Physio: Lung and Renal Flashcards
1
Q
Part of nervous system controlling bronchodilation
A
Sympathetic
2
Q
Part of nervous system controlling bronchoconstriction
A
Parasympathetic
3
Q
Differences between false vocal folds and true vocal folds
A
False folds are proximal and have glands under their epithelium. True vocal folds are distal and have skeletal muscle (the vocalis m.) beneath their epithelium.
4
Q
Sequence of airways from largest to smallest
A
Trachea => primary bronchi => lobar bronchi (R3, L2) => segmented bronchi => smaller bronchi => bronchioles => terminal bronchioles => respiratory bronchioles => alveoli
5
Q
What histology all feature marks the bronchi to bronchiole transition?
A
Bronchioles have no cartilage
6
Q
What histological feature marks the bronchioles to alveoli transition?
A
The alveoli have no smooth muscle in their walls
7
Q
What is a dust cell?
A
A macrophage in the lung
8
Q
Structure and function of type I pneumocytes
A
Cells in alveolar epithelium with flat nuclei. They appear similar to squamous cells and can differentiate into type II pneumocytes
9
Q
Structure and function of type II pneumocytes
A
Rounder and larger than type I pneumocytes, these cells secrete surfactant. They are often found at the junctions of alveolar walls
10
Q
Mechanism of matching perfusion and ventilation
A
As PO2 in an alveolus drops, arteriolar resistance increases. This prevents blood flow to poorly ventilated areas. As PO2 increases, vascular resistance decreases.
11
Q
Pressure in the lung
A
P(lung) = P(alveoli) - P(pleural space)
12
Q
Compliance: definition and equation
A
D: the distensibility of a tissue
Compliance = dV/dP
13
Q
At high volume, the lung has ______ compliance. At low volume, the lunch has ______ compliance.
A
Low; high
14
Q
Concept of interdependence
A
Pressure in a smaller alveolus is higher than pressure in a lower alveolus. Mitigated with surfactant.
15
Q
Surfactant function
A
Modulation of alveolar surface tension
16
Q
How does surfactant balance pressure between large and small alveoli?
A
In small alveoli, it is more concentrated. Therefore the surface tension is lowered and the volume increases. In large alveoli, the diluted surfactant lowers surface tension less, and the volume decreases.
17
Q
Functions or pleurae and pleural fluid
A
Maintain pressure differential
Fluid lubricates
Fluid helps maintain pleural connection
18
Q
Effect of emphysema on compliance and respiratory function
A
Increases compliance, so tissue is more distensible.
Harder to expel air from lung.
19
Q
Effect of fibrosis on compliance and respiratory function
A
Decreases compliance, so tissue is stiffer. It also increases the elastic recoil.
The lung collapses on filling and it is harder to force air into the lung.
20
Q
Method by which O2 moves from alveoli to the blood and from blood to peripheral tissue
A
simple diffusion
21
Q
Factors that proportionally affect rate of diffusion
A
- solubility of the gas in fluid (constant)
- difference in partial pressures between compartments
- cross sectional surface area
- temperature
22
Q
Factors that inversely affect the rate of diffusion
A
- square root of molecular weight of gas (constant)
2. distance of diffusion
23
Q
How has the respiratory system been anatomically optimized for rapid diffusion?
A
- there is a large surface area formed by the capillary sheets
- the membranes across which the gas must diffuse are very thin, and the alveolar lumen and the RBC are in close proximity to one another
24
Q
structure of hemoglobin
A
two alpha chains and two beta chains form a larger molecule. Each chain contains a heme group, which binds one molecule of oxygen
25
What is allosteric binding in hemoglobin?
As one heme group binds/releases O2, the entire molecule undergoes a conformational change that facilitates the binding/release of the other molecules.
26
compare and contrast the oxygen-hemoglobin dissociation curve with the oxygen-myoglobin dissociation curve
The oxygen-hemoglobin dissociation curve has greater variability over the physiological range than the oxygen-myoglobin curve. Therefore, when partial pressure of O2 is high, hemoglobin is saturated. When it is low, hemoglobin releases oxygen. Myoglobin is saturated across the majority of the physiological range.
27
Explain the relationship between rest/exercise and partial pressure of oxygen in the interstitial tissue
During rest, arterial pO2 is about 94mmHg, giving a saturation of ~97%. Interstitial pO2 is about 40mmHg, giving saturation of ~72%. Therefore, hemoglobin supplies about 25% of is O2 content. While exercising, the interstitial pO2 decreases. this causes hemoglobin to supply more O2 to working tissue.
28
What products of exercise cause a shift in the O2-Hemoglobin dissociation curve ("Bohr effect")?
Increased H+ (decreased pH), increased CO2, increased temperature, increased 2,3-BPG (glycolytic product)
29
How do increased H+ ions (decreased pH), increased CO2, increased temperature, and increased 2,3-BPG affect the O2-Hemoglobin dissociation curve?
Each of these things cause a shift to the right. This means that hemoglobin is less saturated at a given pO2 than it would normally be.
A decrease in these factors causes a shift to the left.
This is known as the Bohr Effect
30
How does anemia alter the supply of oxygen to peripheral tissue?
blood O2 carrying capacity is diminished
pO2 in the alveoli and hemoglobin saturation remain the same
may be compensated by cardiac output
31
How does CO poisoning alter oxygen supply to peripheral tissue?
CO irreversibly binds the heme group, preventing O2 transport. This reduces O2 saturation of hemoglobin. Additionally, carboxyhemoglobin causes the other subunits to increase O2 affinity (shift left)
pO2 in the alveoli remains the same
32
How is O2 transported in the blood?
97% bound to hemoglobin
| 3% dissolved in plasma/RBC cytoplasm
33
How is CO2 transported in the blood?
7% dissolved in cytoplasm/plasma
23% bound to protein (mostly hemoglobin)
70% is dissolved in the form of bicarbonate anions (HCO3-)
34
Write the chemical formula of the bicarbonate buffer
CO2 + H20 H2CO3 H+ + HCO3-
carbonic
anhydrase
35
What is the role of chlorine in the bicarbonate transport system?
Chlorine anions are exchanged for bicarbonate anions at the RBC plasma membrane via a bicarbonate-chloride exchanger protein.
It maintains electroneutrality in the RBC.
36
What is the "chloride shift"?
The change in intracellular chloride content. Venous blood has a higher concentration than arterial blood.
37
Explain how shifts in the CO2 dissociation curve happen (the Haldane effect)
O2 binding to hemoglobin causes CO2 to be released from the blood more effectively. This occurs because O2 binding to hemoglobin causes bound H+ ions to dissociate. These ions bind to bicarbonate to form carbonic acid, which dissociates into CO2 and water. CO2 is displaced directly by O2 binding.
38
Calculate pH from pCO2 and bicarbonate
pH = pK + log{ [HCO3-]p / [CO2 + H2CO3] }
| = pK + log{ [HCO3-]p / 0.03 * pCO2] }
39
What part of the bicarbonate buffer system is under respiratory control, and what part is under renal control?
Respiratory system controls pCO2 directly
plasma HCO3- concentration is under renal control
40
Review the Davenport diagram from CO2 transport lecture
YOU BETTER DO IT TOO, FUCKER
41
Describe respiratory acidosis
increased arterial pCO2 => increased H+ and HCO3- => lower pH
arterial pCO2 > 44mmHg
blood pH < 7.35
42
What can cause respiratory acidosis?
```
decreased alveolar ventilation (drug overdose)
decreased lung-diffusing capacity (pulmonary edema)
decreased diffusion (acute respiratory distress)
```
43
How does the body compensate for respiratory acidosis?
The renal system increases HCO3- to return blood pH to normal levels
44
Describe respiratory alkalosis
decreased arterial pCO2 => decreased h+ and HCO3- => higher pH
arterial pCO2 < 35mmHg
blood pH > 7.45
45
What can cause respiratory alkalosis?
hypoxia
anxiety
drug toxicity
fever
46
How does the body compensate for respiratory alkalosis?
renal system decreases HCO3- to return blood pH to normal levels
47
What are some causes of metabolic acidosis and alkalosis?
```
renal failure
shock
diabetes mellitus
vomiting/diarrhea (severe)
**the respiratory system can compensate in these instances
```
48
Define hyperventilation
breathing is increased more than is required, resulting in lower arterial pCO2 than normal
49
define hypoventilation
breathing is decrased more than required, resulting in higher arterial pCO2 than normal
50
Define hyperpnea
increased breathing to match metabolic needs (during exercise)
51
What do central chemoreceptors detect changes in and where are they located?
They detect H+ ions. They are located in the brainstem, separate from the VRG and DRG.
CENTRAL CHEMORECEPTORS ARE NOT SENSITIVE TO HYPOXIA.
52
What do peripheral chemoreceptors detect changes in?
They detect changes in O2, CO2, and H+ ions.
53
Describe the two regulatory groups of cells that reside in the medulla to control breathing.
The dorsal regulatory group (DRG) and ventral regulatory group (VRG) are located in the medulla. The DRG is mainly inspiratory. The VRG is inspiratory and expiratory, including sending signals to the abdominals during exercise. They generate rhythm via a pacemaker effect.
54
Describe the pontine regulatory group (PRG)
There are two groups: the pneumotaxic center (upper pons) and the apneustic center (lower pons).
The pneumotaxic center turns off inspiration to make the switch to expiration. It is stimulated by medullary inspiratory neurons, which shortens inspiration and increases rate.
The apneustic center's role is unclear.
55
How do central chemoreceptors detect changes in blood pH and pCO2?
The blood brain barrier prevents H+ ions and HCO3- from crossing into the brain. However, these ions react in the blood to form CO2, which easily crosses the barrier. Once across, they dissociate again to cause a drop in CSF pH, which stimulates chemoreceptors to send signals to the DRG to increase ventilation.
56
What is the difference between acute and chronic stimulation of central chemoreceptors?
Stimulation of the respiratory center by increased pCO2 declines over 1-2 days as HCO3- diffuses through the BBB and renal adaptation produces increased blood HCO3-.
The acute effect of pCO2 change is strong, but its chronic effect is weak after only a few days.
57
What are the different types and subtypes of peripheral receptors?
The major types are mechano and chemo receptors. Mechanoreceptors are subdivided into airway, pulmonary, and chest wall receptors.
58
What do airway mechanoreceptors do?
They monitor air temperature as air flows by, and they can coordinate breathing/swallowing in the larynx.
59
What are the different types of pulmonary mechanoreceptors?
slow adapting stretch receptors: located in smooth m. of airways
rapidly adapting stretch receptors: located in airway epithelium
J receptors: located near (juxtaposed) pulmonary capillaries
60
How do rapidly adapting and slow adapting pulmonary mechanoreceptors signal lung status to the brain?
Slow adapting receptors fire while the lung volume is changing and when the lung is full. Rapid adapting receptors only fire while volume is changing.
61
Describe reflex control of breathing through inflation reflex and deflation reflex.
An increase in lung volume stops inspiration and promotes expiration. (inflation reflex)
A decrease ends expiration and promotes inspiration. (deflation reflex)
62
What is the pathway of the Hering-Breuer Reflex?
inspiration => lung inflation => stretch receptors => vagal fibers => impulse frequency increases => apneustic center inhibited => expiration
63
Where are peripheral chemoreceptors located and what do they sense changes in?
They are located in the carotid bodies (most important) and in the aortic arch.
They sense changes in arterial pO2, pCO2, and pH.
64
Rank the sensitivity of peripheral chemoreceptors to pCO2, pO2, and pH changes.
They are most sensitive to hypoxia (decreased pO2).
The peripheral response to pCO2 and pH is less than the response to hypoxia and much less than the central response to decreased pCO2/pH. But the peripheral response occurs more rapidly.
65
Define hypercapnia.
Increased pCO2 beyond the normal range.
66
How does increased CO2 affect the ventilatory response?
It causes a linear increase in ventilation.
67
How does decreased pO2 (hypoxia) affect the ventilatory response?
As pO2 decreases, ventilatory response increases curvilinearly.
The relationship is linear when ventilation is plotted against Hb saturation.
68
Compare the responses to acute and chronic hypoxemia and hypercapnia in the peripheral receptors, the central receptors, and the controller.
Peripheral Central Controller
HYPOXEMIA
acute.............................^^.........................v...........................^
chronic..........................^^^.......................0......................^^^
HYPERCAPNIA
acute............................^^.........................^^^.................^^^^^
chronic.........................^...........................^^....................^^^
69
What is a V/Q matching?
In V/Q matching, the body attempts to perfectly match pulmonary blood flow (Q) and ventilation (V). However, more ventilation than blood flow occurs at the lung apex (V/Q = infinity; "dead space"), and more perfusion than ventilation occurs at the lung base (V/Q = 0; "shunt").
70
What are the types of dead space, and what is dead space?
The types of dead space are alveolar dead space (recruitable) anatomic dead space (nonrecruitable; conducting passages).
Dead space is areas that are ventilated but not perfused.
(V/Q = infinity)
71
What is a shunt?
A shunt occurs when a portion of blood flow is able to bypass the lung. Either there is a left/right vascular shunt, or a portion of the lung does not receive ventilation (V/Q = 0).
72
How do you assess for a shunt?
Put the patient on 100% O2 for ___ minutes and obtain a blood gas. pO2 should increase to approximately 700mmHg. For every 100mmHg below 700, estimate a 5% shunt.
73
What is hypoxemia?
A low pO2 in the blood, or a low Hb saturation
pO2 less than 60mmHg or Hb sat less than 90%
74
What is hypoxia?
Low O2 delivery to an organ or tissue
75
What is respiratory failure?
When the lung fails to oxygenate arterial blood adequately and/or fails to eliminate CO2 adequately
76
What are the two types of respiratory failure?
Type 1 failure - hypoxemic respiratory failure
low blood pO2, inability to transfer adequate O2 from alveoli to
capillary space (DOES NOT include anemias)
Type 2 failure - hypercapnic respiratory failure
increased pCO2
77
What are the six types of hypoxemic respiratory failure?
1. low fraction of inspired O2 (Fi O2)
2. low barometric pressure (Pi O2)
3. alveolar hypoventilation/increased CO2
4. shunt
5. ventilation-perfusion inequality
6. diffusion impairment
78
What is the A-a gradient? What is normal and abnormal?
alveolar O2-arterial O2 gradient
Normal is less than 20, but patients with low O2 available (altitude/fire/high CO2) will also have this reading. Elevated is greater than 20, suggesting a shunt, V/Q mismatch, or diffusion impairment.
79
What are the three types of shunts?
1. intrapulmonary: a blockage of an air passage prevents ventilation in a portion of the lung that is being perfused.
2. intracardiac: direct passing of blood from right to left circulation
3. extracardiac: a shunt not in the lungs or heart
80
What are various examples of pulmonary shunts?
- pneumonia
- ARDS
- near drowning
- all alveolar filling processes (blood, pus, cells)
81
What are some causes of cardiac shunts?
- ASD
| - VSD
82
What are some extracardiac shunts?
- arterial-venous malformations
| - hepatopulmonary syndrome
83
What are some possible causes of V/Q mismatch?
- pulmonary embolism
- asthma
- COPD
- CHF
84
What is pascal's law?
Pressure applied to a fluid is transmitted equally throughout the fluid.
85
What is Dalton's law?
Pressure of a gas mixture is equal to the sum of the pressures of the gases that make up the mixture.
86
What is Boyle's law?
For a fixed mass of ideal gas at fixed temperature, pressure and volume are inversely related.
87
What is Henry's law?
At constant temperature, the amount of a given gas dissolved in a given type and volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with the liquid.
88
What are the functions of the kidneys?
1. regulation of total body water
2. long term blood pressure regulation
3. maintenance of the extracellular fluid volume
4. excretion of waste products
5. regulation of electrolyte concentrations
6. elimination/breakdown of foreign substances
7. acid-base balance
8. red blood cell formation (secretes erythropoeitin)
9. bone homeostasis (1-hydroxylation of vitamin D3)
10. gluconeogenesis
89
What is simple diffusion?
Movement of a substance down its electrochemical gradient caused by Brownian motion. No carrier molecules are involved.
90
What is facilitated diffusion?
Net movement of a substance down its electrochemical gradient involving channels. Exhibits specificity, saturability, and competition.
91
What is primary active transport?
Primary active transport uses energy to transport a substance up its concentration gradient.
92
What is secondary active transport?
Secondary active transport is when a second molecule is coupled to the facilitated diffusion of another substance. The diffusion of the carrier down its concentration gradient is used as energy to transport another molecule against its gradient.
93
What is osmosis?
The diffusion of water down its concentration gradient across a semi-permeable membrane. Direction is from areas of low osmolarity to areas of high osmolarity.
94
Review the concentration/volume charts in the body fluid compartments lecture.
I WILL FUCKING STAB YOU IF YOU DON'T, YOU HILLJACK
95
Explain hypotonic expansion, as can occur from the ingestion of water.
An influx of water into the extracellular compartment raises pressure and drives water into the intracellular compartment. This causes decreased osmolarity in both the intra and extracellular compartments.
96
Explain hypertonic expansion, as can occur with the ingestion of hypertonic saline.
An influx of hypertonic fluid into the extracellular compartment draws fluid from the extracellular compartment to the intracellular compartment. This causes an increase in osmolarity in both compartments, and a decrease in volume in the intracellular compartment.
97
Explain isotonic expansion, such as happens when an isotonic IV is given.
The volume of the extracellular compartment increases.
98
Explain hypertonic contraction, as occurs during sweating.
Fluid is lost from all compartments, which causes an increase in the osmolarity in all compartments.
99
Explain hypotonic contraction, as occurs when there is adrenal insufficiency.
Something decreases osmolarity in the extracellular compartment. Fluid is drawn into the intracellular compartment, resulting in decreased osmolarity in all compartments.
100
Explain isotonic contraction, as occurs with hemorrhage.
The volume of the extracellular compartment is decreased, with no effect on the intracellular compartment.
101
What factors govern the flow of water across vascular membranes.
```
Capillary pressure (Pc): higher pressure forces water out of vessels
Plasma colloid osmotic pressure (PIp): higher pressure draws water into vessels
Interstitial fluid pressure (Pif): higher pressure forces water into vessels
Interstitial fluid colloid osmotic pressure (PIif): higher pressure draws water out of vessels
```
102
How does water movement function in peripheral capillaries (arteriolar end vs. venular end)?
On the arteriolar end, capillary pressure is high. There is a net filtration of water into the interstitium.
On the venular end, plasma colloid osmotic pressure is high. There is a net reabsorption of water into the vessel.
103
How are glomerular capillaries different from normal peripheral capillaries?
Capillary hydrostatic pressure is greater than capillary colloid osmotic pressure along their whole length, so they filter water into the interstitium for their entire length.
104
How are peritubular capillaries different from normal peripheral capillaries?
The capillary colloid osmotic pressure is greater than capillary hydrostatic pressure along their entire length, so they reabsorb water along their entire length.
105
How does the collecting duct change its permeability to water in response to the presence of ADH?
Aquaporin 2 (AQP2) channels are expressed on the lumenal membrane of the collecting duct. This allows water to pass into the epithelial cells. The channels are not expressed in the absence of ADH.
106
Describe the two components of renal autoregulation.
1. myogenic: Vascular smooth muscle constricts in response to stress, so increased pressure causes proportional vasoconstriction. This increases resistance and maintains flow at a steady rate. [Flow = change in pressure/resistance]
2. tubuloglomerular feedback: The macula densa monitors flow in the afferent arteriole. When it senses decreased flow or NaCl, it causes dilation in the afferent arteriole. It also stimulates the release of renin, which causes an increase in efferent arteriole resistance. This causes the GFR to increase.
107
What Na resorption proteins are associated with each segment of the nephron?
Proximal Tubule - NHE2
Thick Ascending - NKCC2
Distal Convoluted - NCC
Collecting Duct Principal Cell - ENaC
108
What transport mechanisms for Na+ take place in the early proximal convoluted tubule?
-Na flows down its concentration gradient into the cell (NHE3)
-glucose, phosphare, amino acids are coupled to Na flow
(facilitated diffusion)
-angiotensin II stimulates expression of the Na/H+ exchanger to absorb more Na
-secreted H+ binds to HCO3- to form CO2 and H2O =>
resorbed
-The Na/K ATPase creates the gradient for Na diffusion into the cell
-this is the site of action for carbonic anhydrase inhibitor diuretics
109
What mechanisms to absorb sodium are in the thick ascending limb of the loop of Henle?
there is an Na/2 Cl/K transporter (NKCC2)
- this is the target of loop diuretics (inhibition)
- K+ diffuses back into the lumen
110
What are the sodium resorption methods in the early distal convoluted tubule?
- Active resorption of Na and Cl
| - site of action of thiazide diuretics
111
What is the sodium resorption method in the collectung tubules?
Sodium is resorbed in principal cells in exchange for secreting K+ and H+
- aldosterone activates the expression of this channel on the lumenal side (therefore encourages K+ secretion)
- K+ sparing diuretics act here
112
Why does a decrease in extracellular fluid volume cause an increase in resorption from the kidney?
- When ECF volume decreases, the osmolality of the peritubular capillary increases and the pressure in the capillary decreases. These Starling forces draw more fluid from the interstitium into the capillary. In turn, this increases flow from the tubule into the interstitium.
- The opposite is true if there is an expansion of extracellular fluid.
113
What effect does aldosterone have in the nephron?
It stimulates the expression of ENaC (sodium channels) in the late distal tubule and collecting duct. This allows an increase in Na resorption.
114
The majority of K+ resorption occurs in the proximal convoluted tubule. How does this occur?
It is absorbed along with Na+ and H2O
115
What mechanisms of K+ regulation occur in the thick ascending limb of the loop of Henle?
- K+ is absorbed as part of the Na-K-Cl (NKCC2) pump
| - K+ is secreted by the ROMK channel (maintains slight positivity of lumen)
116
How is K+ regulation handled in the distal convoluted tubule and the collecting duct?
-can either secrete or absorb K+, depending on dietary intake
-reabsorbtion: H+,K+ ATPase on the lumenal membrane
-occurs on a low K+ diet
-secretion: occurs in principal cells of the collecting tubules
-a high intracellular K+ concentration is achieved by the Na,K
ATPase. This concentration drives secretion through channels.
-anything increasing pump activity will increase secretion, and
vice versa
-EX: digitalis blocks the Na,K ATPase. Therefore the intracell.
concentration will decrease, and secretion will decrease.
117
What factors alter distal K+ secretion?
- high dietary K+
- aldosterone
- acid-base concentrations
- thiazide and loop diuretics
- K+ sparing diuretics
- luminal anions
118
How does aldosterone alter K+ secretion?
```
aldosterone increases K+ secretion
-stimulates Na-K ATPase and increases numbers of lumenal
K+ channels
-hyperaldosteronism => hypokalemia
-hypoaldosteronism => hyperkalemia
```
119
How does acid-base chemistry alter K+ secretion?
-H and K effectively exchange for one another across the basolateral membrane
- acidosis decreases K+ secretion
- increased blood H+ drives H+ to enter the cell and K+ to leave.
- the decreased K+ concentration in the cell causes less secretion
-alkalosis causes increased K+ secretion
-the low levels of blood H+ cause H+ to exit the cell and K+ to
enter
-the increased intracellular concentration drives K+ out through channels
120
How do loop and thiazide diuretics affect K+ secretion?
By increasing distal tubule flow rate, they reduce K+ concentration in the fluid in the distal tubule. This drives K+ secretion into the tubule.
These drugs cause hypokalemia.
121
What effect do K+ sparing diuretics have on K+ secretion?
Used alone, they cause hyperkalemia
- spironolactone is the antagonist of aldosterone
- triamerene and amiloride act directly on principal cells
These are primarily used in combination with loop and thiazide diuretics to prevent hypokalemia.
122
How do lumenal anions affect K+ secretion?
Increased anions can cause the tubular fluid to become more negative, which favors K+ secretion.
123
What is the mechanism of urea reabsorption? How is it regulated? What is its function?
Half of filtered urea is reabsorbed passively in the proximal tubule.
The distal tubule, cortical collecting ducts, and outer medullary collecting ducts are impermeable to urea.
However, ADH increases urea permeability for the inner medullary collecting ducts. This contributes to urea recycling in the inner medulla and the development of the corticopapillary osmotic gradient.
124
How is phosphate reabsorbed in the nephron? How is phosphate absorption regulated?
- 85% of the filtered phospate is reabsorbed in the proximal tubule by Na-phosphate cotransport. The rest is excreted.
- Parathyroid hormone (PTH) inhibits phosphate reabsorption by activating adenylate cyclase and generating cAMP. Causes phosphaturia.
125
How is calcium absorbed in the nephron?
The proximal tubule and thick ascending limb absorb 90% of filtered Ca through processes coupled to Na resorption.
The distal tubule and collecting duct absorb a small amount by an active process.
126
What drugs affect Ca secretion/resorption?
- Loop diuretics: increase excretion of Ca
- Ca resorption is linked to Na resorption in the loop of Henle
- inhibiting Na inhibits Ca
- can be used to treat idiopathic hypercalcemia with volume infusion
- thiazide diuretics increase Ca resorption in the distal tubule
127
How is magnesium reabsorbed?
- it occurs in the proximal tubule, the thick ascending limb, and the distal tubule
- in the thick ascending limb, Mg and Ca compete for reabsorption
- hypercalcemia causes increased Mg excretion
- hypermagnesemia causes increased Ca excretion
128
What causes the release of renin in the kidney?
1. decreased arterial pressure
2. increased activity of the renal sympathetic nerves (due to decreased plasma volume, which could be from Na loss)
3. decreased GFR and decreased flow to the macula densa
129
What is the result of renin secretion? What are the effects of the final hormone in the renin-angiotensin pathway?
Renin cleaves angiotensinogen (from liver) to angiotensin I
Angiotensin I is cleaved by ACE to angiotensin II
Angiotensin II...
-acts at AT2 receptors => vasoconstriction => increased BP
-constricts efferent arteriole of glomerulus => increased GFR
-stimulates aldosterone release from the adrenal gland
-stimulates ADH release from posterior pituitary
-increases proximal tubule Na/H cotransporter activity
-stimulates hypothalamus (thirst)
130
What causes the secretion of aldosterone? What are its effects?
- released in response to decreased blood volume (via AT2) and hyperkalemia
- causes
- increased Na resorption by increased Na-K ATPase activity
- increased K secretion by increased ROMK channels
- increased H secretion
131
What causes the release of ADH? What are its effects in the kidney?
- ADH is secreted in response to increased plasma osmolarity and decreased blood volume.
- it binds to receptors on principal cells, causing the expression of AQP2 channels on the lumenal membrane (increased H2O resorption)
132
What causes the release of PTH (parathyroid hormone)? What are its effects?
- PTH is secreted in response to decreased plasma Ca, increased phosphate, or decreased plasma vitamin D
- It causes increased Ca resorption, decreased phosphate resorption, and increased vitamin D production
133
What causes the release of ANP? What are its effects?
- ANP is released in response to increased atrial pressure
- it causes increased GFR and increased Na filtration with no compensatory Na resorption effect (therefore, Na loss and volume loss)
134
Describe the osmolarity of the tubular fluid relative to the blood in each segment of the nephron.
Proximal tubule: isosmotic; water is absorbed with solutes
Thin loop of Henle: hypertonic (high osmolarity); water is
absorbed and solutes are not
Thick ascending limb: fluid is diluted; solutes reabsorbed and
water is not
distal tubule and collecting duct: NaCl resorption; H20 is
absorbed in the presence of ADH
135
What factors are important in maintaining high medullary osmolarity in the kidney?
- countercurrent multiplication: NaCl resorption in the thick ascending limb and countercurrent flow in both limbs of the loop of Henle
- urea recycling from the medullary collecting ducts to the medullary interstitium (also increased by ADH)
- vasa recta serving as osmotic exchanges (and their slow flow rate)
136
What are the countercurrent multiplier and exchanger?
multiplier: active pumping of urea into the thick ascending limb
exchanger: passive diffusion of solutes into and out of the vasa recta as dives from the renal cortex to the medulla and then back to the cortex
137
What is the cycle by which filtered bicarbonate (HCO3-) is resorbed?
-Proximal tubule cells form H+ and HCO3- from CO2 and H2O
-H2CO3 is combined (via intracellular carbonic anhydrase, and
then dissociates)
-H+ is secreted into the lumen via Na-H exchange; HCO3- is
resorbed into the blood
-H+ combines with filtered HCO3- to form H2CO3 which forms
CO2 and H2O (catalyzed by brush border carbonic anhydrase
-H2O and CO2 diffuse into the cell and start the cycle again
138
How is the resorption of filtered HCO3- regulated?
-filtered load: as the filtered load increases, the rate of resorption
increases; however there is a limit at which the rate cannot
increase futher (seen in metabolic alkalosis) (directly related)
-pCO2: as the pCO2 increases, the filtered load increases
due to the increased supply of intracellular H+. (renal comp.
for respiratory acidosis). The reverse is also true. ("" alkalosis)
(directly related)
-volume: as ECF volume increases, HCO3- resorption decreases
and vice versa (contraction alkalosis) (inverse relationship)
-AT2: stimulates Na-H exchange and thus increases HCO3-
resorption (contributes to contraction alkalosis)
139
What is the mechanism of excretion of H+ as titratable acid (H2PO4-)?
- H+ is produced in the intercalated cell along with HCO3-
- H+ is pumped into the lumen by H+ ATPase; HCO3- resorbed
- H+ ATPase increased by aldosterone
- H+ combines with HPO4 to form H2PO4-
- net secretion of H+ and resorption of HCO3-
- urinary pH goes down
140
What is the mechanism for renal secretion of H+ as NH4+?
-NH3 is synthesized in renal cells and diffuses into the lumen
-H+ and HCO3- are formed in the cell from CO2 and H2O
-H+ is pumped into the lumen via H+ ATPase; HCO3 is resorbed
-H+ combines with NH3 to form NH4+
-in acidosis, adaptive increase in NH3 occurs, helping H+ excret.
-hyperkalemia (alkalosis) inhibits NH3 synthesis (decr. H+
secretion as NH4+)
141
What is exclusively absorbed in the proximal tubule?
- glucose
- AA (cysteine, ornithine, arginine, lysine)
- bicarbonate
- phosphate
- uric acid
