Exam 4 Flashcards
1
Q
Main Role of Respiratory System
A
- supply oxygen: creates ATP
- eliminate CO2: comes from krebs cycle and pyruvate metabolism-toxic-acts as acid in the bloodstream so pH lowers; system is built to monitor pH and get rid of CO2 first
- these functions aren’t directly related
2
Q
Conducting Zone
A
- aka anatomical dead space
- tubing through which we pass air-lungs too deep to just diffuse ari-no gas exchange
- functions: warms and humidifies air; uses mucous and cilia to trap foreign objects and move it back
3
Q
Respiratory Zone
A
- site of gas exchange-O2 into blood and CO2 out
- parts: respiratory bronchioles and Type I and II alveolar cells
4
Q
Type I Alveolar
A
- gas exchange
- rely on how thin the water layer inside alveoli are
- want it to be as thin as possible to facilitate quicker gas exchange
- any thickening will decrease diffusion (fill with anything like water or mucus will increase thickness)
5
Q
Type II Alveolar
A
- support type I cells
- regulate Na+ and H20: thin layer of water winding inside type I to make sure it doesn’t dry up or crack-potentially increase distance gas travels so want it as thin as possible-so not enough water they place sodium ion outside to draw water into type II; too thick has potential to draw sodium out and bring water in
- put water next to each other and they pull toward each other and stick to create surface tension which could collapse alveoli and lead to entire lung collapse
- secrete pulmonary surfactant to keep water molecules from attracting each other-break ST
- limit to amount they can secrete so too much water could be bad
- release surfactant especially on deep inhale-respond to physical stretch and squeeze it out during deep inhalation
6
Q
Thoracic Cavity
A
- space within ribcage above diaphragm
- heart and lungs in here
- volume of this space modulated pressure-related voluntarily to skeletal muscles surrounding it
7
Q
Diaphragm
A
- relaxed: domed up into cavity
- contracted: pulls down and away which increases TC volume
8
Q
Secondary Muscles Involved in Inhalation
A
- external and parasternal intercostals: contract and pull ribcage outward to increase TC volume
- scalenes: shorten and lift ribcage up and away from diaphragm increases TC volume
- sternocleidomastoid: shorten and lift up and away from diaphragm to increase TC volume
- pectoralis minor-contracts and pulls rib cage up and out to increase TC volume
9
Q
Secondary Muscles Involved in Expiration
A
- abdominal muscles: contract and pull ribcage down toward diaphragm to decrease TCV
- internal intercostals: contract and squeeze ribcage inward and decrease TCV
10
Q
External Respiration
A
- ventilation: moving air into and out of lungs
- gas exchange: moving gas across capillary wall-only transport
11
Q
Internal Respiration
A
-cellular breathing; actual use of oxygen and production of CO2 which is what keeps us alive
12
Q
Major Functions of Renal System
A
- regulation of ECF volume-important for BP; plasma is in ECF so as volume changes BP changes
- regulation of waste products (not elimination)-saving some waste products like urea
- regulation of electrolytes-important to AP’s (Na+, K+) Ca2+, important to muscle
- regulation of blood pH-kept at very accurate point to facilitate proper enzyme function
13
Q
Renal Cortex
A
- 300 mOsm
- isosmotic still pretty concentrated
14
Q
Renal Medulla
A
- varies ~800 mOsm middle and ~1200 mOsm near the core: water watnes to dilute this
- this is how we reabsorb water in the body
15
Q
Minor Calyx, Major Calyx, and Renal Pelvis
A
-collecting areas considered urine at this point
16
Q
Nephron Anatomy
A
- afferent arteriole-feeds nephron
- glomerulus-capillary network
- glomerular capsule-first part of actual nephron whatever crosses becomes filtrate
- efferent arteriole-what doesn’t enter filtrate exits out of this
17
Q
Flow of Blood/Filtrate
A
- afferent arteriole–>capillaries–>efferent arteriole–>peritubular capillaries
- different because it passes through two capillary beds in series
18
Q
Peritubular Capillaries
A
- surround entire nephron
- dump into venules
19
Q
Filtration
A
- water and anything small enough to cross leaving the capillary; passive process/automatic
- mechanism: only occurs in glomerular capillaries into glomerular capsule-only thing going on here
- Pcap=60 mmHg at arteriole end-pushes water out of capillary (dominant force); glomerular capillaries are fenestrated (300 times more permeable)
- results in a lot of filtration very rapidly to keep proper gradients of electrolytes-eliminates excess as rapidly as you absorb it-maintains electrolyte set points
- combination of high hydrostatic force and fenestrated capillaries allows this
20
Q
Glomerular Filtration Rate
A
- total volume of fluid filtered from plasma per minute
- need relative constant rate no matter how many kidneys
- 20% of plasma that enters the glomerulus is filtered into the nephron tubules
- 120 ml per minute and 180 L per day
- need to reabsorb electrolytes at high rate too
21
Q
Autoregulation
A
- normal circumstances
- intrinsic control of GFR
- goal: constant GFR
- triggered by changes in systemic BP (increase in aortic pressure increases pressures as you travel down through vessels
- we do this because if the rate is too fast we lose important things in the urine and too slow toxins build up
- how: constriction of arterioles, want pressure high at the arterial side
22
Q
What would happen to GFR if arterial BP rises and no corrections are made?
A
- no response would mean filtering would happen too fast because increased BP means increased pressure in glomerular capsule which means increased GFR; only have certain surface area to work with and if you overwhelm it you lose stuff in urine
- autoregulation means vasoconstriction of afferent arteriole which reduces Pgc and GFR back to 60 and efferent arteriole will dilate to let blood in there out
- afferent influences 90% of GFR
23
Q
What would happen to GFR if arterial BP decreased and no corrections were made?
A
- filter too slowly changing concentration gradients and allowing toxins to build up in blood
- efferent arteriole will constrict to let less out so it filters and afferent arterial dilates to let more blood in; increases Pgc and GFR
24
Q
Reabsorption
A
- something goes back into capillary after being filtered out
- mechanism: filtrate in lumenal space moves into intracellular fluid of tubule cells then into interstitial fluid then into blood via peritubular capillaries
- result is moving something from inside the nephron into the capillary then into the blood stream
25
Q
Secretion
A
- specific fine tuning mechanism
- active process; actively move something from inside the capillary out into filtrate (back into nephron)
- blood stream to ISF to ICF of tubule cell to filtrate in lumenal space
- result is moving something from peritubular capillaries into the nephron because if we had reabsorbed too much of something or if we didn’t filter enough of something we push the excess into the nephron to get rid of it
- we have set points for all the different aspects in our blood stream
26
Q
Regulation of Glucose (and amino acids)
A
- filtration: 20% of what is in plasma will all go at same rate and end up in nephron with potential to become urine but we don’t want to lose 20% of glucose because we need it for energy
- reabsorption: want 100% of load in nephron reabsorbed in PCT; secondary co-active transport with sodium; wants to go down gradient so we allow it to do that by bringing glucose with
secretion: not helpful in normal circumstances so normally have 0 glucose in urine
27
Q
Why is the condition glycosuria observed in untreated diabetes mellitus?
A
- too much glucose in the bloodstream and 20% reabsorbed
- doubling the amount in the blood means we double the amount that needs to be filtered but we have a limited amount of pumps and transporters so they become saturated and only pace it can go is out of the urine
- transporters only exist in PCT; glucose draws water toward it as it passes through nephron and prevents reabsorption of water which increases thirst and urination
28
Q
Potassium
A
- found in highest concentration in intracellular fluid
- it does repolarization in AP’s which will stop if it’s not moving how it’s supposed to
- uses secondary co-active transport
- if increased [K+] found in ECF, disruption of AP’s and electrical gradients/potentials so communication breaks down
29
Q
Regulation of Potassium
A
- filtration: 20% of a relatively small quantity because it comes from the ECF
- reabsorption: PCT; sodium potassium pump (primary active transport) K+ in nephron moves from outside cells to inside cells very effectively and 100% is reabsorbed
- why? very few ions and lots of quick working transporters are able to pull every ion back into the body
- secretion: in DCT; K+ reabsorbed too effectively so we have more than we need in bloodstream so eventually peritubular caps secrete excess above set point back into nephron to get rid of it and maintain balance
- see no K+ in loop of henle because they come back in DCT
30
Q
Regulation of Sodium and Water
A
- high concentrations of Na+ and H2O in ECF
- need whole nephron because of large quantity
- filtration: 20% or each in GC but have very large quantities
- reabsorption: PCT almost 99% of each; how: secondary co-active transport pulls sodium across first so water follows-permeability relies on presence of aquaporins-water will only go through if there’s osmotic draw and we create this when sodium goes through
- 65% reabsorbed in PCT
31
Q
Reabsorption of Sodium in Loop of Henle
A
- establishes vertical concentration gradient: as you go down deeper into the medulla, the concentration rises; established in ascending limb because there are no aquaporins so water is not reabsorbed here so prevents dilution and creates this gradient that we use in the collecting duct
- Na+ reabsorption only happens in ascending limb of loop
- osmolarity inside this part of the loop will decrease because water is staying and sodium is leaving
- urea also helps establish concentration gradient
32
Q
Urea
A
- regulated, not eliminated
- metabolic byproduct
- technically waste
- osmotically active-draws water toward it to dilute it
- 50% filtered urea in nephron pulled back into medulla of kidney and stored in ISF to help make concentration gradient
- absorbed by kidney and stays locally in medulla till it’s needed
- combo of urea and sodium creates gradient (1200 mOsm)
- use of urea means we don’t use large amounts of sodium because we’re using this regulated waste product so Na+ can be sent out to body where it’s needed
33
Q
Reabsorption of Water in Loop of Henle
A
- only happens in descending loop because it has aquaporins
- water leaving has no chance to dilute the ISF because peritubular capillaries bring it in: oncotic pressure gabs water due to the plasma proteins and it gets stuck before it even has a chance to dilute ISF
- Na+ not affected here because there are no transport proteins
- osmolarity inside the loop will increase because of water loss and sodium retention
34
Q
Glomerular vs. Peritubular Capillary Pressures
A
- Pcap is 60 mmHG
- oncotic pressure of capillary is 25 mmHg: constant
- glomerular is only filtering because the Pcap is so high
- peritubular: lose large percentage of water which increases osmolarity and decreases total blood volume which means dehydrated blood and a decrease in pressure
- the long and dense peritubular network creates friction and resistance so Pcap is decreasing so you switch to net absorption which means oncotic capillary pressure is dominant force to reabsorb water and re-hydrate blood to send out to body
35
Q
Net Result Through Loop of Henle
A
- another 27% of water and sodium reabsorbed in loop and vertical concentration gradient is made
- 97% overall reabsorption of water and sodium
36
Q
Reabsorption in DCT
A
- sodium reabsorption adjusted here
- final 7-8%
- related to aldosterone levels and dietary sodium levels
- 7500 g of sodium in body and we filter 1500 g/day which is part of our set point
- reabsorption rate is amount reabsorbed/amount filtered (set point sodium and dietary extra)
- no matter high sodium vs. low sodium diet rate is still within the last percentage so what we eat is just a tiny drop in the bucket compared to our overall levels
- net result is 99% reabsorption in DCT
37
Q
Reabsorption in Collecting Duct
A
- water reabsorption adjusted here
- final 5-7%; not 7-8% because we need to lose some water to dilute solutes and create urine
- related to ADH levels and intake of water
- water is not secreted
- ADH inserts aquaporins into collecting duct so water is drawn out
- net result is reabsorption of 97-99% of water
38
Q
Role of DCT
A
- secretion of hydrogen ions from capillaries to the nephron
- reabsorption of bicarbonite ions
- balance between these two keep blood pH at 7.4
39
Q
Metabolic Disorders
A
- systemic disorders that are misbalaance in pH
- metabolic acidosis
- metabolic alkalosis
40
Q
Metabolic Acidosis
A
- 7.35 and below
- increased acid production in body
- systemic cause: stomach tumor increases pH because of increased acid production-proliferation of parietal cells that make this acid which eventually seeps into bloodstream
- kidney secretes hydrogen ions into nephron to try to get rid of them and reabsorb more HCO3- ions
- kidney failure can also lead to this
- also caused by decreased H+ secretion
41
Q
Metabolic Alkalosis
A
- 7.45 and above
- increased base production: pancreatic cancer-pancreas stores HCO3- ions and if it does this at too rapid of a rate and releases these into ISF blood increases in pH
- kidney failure also means too much HCO3- absorption putting it back into bloodstream
- increased H+ loss as in excessive vomiting
42
Q
Effect of Hormones
A
- help regulate ECF volume by monitoring ISF osmolarity, blood volume, and plasma Na+ concentration within the kidney
- ISF osmolarity is monitored by osmoreceptors in hypothalamus so if ISF is more concentrated it draws water from receptors and signals you’re thirsty
- blood volume regulated by barroreceptors that measure stretch on aortic arch and carotid arteries
43
Q
ADH
A
- released when blood volume is low and ISF osmolarity is high
- stimuli to try to get more water
- mechanism: osmoreceptors and barroreceptors stimulate hypothalamus where ADH is made and is then released from posterior pituitary
- effect: ADH binds to receptors in CD and inserts aquaporins so water is reabsorbed and captured by peritubular capillaries to dilute ISF and increase BV
44
Q
Diabetes Insipidus
A
- 8% of what was filtered that enters CD (3-4 gallons) all goes through so you pee a lot and are thirsty a lot
- ISF osmolarity increases and BP decreases so hypothalamus tells you to drink
- treatment: exogenous forms of ADH-ADH receptor agonist; have to use the right amount to maintain number of aquaporins and have to pay attention to intake
45
Q
Syndrome of Inappropriate ADH
A
- too much ADH produced
- very concentrated urine
- ISF osmolarity decreases and have too much reabsorption which can lead to hyponatremia (low [NA+]) so AP’s don’t occur and secondary active transport doesn’t occur; can lead to edema and increased BP
- treatment: ADH receptor antagonist
46
Q
Aldosterone
A
- indirectly released when plasma sodium concentration is low-want more Na+ in the blood
- juxtaglomerular apparatus: where afferent arteriole contacts DCT and contains macula densa and granular cells
- macula densa: sensory cells; part of DCT that touches arterioles (filaments that touch and monitor content)
- granular cells: part of endocrine system; primary; surround afferent and some on efferent-secrete substance
47
Q
Mechanism of Aldosterone Secretion
A
- macula densa senses plasma [Na+]
- granular cells secrete renin if [Na+] is low (renin is a hormone secreted into the bloodstream so it travels everywhere)
- renin converts angiotensinogen into angiotensin I
- angiotensin I converts to angiotensin II by angiotensin converting enzyme (ACE)
- angiotensin I stimulates secretion of aldosterone from adrenal cortex
48
Q
Effect of Aldosterone Secretion
A
- presence of more Na+ transporters in DCT means more reabsorption
- 92% of Na+ reabsorbed before DCT
- remaining Na+ reabsorbed in DCT to meet body’s needs
- no aldosterone means another 7% so 99% total reabsorbed
- aldosterone present means all 8% remaining is reabsorbed
49
Q
Urine Transport and Release
A
-filtrate–>minor calyx–>officially urine–>major calyx–>renal pelvis–>ureters–>bladder–>internal sphincter–>external sphincter–>urethra
50
Q
Ureters
A
-use peristalsis to contract to send down urine to bladder
51
Q
Bladder
A
- stores urine
- smooth muscle
- when stretched enough it opens internal sphincter which signals your brain to tell you you have to pee (involuntary)
- then you have control over external sphincter and then you can pee when it’s convenient
52
Q
Micturition (Urination)
A
- distension of bladder with urine
- stimulates bladder stretch receptors
- sensory input to spinal cord
- autonomic motor control: reflex contraction of bladder smooth muscle; relaxation of internal sphincter
- voluntary relaxation of external sphincter
- urine flows and contents of bladder lost from body
53
Q
What We Need to Breath
A
- a way to move air into the lungs-ventilation
- a way to keep lungs from collapsing when we exhale-lungs get closer and closer as you exhale because they have little/no structural integrity
54
Q
Intrapulmonary Pressure
A
- pressure inside lung itself
- key issue: lung is passive material that won’t change in size or pressure on it’s own so we want pressure in lungs to increase when pressure in TC increases
- TC muscles control this pressure
55
Q
Air Pressure Gradients
A
- this is what moves air
- high pressure to low pressure
- so in order to bring air in we have to change pressure relative to atmosphere which is 760 mmHg
56
Q
Boyle’s Law
A
-volume of gas is inversely proportional to its pressure
57
Q
Mechanics of Inspiration at Rest
A
- goal: want air to rush into lungs
- needs: lower pressure inside TC (757 mmHg) than outside; 3 mmHg difference needed to bring in 500 ml
- mechanics: contract diaphragm to move down and away to increase volume which decreases pressure so gradient is created to allow air to rush in
