exam Flashcards
(128 cards)
1
Q
FIVE FUNCTIONS OF
RESPIRATORY SYSTEM?
A
- Exchange of gases between atmosphere and
blood (or the exchange of air b/w atmosphere and lungs aka ventilation/breathing) - Homeostatic regulation of body pH (by eliminating CO2)
- Protection from inhaled pathogens (mucus layer in constant upward flow which carries pathogens upward too)
- Vocalization (air vibrating across vocal chords)
- Eliminating heat (control water content of body- panting)
2
Q
what are the Important principles of air flow during respiration?
A
- Flow takes place from regions of higher pressure to
regions of lower pressure - A muscular pump creates pressure gradients by expanding/compressing thoracic cavity (volume/pressure relationship)
- Resistance to air flow is influenced primarily by the
diameter of the tubes through which air is flowing (when tubes dilate= less resistance= more air flowing in/out
3
Q
Gas exchange from environment to cells occurs in 4 stages; what are they?
A
- Ventilatory flow
- (air from atmosphere to lung) - Diffusion (of CO2/O2 b/w lungs and blood across respiratory epithelium)
- Circulatory flow (O2/CO2 transport in blood)
- Diffusion (exchange of gases into cell from blood)
4
Q
what is the primary stimulus to an increase in ventilation?
A
a build up of CO2 (NOT a drop in O2)
5
Q
describe the upper and lower respiratory system
A
lower: trachea branch out into right and left bronchi which then divide into secondary and tertiary bronchi and then into bronchioles which connect to alveoli sacs. includes diaphragmarm
upper: (the conducting zone) includes the nose and nasal passages, paranasal sinuses, the pharynx, and the portion of the larynx above the vocal folds (cords)
6
Q
action of the conducting zone? (upper RS)
A
- Warm air (cant take in really cold air bc we have to maintain a core body temperature and it may damage alveoli)
- Add water vapor to air (increases moisture/humidity bc we dont want dry air reaching the alveoli-it will dry out moist exchange epithelium does not dry out)
- Filter out foreign material (mucus and cilia aid in moving mucus upwards in watery saline layer) *goblet cell secrets mucus
7
Q
how do we achieve a saline layer (salty solution) in the airways?
A
-saline produced by epithelial cells when Cl- is brought into epithelial cell from ECF by NKCC transporter (move 1 Na+, 1 K+, 2Cl- into REC) and then moves into lumen. Na+ goes into lumen by paracellular pathway by electrochemical gradient. NaCl movement from ECF into lumen creates a conc. gradient so water follows into lumen
8
Q
describe the lung structure
A
light spongy tissue, volume mostly occupied by air spaces -Each lung is surrounded by a double-walled pleural sac ->Fluid in pleural sac keeps lungs stretched (even at rest) and stuck to thoracic cage -prevents them from collapsing -left lung has 2 lobes and a cardiac notch where heart sits
9
Q
describe type 1 and 2 alveoli/epithelial cells
A
type 1:
high in number and very thin (rapid gas exchange)
type 2:
fewer in number, smaller but thicker (synthesize and secret the chemical surfactant which aid lungs in expanding )
10
Q
Dalton’s law ?
A
states that the total pressure exerted
by a mixture of gases is the sum of the pressures
exerted by the individual gases
*air= a mixture of gasses (lots of N2, some O2)
11
Q
partial pressure ? (*bring calculator!)
A
The pressure of a single gas in a mixture is its partial pressure (Pgas) Pgas = Patm x % of gas in atmosphere ex Patm= 760mmHg at 21% O2 Pgas (O2) = 760 x 0.21 = 160mmHg
12
Q
what is Boyle’s law?
A
inverse relationship b/w volume and pressure (V=1/P =decreased volume=increased pressure)
P1V1 = P2V2
-Pressure is doubled when volume is decreased by 2 (half)
*sets pressure gradients
Changes in lung volume → pressure gradients → air flow
13
Q
Tidal volume (VT)
A
Volume of air that moves during a single inspiration or expiration
14
Q
Inspiratory reserve volume (IRV)
A
Additional volume inspired above tidal volume
15
Q
Expiratory reserve volume (ERV)
A
Additional volume forcefully exhaled at the end of a normal expiration
16
Q
Residual volume (RV)
A
Volume of air in resp. system after maximal exhalation- we can never breathe everything(all air) out
17
Q
lung capacity
A
Two or more lung volumes together
18
Q
Total lung capacity
A
Maximum volume to which the lungs can be expanded with the greatest possible inspiratory effort
Total lung capacity = Vital capacity + Residual volume
* (all air)
19
Q
Vital capacity (VC)?
A
The maximum amount of air that can be moved into and out of lungs with one breath
Vital capacity = Inspiratory reserve volume + Tidal volume + Expiratory reserve volume
*One breath (everything but residual volume)
20
Q
Inspiratory capacity?
A
Amount of air that can be inspired beginning at normal expiratory level and distending lungs to maximum amount
Inspiratory capacity = Tidal volume + IRV
21
Q
Functional residual capacity?
A
Amount of air that remains in the lungs at the end of a normal expiration
Functional residual capacity = ERV + RV
22
Q
Anatomical dead space*
A
volume of air in trachea and bronchi not involved in gas exchange
23
Q
Physiological dead space
A
volume of air in all other lung regions(i.e. alveoli that are not functional or are already maxed out) that is not involved in gas exchange
24
Q
ALVEOLAR VENTILATION
VOLUME (VA)
**Exam
A
VA = (tidal volume(VT) - dead space(VD))*breathing frequency(f)
= the total effective ventilation of the lungs per unit time
ex. VA = (500 - 150 ml/breath) x 12 breaths/min = 4200 ml/min
25
Minute Ventilation (VE)
Minute Ventilation = tidal volume(VT) * breathing frequency(f)
*includes dead space unlike VA
26
*why is Increased depth of breathing more effective than increased rate
shallow/fast breathing is not good because there is too much dead space and so less O2 getting in and CO2 getting out
27
describe how the pressure gradient for air flow is created during inhalation/inspiration
Somatic motor neurons trigger
contraction (by releasing Ach) of:
1. diaphragm
(moves downward)
2. external intercostal muscles
of ribcage and scalenes (ribs move outward/
upward)
*Muscle contraction increases volume of thorax
-Outer layer of pleural sac pulled outward = decrease in
intrapleural pressure
-Lungs expand and alveolar pressure decreases
->Air flows into the lungs
28
describe how the pressure gradient for air flow is created during exhalation/expiration
Nerve impulses from somatic motor neurons stop =
muscles stop contracting:
Thorax decreases and intrapleural pressure increases
- Elastic recoil of lungs decreases lung volume
- Air is forced out of lungs
diaphragm moves up and ribs move down
29
describe intrapleural pressure
Cohesive forces exerted by the fluid between the
two pleural membranes cause the lungs to adhere
to the thoracic cage
-Intrapleural pressure is subatmospheric (created by outward pull of the thoracic cage and inward pull of elastic lungs)- helps to keep lungs inflated
-if the sealed plural cavity is opened to the atmosphere, air flows in and lungs collapse to unstretched size)
30
THE WORK REQUIRED TO
| VENTILATE/BREATHE DEPENDS ON:
Compliance:
- Ability of the lung to stretch (reduced by *surface tension) -surfactant aids with compliance by reducing surface tension
-Affected in fibrotic lung disease- scar tissue makes lungs inelastic (CF)
Elastance:
- Ability of the lung to return to its original shape
- Affected in emphysema(have to force air out consciously bc lose ability to deflate naturally), COPD/smokers
31
SURFACTANT
Lipoprotein complex that reduces surface tension
(reduces tendency of airway alveolar walls to stick
together)
-Produced by type II alveolar cells
32
LAW OF LAPLACE
-Surface tension created by
thin film of fluid is directed
toward the center of alveoli bubble
and creates pressure in
interior of bubble (O2 cant cross large fluid layer to capillary)
-law states that the
pressure is a function of the
surface tension of the fluid
and the radius of the bubble (small bubble = more pressure)
Pressure = (2 * ST of fluid)/Radius of bubble
33
SURFACTANT IN NEWBORNS
Synthesis begins ~25th week of fetal development (adequate levels by 34th week)
-Premature babies = respiratory distress syndrome bc they dont have enough surfactant to reduce surface tension in alveoli and so they collapse
Treatment: artificial surfactant and ventilation
34
by the time O2 reaches the capillaries it is around a Partial pressure of around 100mmHg instead of 160mmHg like it was to begin with in dry air. why might this happen?
-it decreases because it mixes with stale air in dead space on its way to capillaries
35
What can cause a decrease in the PO2 in the arterial blood? (what changes the partial pressure of O2 in the blood?)
- not good diffusion
- sickle cell anemia (O2 not easily transported)
- Less O2 coming in from environment
36
what are the two causes of low alveolar PO2?
1. Inspired air has low O2 content
2. Alveolar ventilation is inadequate (hypoventilation)
- Due to shallow breathing, decreased lung compliance, increased airway resistance (asthma and CF), CNS depression
37
Diffusion rate of O2 into arterial blood is directly proportional to:
Surface area x concentration gradient x barrier permeability of walls
38
Diffusion rate of O2 from alveoli into arterial blood is inversely proportional to:
Diffusion distance
| -shorter distance = greater diffusion rate
39
describe some pathologies that lead to hypoxia (less O2 getting into blood from alveoli)
1. emphysema- alveoli have less SA for gas exchange
2. CF- alveoli walls are thick decreasing lung compliance and therefore slowing gas exchange
3. pulmonary Edema- increased diffusion distance due to fluid build up in interstitial space
4. Asthma- increased airway resistance bc bronchioles constricted (decreases alveoli ventilation-less O2 in alveoli)
40
O2 Transport in the Blood?
a little dissolves in the plasma/blood, but 98% binds to hemoglobin inside RBC's and transported throughout blood (Leaves RBC where needed)
41
what is our healthy O2 carrying capacity of RBC's?
200mL O2 per L of blood =total amount of O2 that can be carried by each unit of volume
42
what determines how much O2 is bound to hemoglobin ?
1. how much O2 is in the bloodstream/plasma (determines % saturation of Hb)
2. Amount of Hb (determines total # of Hb binding sites-Hb content per RBC * # of RBC's)
therefore, amount of O2 bound = % saturation of Hb * # of Hb binding sites
43
what is blood doping
people inject themselves with erthropoictin to increase RBC's(Erythropoiesis) and increase O2 carrying capacity
44
*oxyhemoglobin
If O2 is bound
45
*deoxyhemoglobin
If O2 is absent
46
methemoglobin
If oxidation occurred, iron atoms would be converted from F2+ to F3+ → Hb could not bind to O2
47
O2 BINDING
| CHARACTERISTICS (to Hb)
1. O2 binds to heme groups (1:1)
2. Four O2 bind to one molecule of Hb
3. The extent to which O2 is bound to Hb varies with PO2 (higher PO2 in blood=more binding to Hb)
4. Affinity of Hb for carbon monoxide is ~200x greater than O2
48
how do you use graph to determine what has a greater affinity for O2 (myoglobin or Hb?)
*******ON EXAM
you find P50 for both (the PO2 at which 50% of Hb is saturated with O2)
• low PO2 (i.e. low P50) = high affinity for O2
• high PO2 (i.e. high P50) = low affinity for O2
(Affinity and P50 are inversely related: as P50 increases, O2 affinity decreases)
49
THE POSITION OF THE OEC (P50 or % saturation of Hb?) IS ALTERED BY A
NUMBER OF FACTORS:
```
pH (Bohr effect)
CO2
Temperature
Organic phosphates
Development
```
50
What happens when you change the pH of the blood?
| *****exam
A decrease in pH/more acidic shifts the curve to the right (Less affinity for O2 bc a higher P50)
ex. muscles need O2 when doing cardio, lactic acid build up makes blood more acidic and lowers Hb affinity (offload more O2 onto tissues)
51
How does shifting pH affect Hb – O2 binding?
* changes Hb affinity
HbO2 + H+ ↔ HbH+ + O2 (H+ acts as an allosteric
modulator)
-Increasing H+ concentration (decreasing pH) favours the dissociation of O2 which dissolves into tissue
52
How does CO2 affect Hb – O2 binding?
| ****** Exam
CO2 + H2O ↔ H2CO3 (carbonic acid doesnt stay long)
H2CO3 ↔ H + + HCO3- (bicarbonate)
CO2 + H2O ↔ H + + HCO3- (overall)
-CO2 interacts with water to make carbonic acid which quickly forms bicarbonate (Makes blood more acidic and protons kick off O2 from Hb)
53
explain the Bohr effect
-In the systemic tissues, CO2 is higher and pH is lower
than in lungs
-Bohr effect shifts to lower Hb-O2 affinity in systemic
tissues
Bohr effect shifts to higher Hb-O2 affinity in respiratory
organ
*goal is to maximize O2 delivery to tissues
54
Fixed-acid Bohr effect vs CO2 Bohr effect
Fixed-acid Bohr effect: results from the influences
of the H+ concentration on Hb
CO2 Bohr effect: results from the direct influences
of PCO2 on Hb
55
What happens with Hb affinity when you change the temperature of the blood?
higher temps = less Hb affinity for O2
56
WHAT HAPPENS WITH ORGANIC
| PHOSPHATES (on Hb affinity)?
more organic phosphates/2,3 DPG(diphosphoglyceric acid) = lower O2 affinity
during fetal development 2,3 DPG control is higher than in adults and lowers the affinity for O2 and takes O2 from maternal blood (everything set up so more O2 is offloaded to fetus)
57
CO2 TRANSPORT IN BLOOD
-Only 7% of the CO2 remains dissolved in plasma
->At the lungs, dissolved CO2 diffuses out of the plasma.
-Nearly a fourth of the CO2 binds to hemoglobin, forming carbaminohemoglobin
-70% of the CO2 load is converted to bicarbonate and H+ (Hemoglobin buffers H+)
->HCO3 enters the plasma in exchange for Cl-
(the chloride shift)
*transformed back to CO2 when gets to lungs where is it diffuses across alveoli membrane then out
58
how is ventilation influenced?
-Neurons in the medulla control breathing(and HR)
-CO2 is the primary stimulus in mammals
-Sensory input from chemoreceptors to the medulla
helps maintain blood gas homeostasis
59
role of peripheral chemoreceptors in ventilation
- Located in carotid and aortic arteries
- Constantly sensing the pressure in blood (How much O2 and CO2 in blood before it gets to brain)
- always relaying info to the brain
- respond primarily to PO2 changes (opposite to the central receptors in brain which primary responds to PCO2 changes)
- signals medulla to increase ventilation if PO2 is low (less O2=less ATP = K+ channels cant open and cell becomes more positive= cell depolarizes and Ca2+ channels open= NT's released to sensory neurons and info sent to medulla to control ventilation)
60
Intracellular responses to low PO2 levels
hypoxia-inducible factors are formed and responses are elicited to cope with low intracellular O2
Erythropoiesis(make new RBC's)
Synthesis of glucose transporters
Synthesis of enzymes of anaerobic glycolysis (to speed up ATP production)
Angiogenesis (new blood vessels)
61
CIRCULATORY SYSTEM?
Pressure driven bulk flow of fluid that rapidly transports O2, CO2, nutrients, organic wastes, hormones, immune system agents, heat, and other commodities throughout the body
62
Peripheral circulation?
1. Propulsive/pushing forward organ
2. Arterial system
3. Capillaries
4. Venous system
63
BLOOD FLOW THROUGH THE CIRCULATORY SYSTEM
Lungs → L. atrium (via pulmonary vein) → L. ventricle
(via bicuspid valve) → body (via systemic aorta)
Body → R. atrium (via superior and inferior venae
cavae) → R. ventricle (via tricuspid valve) → lungs (via
pulmonary arteries)
64
what is unique about the fetal heart
| ******EXAM
has two shunts to avoid blood to lungs(dont need to go to lungs bc O2 is from placenta):
1. Most of blood ejected by R. ventricle is returned to
systemic circuit via *ductus arteriosus
2. R → L atrium shunt through
*foramen ovale causes blood to
be shunted away from the
*Blood flow through pulmonary
circuit is greatly reduced but not completely
65
**Atrioventricular(AV) valves
tricuspid (right) and bicuspid/mitral (left)
| -promote one way flow of blood through heart
66
*Chordae tendineae
prevent AV valves from being pushed into atria
67
what is the Cardiac cycle
from the beginning of one heart beat to the beginning of the next heart beat
Systole = contraction
Diastole = relaxation
(Contraction increases pressure; relaxation decreases pressure)
68
what are the steps of the Cardiac cycle
1. ventricles relax and fill passively with blood (diastole)
2. atria fill the remaining 20% with blood (SL valves still closed and AV valves close *first heart sound-beginning of systole)
3. Enough ventricular pressure to open SL valves and blood is ejected (systole)
4. ventricles relax/ pressure drops and begin to fill passively with blood again (SL valves close-second heart sound- diastole)
69
how is the cardiac cycle started?
| *************EXAM
cumulative depolarizations of the heart muscles within the atria ->initiated by sinoatrial (SA) node*Pace maker of heart
-Autorhythmic (pacemaker) cells in the right atrium
responsible for generation of the rhythm of the heart
->Cells exhibit the highest frequency of spontaneous
depolarization
->Initiates *conduction (process by which depolarization
spreads through the heart) via gap junctions
70
Ventricles contract simultaneously and eject equal
volumes of blood, but why does left ventricle develop
higher pressure
-it is larger and generates more pressure bc it has to bring blood a much greater distance and there is more resistance
Lower resistance in pulmonary circuit
-Many capillaries arranged in parallel
-Relatively short distance
71
End-diastolic volume:
| End-systolic volume:
- maximum volume of blood in the ventricle
| - volume of blood in ventricle at end of contraction
72
what is stroke volume (SV)
| ***********EXAM
volume of blood pumped by one ventricle in one heart beat
EDV – ESV = stroke volume(mL/beat) OR
cardiac output (CO) / heart rate = stroke volume
(mL/min)/(beats/min) = mL/beat
70mL = normal SV
73
what is cardiac output?
volume of blood pumped by the heart in 1 minute (mL/min)
74
describe the depolarization spread from SA node to ventricle contraction (conduction)
autorhythmic cells in SA node in right atrium spontaneously depolarizes and spreads to AV node which electrically connects atria to ventricles, where depolarizations spread down bundle branches->parkinje fibres-> to apex and travels upward to stimulate AP which makes ventricles contract
-spreads via gap junctions to contractile cells
75
THE ELECTROCARDIOGRAM?
| ********know heart traces
Recording of the summed electrical activity of the heart (indirectly measures the depolarizations and depolarizations of the heart cells
-has 5 identifiable deflections (P,Q,R,S,T)
76
explain the different waves from an electrocardiogram
P wave = cumulative depolarizations of atria (started from SA node)
QRS wave = depolarizations of the ventricles and atrial repolarizations (masked bc smaller)
T wave = ventricle repolarizations
77
explain the different intervals/segments from an electrocardiogram
P-Q/P-R interval = time b/w beginning of atrial depolarization and beginning of ventricle depolarization (conduction b/w AV node and AV bundles)
ST interval = ventricles contract
78
what is Sinus Bradycardia?
slowing of heart rate -takes longer to depolarize and repolarize heart muscles
*only dangerous if HR is too slow, otherwise this is good
79
Sinus Bradycardia?
sinus rhythm with an elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult
80
Arrhythmia
lack rhythm to HB (distance b/w complexes change)
81
describe 1st,2nd and 3rd degree AV block
| *results in bradycardia
1st degree: disease of the electrical conduction system of the heart in which the PR interval is lengthened(constant) slightly
2nd degree: even longer interval and may even skip QRS complexes
3rd: most QRS complexes are missing (complete block at AV node and no conduction to ventricles)
82
Left Ventricular Hypertrophy?
enlargement and thickening (hypertrophy) of the walls of your heart's main pumping chamber (left ventricle) and QRS complex really large
-may be due to high BP or heart condition
83
what is atrial and ventricular fibrillation
atrial fibrillation: absence of P waves and irregular ventricular rhythm
ventricular fibrillation: absence of QRS complexes
84
BLOOD PRESSURE? what is it and what does it depend on
Force exerted by the blood against a vessel wall
-Depends on the volume of blood contained within the
vessel and the compliance of the vessel walls
85
what is systolic and diastolic pressure
| ****************KNOW
Systolic pressure: max pressure exerted in the arteries
when blood is ejected in them during systole (~120
mmHg)
Diastolic pressure: min. pressure in arteries when blood is draining into other vessels during diastole (~80 mmHg)
86
what is pulse pressure
systolic pressure - diastolic pressure
87
MEAN ARTERIAL PRESSURE? what is it proportional to?
| ****************KNOW
MAP = diastolic pressure + 1/3 (systolic pressure - diastolic pressure)
MAP = DP + 1/3(pulse pressure)
= 80 + 1/3 (120 – 80 mm Hg)
= 93 mmHg
-MAP is proportional to cardiac output x arteriolar resistance
88
Korotkoff sounds
sounds are
created by pulsatile blood
flow through compressed
artery
89
THE RELATIONSHIP BETWEEN
| PRESSURE, RESISTANCE, AND FLOW
Blood flows down a pressure gradient
- >Flow depends on ∆ pressure, not absolute pressure
- >Flow is directly proportional to ∆ pressure/resistance (no change in pressure = no blood flow in artery)
90
Three factors affect resistance:
| **********KNOW
1. Length of blood vessels
2. Viscosity of blood
3. Radius of blood vessels
91
Vasoconstriction vs vasodilation
Vasoconstriction: decrease in blood vessel diameter
Vasodilation: increase in blood vessel diameter
92
DISTRIBUTION OF BLOOD TO THE TISSUES (is dependent on what??)
Varies depending on metabolic need (blood distributed differently depending on what youre doing. ex. when exercising more blood to legs)
Determined by:
1. Number and size of arteries supplying organ
2. Resistance of arterioles
*Kidneys receive 20-25% of cardiac output even though they only constitute ~0.4% of total body weight!
93
how is blood Flow through capillaries regulated by precapillary sphincters
- If precapillary sphincters are constricted, blood flows through metarterioles to venous circulation (bypass capillaries)
- if precapillary sphincters are relaxed, blood flows through all capillaries in bed
94
Factors that enhance exchange of O2/blood at the capillaries? (3)
1. Capillary walls are very thin (1 μm)
2. Capillaries are very narrow (7 μm diameter)
3. No cell is farther than 0.1 mm away from a capillary
95
how does xchange of O2/blood at the capillaries occur? (3 ways)
Exchange can occur through:
1. diffusion-
2. vesicular transport-
3. bulk flow- mass movement of fluid between the blood and interstitial fluid (absorption and filtration of fluid via
96
Forces influencing bulk flow? (4)
| ***********KNOW
STARLING FORCES:
1. Capillary blood (hydrostatic) pressure
- Fluid pressure exerted on inside of capillary walls by blood
2. Plasma-colloid osmotic pressure
- Osmotic pressure exerted by plasma proteins
3. Interstitial fluid hydrostatic pressure
- Fluid pressure exerted by interstitial fluid on outside of capillary walls
4. Interstitial fluid-colloid osmotic pressure
- Osmotic pressure exerted by interstitial fluid proteins
97
Hydrostatic and colloid pressure gradient favor absorption or filtration?
*******
```
Hydrostatic pressure gradient (Pcap – PIF):
favors filtration (movement OUT of capillaries)
```
```
Colloid osmotic pressure gradient (πcap – πIF):
favors absorption (movement IN capillaries)
```
98
how to find net pressure at capillaries (will there be filtration or absorption??)
Net pressure = hydrostatic pressure gradient - colloid osmotic pressure gradient
= (Pcap – PIF) - (πcap – πIF)
-Net fluid flow across the capillary is determined by
the difference between the hydrostatic pressure
gradient favoring filtration and the colloid osmotic
pressure gradient favoring absorption
99
describe the net pressure at arteriole and venus end of capillary bed
***********EXAM calculation question
arteriole end favors filtration and venus end favors absorption
(Net pressure = neg, then absorption is happening)
100
In detail, what happens with an increase in Blood Pressure?? (include every system)
********potential exam essay question
- BP increase is picked up by stretch sensitive mechanoreceptors (baroreceptors) and relayed to brain
- SP NS will decrease force of contractile cells (so ventricle will contract with less force decreasing cardiac output) and decrease activity of pace maker cells in SA node to slow HR (release NE)
- PS NS cause smooth muscle to dilate (vasodilation) so BP goes down (release Ach)
- greater parasympathetic control of autorhythmic cells (decreases cardiac output which decreases stroke volume which decreases BP and neg feedback to baroreceptors to stop firing)
- angeotensin 11 decreases Sympathetic output to lower BP
- ADH release is inhibited bc it constricts blood vessles causing increase in BP in order to increase blood vol
101
BARORECEPTOR REFLEX?
```
Homeostatic control of blood pressure:
-Baroreceptors: tonically active stretch-sensitive
mechanoreceptors located in walls of carotid arteries
and aorta (sense pressure changes by responding to change in the tension of the arterial wall and relay info to medulla cardiovascular control centre which alters S and PS control on heart)
```
↑ blood pressure = ↑ in baroreceptor firing
↓ blood pressure = ↓ in baroreceptor firing
102
MAIN FUNCTION OF THE KIDNEY:
Homeostatic regulation of the volume and composition
of the blood plasma by means of controlled excretion of
solutes and water
103
other functions of kidney?
- Excretion of wastes
- Homeostatic regulation of pH
- Production of hormones
104
pathway from surface of kidney(renal pyramid) to inside/ureter
Renal pyramid → renal papilla
→ minor calices → major calyx
→ renal pelvis → ureter
105
location of nephron in kidney
80% contained in cortex; 20% in medulla
- Cortex contains all Bowman’s capsules and tubules
- Medulla contains loops loops of Henle and collecting ducts
- each nephron has two sets of capillaries(glomerulus and peritubular) and two arterioles(efferent and afferent)
106
describe pathway of Portal system:
afferent arterioles → glomerulus → efferent arteriole
→ peritubular capillaries → renal venules
-vascular system in which blood flows
from one capillary bed to another capillary bed
without passing through the heart in between
107
juxtaglomerular apparatus
a structure that regulates the function of the nephron; secretes renin
108
Vasa recta:
the peritubular capillaries that surround the loop of Henle
109
4 processes in the nephron
| *********
1. Filtration: movement of fluid from blood to nephron/lumen (= filtrate)
2. Reabsorption: movement of substances in the filtrate from nephron/lumen back into blood/peritubular capillaries
3. Secretion: movement of selected molecules from blood to the nephron/lumen
4. excretion: water/solutes from lumen to external environment
110
how to calc the amount of solute excreted?
amont filtered - amount reabsorbed + amount secreted (usually less than 1% from initial 20% of fluid is excreted from nephron)
111
Filtration fraction:
the percentage of total plasma volume
| that filters into the tubule
112
Three filtration barriers?
1. Glomerular capillary endothelium
- Mesangial cells (smooth muscle cells that regulate blood flow through capillaries)
2. Basal lamina
- Acellular layer of extracellular matrix
3. Epithelium of Bowman’s capsule
- Podocytes
113
GLOMERULAR FILTRATION RATE
| *********
the volume of fluid that filters into Bowman’s
capsule per unit time (avg = 125 ml/min or 180 L/day)
-Influenced by filtration coefficient and net filtration
pressure
GFR = Kf x net filtration pressure
114
Filtration coefficient depends on:
- Surface area of glomerular capillaries
| - Permeability of interface between capillaries and Bowman’s capsule
115
NET FILTRATION PRESSURE
1. Hydrostatic pressure: pressure of blood flowing through glomerular capillaries
2. Colloid osmotic pressure: pressure of proteins in plasma
3. Bowman’s capsule hydrostatic pressure: pressure of fluid within Bowman’s capsule
116
what happens when Vasoconstriction of afferent arteriole?
- increases resistance
- decreases renal blood flow(less blood to kidneys)
- decreases capillary blood pressure(bc less blood to push on walls)
- decreases GFR
117
Vasoconstriction of efferent arteriole:
- increases resistance
- decreases renal blood flow(slower)
- increases capillary blood pressure(resistence causes blood to flow backwards=more p)
- increases GFR (more blood getting kidneys)
118
what is the primary driving force for renal reabsorption
Active reabsorption of Na+
119
NA+ REABSORPTION IN THE
| PROXIMAL TUBULE
Na+ concentration in filtrate is higher than in cells →
Na+ can passively enter tubule cells down its
electrochemical gradient
-Once inside tubule cells, Na+ is actively transported
out across basolateral membrane in exchange for K+
120
what does renin do
convert angiotensinogen to angiotensin 1 which is converted to angiotensin 11 at the lungs which stimulates brain to release ADH and stimulates adrenal gland to release aldosterone (which both act on kidney to reabsorb Na+ and water)
-Cells in juxtaglomerular apparatus secrete renin
121
when is renin secreted
Renin secreted in response to low blood volume, low blood pressure, or ↓ in NaCl
122
function of aldosterone in kidney (2)
1. changing expression of proteins (increasing pumps/channels)
2. increasing activity of channels (stay open longer for Na to go out of nephron and K to come in)
123
WHY IS COUNTERCURRENT FLOW IN
| THE VASA RECTA IMPORTANT?
It establishes a vertical osmotic gradient that
| can be used by the collecting duct to reabsorb water
124
renal threshold
```
conc in plasma in which saturation occurs
-At saturation, the
remaining
concentration of
the substrate will
be excreted in the
urine
```
125
Clearance
Rate at which a solute disappears from the body by excretion or by metabolism
-Clearance is ml of plasma cleared of a substance per
min
Clearance of X = Excretion rate of X (mg/min) / [X]plasma (mg/ml plasma)
126
Inulin
polysaccharide
used to
determine
clearance
127
when does clearance = GFR
| **********
when no reabsorption or secretion
128
hormone types
1. Peptide hormones- need preprohormomne, vesicles, dissolve in plasma, cant freely cross membrane so binds to MBR's, terminated by peptidase
2. Steroid hormones-derived from cholesterol, Synthesized and secreted from the gonads, adrenal gland, and placenta(no vesicles), freely crosses membrane, longer half life, may enter cell(slow gene expression) or bind on surface receptors, broken down by liver and excreted
- estrogen, testosterin, progesterone,Glucocorticoids(cortisol), Mineralocorticoids(aldosterone)
3. Amine hormones:
made from tyrosine, some act liike peptide h, some act like steroid h
Exocytosis (catecholamines) and diffusion (thyroid hormones)
Membrane-bound receptors (catecholamines) and
intracellular receptors (thyroid hormones)
Epinephrine
Norepinephrine
Dopamine
Triiodothyronine (T3)
Thyroxine (T4)
Melatonin
