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Flashcards in First Pass Miss Exam 2 Deck (80):

What areas of the medulla are involved in inspiration?

pre-Botzinger = pacemaker
rVRG (nucleus paraambiguus)
Nucleus ambiguus = tense CN12, CN9, CN10 during inspiration to keep upper airway muscles clear


What areas of the medulla are involved in expiration?

cVRG (nucleus retroambiguus)
Botzinger (inhibits inspiratory muscles)


What is congenital hypoventilation syndrome?

Disease reducing phrneic nerve activity and altering respiratory frequency

can cause respiratory arrest during sleep


What is Rett syndrome?

Brainstem abnormality most common in females that can lead to breath holding / breathing arrythmia


What is Analgesia / respiratory depression?

Opoids can suppress breathing at pre-Botzinger complex, slow breathing.


What is the recoil pressure of a system defined as?

Pressure inside - pressure outside

If it were positive, the system would have a propensity to recoil outwards

Thus, a positive value across the lung wall = lung inflated. A negative value across the chest wall = chest is slightly collapsed at FRC relative to its resting point


What is the point which the lung deflates to if uncoupled from the chest wall?

Minimal volume

(not reserve volume, which is max you can deflate with expiratory effort)


What is the transpulmonary pressure vs transrespiratory system pressure?

Transpulmonary = pressure across the lung wall
Transrespiratory = Palv - Patm


What accounts for 1/3 and 2/3 of the compliance behavior of the lungs, respectively?

1/3 - elastic behavior - inflation of one alveoli tends to inflate adjacent ones
2/3 - surface tension - propensity of liquid to try to reduce the air/liquid interface as much as possible


What is the function of surfactant?

Decreases work of breathing, increases compliance, stabilizes alveolar size, reduces hysteresis, dries alveoli


Why is the law of Laplace important for alveolar size?

Since P = 2T/R, if you decrease the radius of an alveoli, its pressure will be greater. If surface tension is not reduced by a higher concentration of surfactant here, it will further collapse. A reduction in T by surfactant prevents airflow away from the smaller alveoli


Why does pulmonary fibrosis lead to increased breathing effort?

Reduces lung compliance, requiring a more negative intrapleural pressure for the same volume (chest wall has to work harder to generate that more negative pressure)


What happens to resistance as lung volume increases, and how does the differ in COPD?

Airway resistance decreases as lung volume increases due to radial tension. COPD people have floppy lungs so at any given lung volume they have a greater resistance to flow as their alveoli / bronchi are always collapsed.


How do PANS and SANS affect airway resistance?

PANS - muscarinic Ach to constrict
SANS - beta2 receptor to dilate. circulating catecholamines are most important


What happens to blood flow in hypoxic alveoli? When is this really bad?

Blood vessels are vasoconstricted, really bad when living at high altitudes, can lead to chronic pulmonary hypertension


Why might vascular remodeling lead to decreased ability to accommodate cardiac output?

Normally, vascular tissues are compliant enough to store about 500 mL of blood for increased CO. If compliance is decreased because vessels thicken, then this blood will not be stored for LV increased loads.


What is the alveolar air equation?

PaO2 = PinspiredO2 - (PaCO2/R)

R = respiratory quotient, rate of CO2 production / oxygen consumption

Thus, if you tend to create more CO2 per oxygen, and your CO2 is that high, your O2 will be relatively lower.


What factors does the rate of the diffusion depend on?

1. Diffusion coefficient - ^ with solubility, decrease with MW
2. Area - increases diffusion rate
3. Thickness - decreases diffusion rate
4. Pressure gradient - increases diffusion rate

Vdiffusion = A/T * (P1-P2), which is the pressure gradient


Where is the highest ventilation / perfusion ratio in the lung?

At the apex, where there is minimal flow and lots of ventilation


What are the two compensatory mechanisms by which a lung with excellent ventilation but poor flow due to blockage would divert air to the opposite lung?

1. Increased O2 causes bronchoconstriction of deadspace lung, diverting flow towards opposite
2. Type II cells will decreased surfactant production when there is less flow -> increasing alveolar collapse


What are normal values for arterial and venous pCO2 and PO2?

O2 = 100 mmHg
CO2 = 40 mmHg

O2 = 40 mmHg
CO2 = 46 mmHg


How is most CO2 in the body carried?

only 7% dissolved (but 24 times more soluble than O2). Rest as bicarbonate. Although venous blood has as much as 23% due to carbamino compounds (CO2 attached to amine of hemoglobin)


What three factors can lead to an increased A-a gradient?

V/Q defect
Diffusion defect
Right to left shunt


What are the two locations of the peripheral chemoreceptors?

1. Carotid bodies - bifurcation of common carotid, afferents CN9
2. Aortic body - superior wall of aortic arch


What do the peripheral chemoreceptors respond to?

CO2, H+, K+ and PO2 (only one to do this). Only get dramatic increases in minute ventilation at less than 60 mmHg O2


What do central chemoreceptors respond to?

increases H+ concentration, which gets across blood brain barrier via CO2.


What is the primary and then two additional functions of the stretch receptors?

Main function: terminate inspiration when lung volume is large enough
1. Control breathing pattern -> frequency and tidal volume. Allows for shallower breaths if lung compliance is low to reduce the work of breathing
2. Feedsback to give breathing discomfort if work achieved does not equal work demanded. -> dyspnea


What is the general function of irritant receptors?

Found all through airway, respond to mechanical / chemical stimuli and trigger a different reflex based on where you are.

I.e. Nasal = CN5 = sneeze
Tracheal = CN10 = cough
Epipharyngeal = CN9 = aspirate


What is the general function of irritant receptors?

Found all through airway, respond to mechanical / chemical stimuli and trigger a different reflex based on where you are.

I.e. Nasal = CN5 = sneeze
Tracheal = CN10 = cough
Epipharyngeal = CN9 = aspirate


What is the function of juxtapulmonary capillary (J receptors)?

They respond to engorgement of pulmonary capillaries / increases in interstitial volume of the alveoli. Feedback via vagus -> cause rapid shallow breathing, especially in heart failure / interstitial lung disease

They are a type of irritant receptor


What do all irritant receptors do? Why is this bad with asthma?

All stimulate breathing and produce bronchoconstriction. This is meant to increase airway velocity to flush things out. Like via coughing. Bad in asthma because you already have bronchoconstriction from active agents


What determines the fate of an upper airway particle?

Size. This dictates where they get trapped and their method of expulsion

Large - Trapped in nose + pharynx
Medium - small airway

Large/medium cleared via cilia / expectoration

Small - alveoli - cleared by alveolar macrophages. i.e. sulfur and nitrogen oxides


What are the Type 3 or 4 afferents which are responsible for ventilation increase during exercise?

Metabolic receptors - with slow, unmyelinated fibers conducting in response to metabolites

1/2 are golgi tendon organs + intrafusal fibers with fast conduction velocity


What is the intrinsic potentiating mechanism?

Even after stimulus is removed, carotid bodies has a continued short term effect of elevating inspiration signals to phrenic nerve


What are anaerobic threshold and respiratory compensation?

Anaerobic threshold - point where lactic acid is building up, and more CO2 trips peripheral chemoreceptors to increase ventilation rate. H+ ions are still buffered by bicarbonate, however.

Respiratory compensation - lactic acid is too much, hyperventilation increases to blow off CO2 to prevent further acidosis, buffering by bicarbonate is no longer adequate and H+ stimulates peripheral chemoreceptors


How do we know that under normal exercise conditions, H+ / lactic acid buildup is not actually the cause of increased ventilation rate?

McArdle's patients which cannot do fermentation and thus have minimal acid buildup show the same exercise patterns.

-> must be due to central command, increasing the number of alpha-motoneurons recruited increases ventilation rate


What are the fast and slow response phases of exercise?

Fast - abrupt increase in minute ventilation due to central command + Types 1/2 afferents. Types 3/4 have minimal effect
Slow - exponential increase overtime due to short term potentiation in moderate exercise. Only in severe exercise will activation of Types 3/4 afferents + peripheral chemoreceptors directly increase breathing rates (increases in K+ and H+ concentrations, respectively)


What is the final phase of exercise breathing?

Steady state phase - a complex interaction of all afferents. There is a "slow drift" upwards in steady state in severe exercise.


What is the primary thing that's different in OSA with regards to chemoreceptors?

Apneic threshold is high, and there is a higher slope / sensitivitity so when they do start breathing again, they hyperventilate more to make them hypercapnic.


What is the primary treatment for OSA?

Have patients sleep on their side to get their tongue out of the way


What are two mechanisms by which an increase in GFR will be met with a parallel increase in proximal tubule reabsorption (glomerotubular balance)?

1. Osmotic concentration of plasma proteins will increase with higher GFR, pulling solutes in
2. As filtered load of solutes goes up, Na+ reabsorption goes up as well as they are co-transported


What is threshold defined as?

The highest plasma concentration at which the excretion of a substance is 0, because Tm will be saturated (max reabsorption rate)


What are the two mechanisms by which PTH increases phosphate excretion?

1. Decreases the Tm for phosphate, lowering the threshold
2. Increases the GFR, lowering the threshold for excretion


Give an example of an organic cation and an organic anion?

cation: creatinine
anion: PAH or urea


How is bicarbonate co-transported with sodium?

Na/H exchanger makes H+ excreted from proximal tubule cell = to HCO3 reabsorption, carbonic anhydrase mechanism


What factors affect HCO3- reabsorption?

1. Carbonic anhydrase blocker - needed on both brush border and inside the cell, otherwise you have diuresis
2. Change in partial pressure of CO2 (mass action) -> increased pCO2 = more HCO3- in proximal tubule, leading to greater reabsoprtion
3. filtered HCO3 - = higher = lumen more negative, more favorable for H+ to leave and Na + reabsorption


How do early and late proximal tubule Cl- absorption differ?

early: Lumen is slightly negative so Cl- can leak through paracellular with water following
late: Lumen is slightly positive but the Cl- gradient is favorable and it is antiported with a negative base, also H+/Na+ exchanger. NET TRANSPORTED WITH SODIUM


What factors affect PROXIMAL Na reabsorption?

Catecholamines / Angiotensin 2 -> increase BP by increasing the activity of the Na/H exchanger.

ANP -> decreases proximal NA reabsorption to lower blood pressure


What is the only condition under which Na is secreted?

Osmotic diuresis, when concentration of sodium becomes lower in the tubular fluid because water is left behind balancing out the osmolytes, Na+ can actually leak out through the proximal tubule intracellular tight junctions


What are the functions of the ascending and descending limbs of the loop of Henle?

Descending limb: concentration urine, mostly reabsorbs water and not many solutes
Ascending limb: dilute the urine while sending solutes into the ISF to make it hypertonic, so it can be concentration later.

Length of the loop is most important factor


What tends to keep the thick ascending loop of Henle tubular fluid positively charged? Why is this important?

Even though Na/K/2Cl- are cotransported, K+ still tends to leak out into the lumen, making the fluid positively charged.

Allows us to move Na, K+, Ca+2, and Mg+2 paracellularly through claudins (in zonula occludens)


Why is TALH HCO3- absorption not as good as proximal tubule, even though there IS a Na/H exchanger?

There is no brush border carbonic anhydrase, making it difficult to have CO2 diffuse from the tubule lumen


What is the action of furosemide?

"Loop diuretic" - Inhibits the Na/K/2Cl transporter, thus inhibiting the dilution and concentration of urine, and decreasing reabsorption of solutes -> plasma becomes dilute, can cause brain edema.


Where can urea be reabsorbed?

Terminal collecting duct (Facilitated diffusion) as well as proximal tubule (paracellular). It is used as a secreted in descending and thin ascending limb. Mainly distributed to maintain medullary gradient via the vasa recta


What three things control ADH secretion?

1. Increase in blood osmolarity, sensed by osmoreceptors with 1% change sensitivity
2. High pressure baroreceptors in carotid sinus, increase their firing at high blood pressures to inhibit ADH secretion / SANS
3. Low pressure receptors which measure stretch of left / right atria and are inhibited from firing at low pressures


What circulating factors stimulate ADH?

Angiotensin 2, catecholamines, nicotine, hypoxia, hypercarbia


What inhibits ADH?

Alcohol and cold -> gotta pee like a racehorse


What is the mechanism of action of ADH?

Bind V2 receptors on basolateral membrane of principal cells of collecting duct -> activate cAMP, and PKA pathway, phosphorylates AQP2 and are transported in vesicles to apical membrane


What are two causes of diabetes inspidus?

1. Neurogenic / central - lack of ADH secretion
2. Nephrogenic - mutation of V2 receptors or AQP2 channel


What are granular cells?

Juxtaglomerular cells - cells of afferent arteriole which are Vascular Smooth Muscle and secrete renin


How does the juxtaglomerular apparatus system of renin-angiotensin-aldosterone system work?

-> Less NaCl to macula densa cells in distal tubule -> there must be less filtered load -> need to increase BP -> extraglomerular cells transduce signals via prostaglandins / adenosine to get JG cells to release renin


What 3 factors increase renin secretion?

1. Decreased perfusion pressure - sensed by JG cells
2. Sympathetic nerves -> SANS to Beta receptors of JG cells
3. Decreased NaCl load to macula densa


What are the functions of angiotensin 2?

1. Constrict vascular smooth muscle
2. Increase Na reabsorption from proximal convoluted tubule
3. Constrict efferent arteriole
4. Stimulate ADH / Aldosterone / thirst


What is the function of aldosterone?

Increase Na reabsorption via principle cells of the distal tubule


What is the function of thiazide diuretics?

Act on distal convoluted tubule cells to inactivate the Na/Cl cotransporter.


How is the -55mV lumen potential of the tubular fluid maintained?

the sodium permeability on the apical side of principle cells is about equal to potassium permeability (cell is relatively -25 mV potential compared to lumen, which is the equilibrium between the two permeabilities)


How is Cl- reabsorbed by distal tubule principle cells?

enters ISF paracellularly since lumen potential is so negative


What are the channels on the apical surface of the distal tubule principle cell?

ENaC - Sodium Channel
ROMK - Potassium Channel


What three factors trigger the release of aldosterone? What does it do?

1. Angiotensin II
2. Increased plasma K+
3. Decreased plasma Na+

Functions to add more channels to apical membrane + speed Na/K-ATPase


What is special about aldosterone's function on principle cells in the presence of angiotensin II?

When blood volume is low, we don't also want to make ourselves hypokalemic, so we inhibit ROMK


What also binds the aldosterone receptor with high affinity?

Cortisol - must be actively modified in principle cells by hydroxysteroid dehydrogenase 2


How will principle cells respond to higher Na+ load?

Start reabsorbing more Na+. If it's gotten here, we still want to try to reabsorb it. If GFR drops, Na load would drop but the effects of aldosterone would still increase Na+ uptake because we want to protect blood pressure.


What effect do non-reabsorbable anions have?

Make the lumen potential more negative, thereby decreasing reabsorption of sodium and increasing K+ secretion


What effect does tubular flow rate have on the principle cells?

Increases K+ secretion via the cilia. (opens Ca+-gated K+ channels)


Where does the ammonia come from to create "new HCO3" in alpha-intercalated cells?

Secreted via Na/H transporter in place of H in proximal tubule, or
in place of K in TALH in Na/K/2Cl- transporter


Why is a more negative lumen potential not allowing more K+ reabsorption when the H/K ATPase antiporter runs faster in alpha-intercalated cells?

Negative lumen potential has a greater effect on distal tubule principle cells to increase K+ secretion.


What is meant by "titratable acid"

Phosphates which are secreted into tubule. More phosphates -> more meat was eaten -> generally, more H+ needs to be mopped up


Why does H+ excess actually lead to K+ deficit?

The etiology of H+ excess is typically loss of base (diarrhea). Thus, blood volume must be recovered, and aldosterone is stimulated, which causes more K+ secretion.

This is even worse in diabetes because of the diuresis increasing sodium load + nonreabsorable anions which increase K+ secretion


What is the main way by which we deal with metabolic or respiratory alkalosis in the kidney?

We excrete less acid / reabsorb less bicarbonate via the alpha-intercalated cells


Which receptor on parietal cell works via GalphaS? Why is this important?

H2 -> increase cyclic AMP. Important because somatostatin + prostaglandins are Galphai