & weight gain

increases HCl secretion & gastric motility – impacts capability of system to engage in digestion

increases CO & reduces SVR (systemic vascular resistance) - increases blood flow to gut and elsewhere

125
Q

how to infants get immune benefit from breastmilk (immunoglobulins are proteins)

A

immunoglobulins are able to survive trip through stomach so they can be absorbed

  • higher pH in newborn stomachs (avg 4.6)
  • ability to produce pepsin in stomach is not mature in infants (less HCL)
126
Q

cells of pancreas

A

islets of langerhorn: endocrine portion of pancreas

  • beta cells: release insulin
  • alpha cells: release glucagon

acinar cells: exocrine portion of pancreas
- produce inactive and active digestive enzymes

ductal cells: produce HCO3- and H2O for release into SI

127
Q

pancreatic juice composition - changes with flow (secretary rate (ml/min) from pancreas

A

slow rate: high NaCl

fast rate: HCO3- levels rise and Cl- levels fall (since anti-port)
- high Na+ and HCO3-

128
Q

stimulus for HCO3- release from pancreatic ductal cells

A

low pH (pH of 4.5 and below is large stimulus; under 3 no additional HCO3- will be released)

  • Secretin: low pH (protons) and fats entering duodenum actually stimulate secretion release, which directly stimulates ductal cells
  • Ach: direct neural innervation from vagus nerve stimulates ductal cells
  • CCK: pH and chyme stimulate CCK release; secondary stimulator of ductal cells (primary simulator of acing cells)
129
Q

enterokinase

A

protease present on brush border of duodenal cells
- engages in partial proteolytic cleavage of AA sequences that result in activation of key digestive enzymes (trypsinogen to tyrosine)

Note: key for protein digestion!!

130
Q

role of liver in digestion

A

contends with nutrient flow from GI tract prior to it entering circulatory system

131
Q

what does liver do with glucose?

A

Glucokinase is activated by virtue of concentration: stimulates glycolytic activity and ultimately glycogen synthesis (high KM – will see big increases in activity only when levels rise dramatically)

132
Q

cause of gallstone formation

A

when sphincter of Oddi is not stimulated to be open, bile is stored in gallbladder (and concentrated)
- precipitation of substances due to high concentration creates stones

133
Q

micelles

A

formed by bile; hydrophobic portion on inside and hydrophilic portion on outside
- role in digestion of hydrophobic substances (free fatty acids, triglycerides, cholesterol fat soluble vitamins - ADEK)

134
Q

mucosal barrier (brush border) of small intestine

A

very important for digestion

  • large surface area
  • location of intrinsic enzymes of digestion (glycocalyx sets up key microenvironment)
  • unstirred layer allows diffusion

Enterokinase: activates key enzymes for protein digestion

lactase, maltase, sucrase, limit dextrinase, trehalase: CHO digestion to monosaccharides

135
Q

why are enzymes responsible for digestion of proteins secreted from pancreas in inactive form

A

so they do not consume the very proteins that are making them - key regulation!!

136
Q

lactose intolerance

A

lack enzyme lactase, so disaccharide lactose cannot be broken down into monosaccharide (glucose and galactose)
- presence of lactose in GI lumen of intestine creates large osmotic draw (water = diarrhea, gas)

137
Q

GIP - gastric inhibitory peptide

A

hormone secreted by K cells of GI tract (mainly SI)

  • stimulators of release: CHO and TG content of chyme
  • incretin: stimulates insulin release (why oral glucose more effective then IV)
  • DPP IV cleaves GIP and renders it non-insulinotropic (inhibit DPP IV to prolong existence of GIP and enhance insulin production for people with DM)
138
Q

why is oral glucose better than IV glucose for diabetic going into hypoglycemic shock

A

oral glucose activates hormone GIP release from K cells of GI tract

GIP is an incretin - stimulates insulin release

Note: IV glucose administration does no activate GIP (only in GI tract)

139
Q

where is absorptive capacity - where are different things absorbed

A

Most absorption is in the small intestine (few substances can be absorbed in the stomach)

Fats, carbs, fat-soluble vitamins (ADEK) - absorbed in the proximal gut and tapers off distally

Protein and water soluble vitas are mostly absorbed in the proximal SI, too

Bile salts can occur throughout - mainly at the ileum (distal SI)

Cobalomin - B12 (need intrinsic factor) - Ileum (distal SI)

140
Q

diarrhea - metabolic changes seen

A

hypokalemic, metabolic acidosis - losing K and losing frank base (HCO3-)
- since HCO3- is pumped out in exchange for Cl in SI (a lot in colon)

141
Q

vomiting - metabolic changes seen

A

hyperkalemia, metabolic alkalosis - constantly putting HCO3 back into ECF since trying to replace H+ in lumen (since puking out)

142
Q

proton pump inhibitors (parietal cells of stomach) - what positive and negative effects do they have

A

block H+/K+ ATPase pump so H+ is not pumped into lumen

positive: reduce acidity (inc. pH) of lumen
negative: low pH key for absorption of important nutrients (namely iron)

143
Q

calcium absorption in small intestine

A

low calcium levels stimulate release of PTH from parathyroid glands

PTH activates vitamin D (in kidney)

Active vit D3 binds epithelial cell, resulting in inc. RNA and inc. in intracellular machinery needed to drive Ca absorption

Ca crosses apical membrane into cell:
- intracellular free Ca levels are held VERY low in cells

Ca is extruded into ECF by:

  • primary active transport out into the plasma
  • can be sequestered by ER and mitochondria
  • Ca/Na exchange
144
Q

hepcidin

A

protein responsible for inhibiting iron uptake

Factors that increase hepcidin: chronic inflammation, high iron levels

Factors that reduce: generation of RBCs (erythropoietic signal), low iron levels (results in inc. duodenal absorption of iron)

145
Q

motility of colon

A

non-propulsive movements: back and forth

propulsive movements:

  • irregular contractions (basic electrical)
  • mass peristalsis: smooth wave that moves contents of colon though colon (under control of reflexes)
146
Q

reflexes involved in mass peristalsis

A

Ortho-colic reflex → in the am when you get up

Gastro-colic reflex → after feeding

Gastro-ileal reflex → chyme into the ileum

147
Q

3 things that neutralize pH in small intestine

A

pancreatic secretion of HCO3- (CCK)
bile secretion of HCO3- (CCK)
Duodenal secretions