exam 3 Flashcards

1
Q

gas exchange in respiration

A

exchange 1: atmosphere to lung (ventilation)
exchange 2: lung to blood
transport: transport gases in blood
exchange 3: blood to cells

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2
Q

anatomy of airway

A

pharynx
larynx
trachea
bronchi
bronchioles
alveoli

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3
Q

anatomy of airway

A

pharynx
larynx
trachea
bronchi
bronchioles
alveoli

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4
Q

pharynx

A

passageway for ingested materials and air

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5
Q

trachea

A

windpipe
flexible tube help by c-shape rings of cartilage

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6
Q

larynx

A

contains the vocal cords
bands of connective tissue tightened or loosed by muscles to create sound when air passes

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7
Q

bronchioles

A

small collapsible passageways
smooth muscle walls
branch until the reach the exchange surface (Alveoli)
total cross sectional diameter increases as they branch

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8
Q

goblet cells

A

secreted by goblet cells
contain ciliated epithelial cells which move the mucus toward the pharynx

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9
Q

alveoli

A

exchange surface of lungs
where O2 and CO2 move between air and blood

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10
Q

type 1 alveoli

A

thin gas exchange cells
majority of alveolar surface
close association with pulmonary capillaries to permit gas exchange
0.2 um thick

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11
Q

type 2 alveoli cells

A

produce surfactant
substance that acts to ease expansion of lungs during inspiration

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12
Q

elastin fibers

A

connective tissue fibers between alveoli
contribute to elastic recoil

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13
Q

pleural sac

A

membrane surrounding lungs
pleural tissue held by fluid
holds lungs against thoracic wall by intrapleural pressure

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14
Q

intrapleural vs interpulmonary pressure

A

intrapleural is always less

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15
Q

inspiration

A

external intercostal contacts
diaphragm contracts
chest wall and lungs expand
sterum moves up

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16
Q

expiration

A

passive! due to elastic recoil
external intercostal relaxes
diaphragm relaxes
chest cavity and lungs contract
ribs and sternum decompress

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17
Q

active expiration

A

internal intercostal muscles contract
abdominal muscles contract

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18
Q

alveolar (interpulmonary) pressure during inspiration and expiration

A

low during inspiration
high during expiration

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19
Q

resistance effect

A

decrease alveolar pressure during inspiration
increase alveolar pressure during expiration
increases energy required for breathing (normally 3%)
decrease compliance

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20
Q

lung compliance

A

change in lung volume/change in transpulmonary pressure

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21
Q

transpulmonary pressure

A

alveolar (interpulmonary) pressure - intrapleural pressure

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22
Q

what affects compliance

A

intrinsic elastic properties
surfactant

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23
Q

what affects compliance

A

intrinsic elastic properties
surfactant

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24
Q

surfactant

A

made of phospholipids and proteins
secreted by type 2 alveoli cells
decrease surface tension!

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25
surfactant effect on compliance
decrease surface tension increase compliance easier for lungs to expand greater effect in smaller alveoli which equalizes pressure between large and small alveoli
26
tidal volume
volume of gas that moves in and out 500 ml per breath
27
functional residual capacity
2100 ml volume left in system at end of expiration
28
expiratory reserve volume
extra 1100 we can force out using expiratory muscles
29
residual volume
remaining 1000 ml left after we force out extra air
30
inspiratory reserve volume
3000 ml air we can bring in if we breath deeper
31
total maximal inspiratio volume
3500 500 from normal tidal volume extra 3000 from inspiratory reserve volume
32
vital capacity
total maximalvolume we can move in and out 4600 500 + 3000 + 1100
33
forced expiratory volume
volume actively expired in 1 second typically 80% of todal goes down as airway resistance increases
34
minute ventilation
tidal volume x breathing rate amount of air moved in and out per minute
35
alveolar ventilation
takes into account dead space of tidal volume (150 ml) amount of fresh air brought to alveoli per minute = (tidal volume-dead volume) x breathing rate
36
respiratory quotient
1 molecule O2 consumed = 0.8 CO2 generated
37
normal alveolar ventilation per minute
approximately 12 breaths/min * 350 ml = 4200 ml 21% of volume is O2=882 ml/min of oxygen entering lungs
38
increase pCO2
dilate bronchioles constrict pulmonary arteries dilate systemic arteries
39
increase pO2
constrict bronchioles dilate pulmonary arteries constrict systemic arteries
39
gas exchange occurs by
simple diffusion proportional to: concentration gradient, surface area inversely proportional to: thickness, distance
40
atmospheric o2 alveolar pressure
160 mmHg vs 100 mmHg difference because: dead volume, rapid diffusion between alveoli and pulmonary capillaries
41
normal arterial blood values
pO2= 95 pCO2 = 40 pH = 7.4
42
normal venous blood values
pO2 = 40 pCO2 = 46 pH = 7.37
43
what happens to arterial oxygen
2% dissolves in plasma 98% binds to hemogobin
44
exchange between alveoli and capillaries
occurs within first third of capillary length
45
hypoxia
less oxygen
46
asthma
causes hypoxia increased airway resistance decreases alveolar ventilation
47
pulmonary edema
causes hypoxia fluid in interstitial space increases diffusion distance
48
fibrotic lung tissue
causes hypoxia thickened alveolar membrane slows gas exchange
49
emphysema
causes hypoxia destruction of alveoli decreases surface area
50
binding of oxygen and hemoglobin
1 gram of hemoglobin combines with 134 ml of O2 each of 4 subunits can be oxygenated or deoxygenated reversible, fast Hb + O2 <-> HbO2
51
percent oxygenated substrate
percent of hemoglobin saturation of oxygen
52
hemoglobin concentration
150 g/liter 15%
53
what happens to CO2 in blood
7% remains dissolved 70% converted to bicarbonate and H+ 23% binds to Hb
54
CO2 and Hb binding
forms cabaminohemoglobin
55
Hb-O2 curve shift to right
curve shifs to the right causes more O2 to be delivered to the tissue
56
what causes right shift of curve
increase of DPG decrease pH increase temp
57
what causes decrease pH which leads to curve shift to right
skeletal muscles are more active acids build up of lactic acid decrease pH increase oxygen delivery
58
regulation of inspiratory muscles
phrenic nerve innervates diagphram intercostal nerve innervates external intercostal originate from cervical spinal cord (C3-C5)
59
what controls the nerves innervating inspiratory muscles
central rhythm generator located in medulla
60
central rhythm generator
generates oscillitaroy activity which excites DRG and VRG
61
DRG and VRG
dorsal/ventral respiratory group neurons that innervate motor neurons that control respiratory muscle DRG fires I neurons VRG fires both
62
pre-Botzinger nucleus
found in VRG fires I neurons or E neurons
63
I neurons vs E neurons
I neurons: active during inspiration, silent during expiration E neurons: silent during inspiration, active during expiration
64
where are peripheral chemoreceptor sites
cartoid bodies aortic bodies
65
peripheral chemoreceptors respond to
changes in arterial blood - significant decrease Po2 (Hypoxia) - increased H+ (metabolid acidosis) - increased pCO2 (respiratory acidosis)
66
central chemoreceptors
medulla oblongta respond to changes in brain extracellular fluid - increased pCO2 associated with changes in H+
67
blood brain barrier
CO2 can cross H+ cant cross
68
peripheral vs central chemorceptors
low O2 only affects peripheral chemoreceptors peripheral: increase arterial H+ central: increase ECF H+
69
what happens after chemorceptors fire
fire medulla inspiratory neurons (DRG and VRG) fire neurons to diagphragm and inspiratory intercostals (phrenic and intercostal) causes diagphragm and external intercostal to contract breathign!
70
effect of exercise on ventilation
increase minute ventilation decrease arterial co2 increase arterial H+ O2 stays same feed forward mechanism because minute ventilation changes before others
71
sneezing
receptors in nose and pharynx stimulate deep inspiration and forced expiration
72
coughing
receptors in trachea stimulate deep inspiration and forced expiration
73
speech
requires fine control of respiratory muscles
74
2,3DPG
compound made from intermediate in glycolysis increased levels of DPG in red blood cells with hypoxia increased DPG shifts curve to right
75
breathing at high altitude
barometric pressure is low alveolar O2 is low hard to get O2
76
increase red blood cell count
if there is low o2=hypoxia so kidneys release erythropoiten to produce erythrocytes which increases hematocrit and blood volume
77
great increase in pulmonary ventilation
if there is low o2=hypoxia so small increase in pulmonary ventilation but kidney normalizes pH by secreting bicarbonate ion which increases ventilation by a lot
78
increase cellular metabolism
if there is low o2=hypoxia but produce more cells, more mitochondria, more energy
79
increased vascularity of tissue
if there is low o2=hypoxia but increase # of capillaries to make more o2 which also increases surface area for gas exchange between alveoli and blood
80
ways to acclimate to low po2
increase cellular metabolism increase # RBC increase vascularity of tissue large increase of pulmonary ventilation change O2-Hb curve
81
change O2=Hb curve
low O2=hypoxia=curve shift to left over time 2,3-DPG brings curve back to the right
82
function of kidneys
regulate blood pressure, osmolality, electrolyte concentration, erythrocyte maintain ph and h2o excrete metabolic waste produce glucose
83
urinary system
kidney ureter bladder urethra
84
kidney anatomy
nephrons bowmans capsule/proximal distal tubules: inner medulla loop of henle/collecting ducts: outer cortex
85
nephrons
1 million per kidney juxtamedullary (20%) long loop cortical (80%)
86
renal autoregulation
myogenic mechnisms tubuloglomerular feedback
87
path of urine
glomerulus bowmans capsule proximal convulted tubule proximal straight tube descending limb ascending limb distal convoluted tubule cortical collecting duct medullary collecting duct renal pelvis
88
arterioles and capillaries of nephron
afferent arterioles to glomerular capllaries transition to efferent arteriole to peritubular capillaries
89
excretion formular
filtration-reabsorption+secretion
90
filtration equation
net filtration pressure x Kf (filtration constant) net filtration pressure: hydrostatic and osmotic pressure filtration constant:how leaky capillary is
91
hydrostatic pressure
blood pressure
92
osmotic pressure
due to proteins being in plamsa but not in bowmans capsule
93
layers of filtration
1.capillary endothelial cells: more holes, coarsest level 2.basal lamina: noncellular matrix between endothelial cells 3.podocytes:filtration sites, finest level, specialized epithelial cells that line glomerular capillaries
94
GFR
normal glomerular filtration rate 125 ml/min=180 L/day = V * Us/Ps only works for a substance filtered but not secreted
95
clearance rate
how much blood is excreted (renal plasma flow) (600mL) totally reabsorbed: clearance rate =0
96
filtration fraction
= GFR/RPF
97
reabsorption
most occurs in proximal tubule regulated occurs in distal segment of nephron (collecting duct)
98
reabsorption pathway
transport molecules from lumen of tubules across epithelial cells into interstitial space into peritubular capillaries
99
apical vs basolateral membrane
apical(Lumen: face tubular lumen, highly convoluted, large surface area basolateral: face renal interstitial fluid
100
transport maximum
due to limited transporters or transport time maximum rate at which a membrane can transport substance
101
Na+ reabsorption
enters lumen membrane through concentration gradient crosses basolateral membrane by secondary conc. gradietn
102
glucose reabsorption
sodium enters lumen membrane down conc. gradient, SGLT protein pulls glucose with it glucose diffuses basolateral membrane using GLUT Na crosses baoslateral by secondary active transport
103
impermeability of water
collecting duct is impermeable to water ascending limb: not permeable to water, permeable to sodium descending limb: not permeable to sodium, permeable to water
104
permeability of collecting duct regulation
aquaporin 2 on apical membrane ADH released into blood stream and acts on receptors on basolateral membrane ADH binding activates cAMP fusion of vesicle with membrane: insert AQ2 on apical membrane
105
where is ADH made
hypothalamus
106
osmosensors
located in hypothalamus in close proximity to ADH
107
diabetes insipidus
central: problem with ADH syntheis or secretion nephrogenic: problem with renal response to ADH
108
deeper into kidney
interstitial fluid becomes more hypertonic
109
plasma osmolarity and vasopressin
osmolarity increases vasopressin (adh)increases urine volume decreases uring osmolarity increases
110
ADH secretion
decreased blood pressure decreased atrial stretch increased osmolarity all increase vasopressin (ADH) which inserts water pores increase water reabsorption to convserve water
111
Na+ reabsorption
most in proximal tubule (2/3) least in collecting tubule none in descending loop main transporter of apical membrane is Na/K/2Cl transporter
112
aldosterone
acts on collecting tubule regulated by angiotensin 2 which is controlled by renin aldosterone increases Na+ reabsorption and K+secretion
113
what controls renin
increase renal sympathetic nerves (b-adrenergic receptor) decrease atrial presure decrease GFR
114
control of plasma osmolality
regulating how much water there is to dilute or concnetrate solutes
115
mechanisms to regulate water
control of water loss by kidneys control of water intake (thirst)
116
aldosterone
steroid hormone released from adrenal cortex acts on collecting ducts to promote na+ reabsorption and K+ secretion
117
absence of aldosterone
2% of filtered Na+ is excreted (a lot)
118
presence of aldosterone
all Na+ is reabsorbed
119
how does aldosterone control reabsorption of Na+
synthesizes new Na,K,ATPase molecule in basolateral membrane stimulates insertion of Na+ channels in apical membrane increases transcription/translation
120
what controls release of aldosterone
angiotensin acts on aldosterone releasing cells of adrenal cortex
121
renin
released from juxtaglomerular cells lie next to macula densa surround afferent and efferent arteriole
122
atrial natriuertic hormone
released from right atrium in response to stretch promotes Na+ excretion decreases Na+ reabsorption increases GFR inhibits renin secretion, aldosterone, and ADH
123
potassium homeostasis
regulation occurs by secretion at level of cortical collecting ducts regulated by aldosterone because it increases Na/K channels, promote K+ secretion
124
calcium homeostasis
conc. in ECF is low regulated at collecting duct controlled via an endocrine feedback mechanism controlled by PTH low Ca = secrete PTH = increase Ca promote Ca reabsorption
125
H+ homeostasis
buffer respiration kidneys
126
osmotic diuretics
ex: mannitol provide large amount of filtered but not reabsorbed solute --> get excreted and bring water with them
127
aldosterone antagonists
ex: spironolactone block aldosterone receptors which promotes Na+ excretion, bring water wih it
128
loop diuretic
ex: furosemide inhibit Na+ transporter