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MSAP 2015 > PHYSIOLOGY: RENAL SYSTEM > Flashcards

PHYSIOLOGY: RENAL SYSTEM Flashcards

1
Q

What are the functions of the kidney?

A

•Excretory, regulatory, & endocrine organ

Responsible for:

a) Producing urine (1 L/day excreted): Maintains proper balance between water, salts, acids and bases
b) Controlling blood pressure, blood volume, blood constituents
c) Filtering and cleaning blood: Allows toxins, metabolic wastes, and excess ions to be excreted in the urine à Body’s “washing machine”
d) Synthesizing and secreting hormones: Renin to regulate blood pressure; erythropoietin to stimulate red blood cell production, activates vitamin- D -1,25-dihydroxycholecalciferol)

  • Total renal blood flow ~25% of cardiac output (1800 L/day or 1.25 L/min)
  • From 1800 L/day à filters about 180 L/day; reabsorbs >99% of plasma ultra-filtrate to make urine
  • Nephron: functional unit of kidney
  • millions per kidney
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2
Q

Which nephron is most responsible for urine?

A

the Juxtamedullary

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3
Q

How does blood supply get to the nephrons?

A

Vasculature on top of tubules – arterioles on either side of glomerular capillaries

Afferent artery - glomerular capillaries (filtration here) (Not all blood is filtered)

Efferent artery via peritubular capillaries (wrap around epithelium portion of nephron (proximal/distal tubules))

  • 99% reabsorption - proximal tubules into peritubular capillaries into vasculature

Vasa Recta - capillaries close to juxtamedullary nephrons only

  • Specialized peritubular caps
  • Hairpins close to thin/thick ascending and thin descending limbs of loop of Henle
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4
Q

What two components determine flux across the glomeruls during glomerular filtration?

A

2 components to determine flux across glomerulus:

1) Permeability

2) Glomerular filtration pressure

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5
Q

How does size and charge effect permeability with GFR?

A

a. Size:
- Small molecules radii
- 15 - 35 Å : inverse relationship with size and filterability
- Large molecules > 35 Å : no filterability at all

Freely filtered molecules: [plasma] = [Bowman’s space]

Non-freely filtered molecules: [plasma] > [Bowman’s space]

b. Charge: 15 - 35 Å : Cations > neutral > anions

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6
Q

What are the “Starling Forces”?

A

“Starling Forces”: 4 pressures affecting fluid movement across capillary wall

–2 hydrostatic pressures: push H2O away (out capillary/interstitium)

–2 oncotic pressures: proteins drawing H2O towards them (into the capillary/interstitium)

  1. Hydrostatic pressure of capillary (PG) – favours filtration
  2. Hydrostatic pressure of interstitium (PB) – opposes filtration/ favours reabsorption
  3. Oncotic pressure of blood ( plasma) (pG) – opposes filtration/ favours reabsorption
  4. Oncotic pressure of interstitial fluid/Bowman’s space (pB) – favours filtration (+) – no proteins in Bowman’s space (0 mmHg)
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7
Q

If a kidney stone blocked a renal calyx, how would this affect filtration pressure in the nephrons emptying into it?

A

It would increase hydrostaic pressure in the bowman’s space fluid would move back int the capillary. It may oppose filtration where ther’s no movement of fluid at all. Net pressure = 0

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8
Q

Nephrotic Syndrom results in an increased permeability of glomerular capillaries to plasma proteins. What Starling Force will be affected and why?

A

This results in increased oncontic pressure of intersititial fluid/Bowman’s space (πB) (favours filtration (+)- no protiens in Bowman’s space (0 mmHg). It should normally be zero.

Protein is being filtered out and water is collecting in places it’s not suppose to.

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9
Q

Urinary track obstruction (obstructive uropahty) results in back up tubular flow. What does this result in?

A

Increased hydrostaic pressure PB (opposes filtration/favors reabsorption)

Backs up tubular flow

Kidney stones cause increased movement of reabsorption force.

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10
Q

Glomerular blood hydrostatic pressure varies with constriction of afferent and efferent arterioles.

What would be the effect of afferent arteriole constriction and dilation?

A

Constrict afferent:

Decreased Renal plasma flow (RPF)

Decreased GFR

Deceased Hydrostatic Pressure

Dilate afferent:

Increased RPF

Increased GFR

Increased Hydrostatic Pressure

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11
Q

Glomerular blood hydrostatic pressure varies with constriction of afferent and efferent arterioles.

What would be the effect of efferent arteriole constriction and dilation?

A

Constrict afferent: (Blood backs up & pools)

Decreased Renal plasma flow (RPF)

Increased GFR

Increased Hydrostatic Pressure

Dilate afferent:

Increased RPF

Decreased GFR

Decreased Hydrostatic Pressure

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12
Q

What’s the difference between filtration and reabsorption?

What’s the difference between secretion and excretion?

A

Filtration: Movement of solutes from glomerular capillaries to Bowman’s Space

Reabsorption: Returns most filtered solutes to circulation

Secretion: Transports solutes from peritubular capillaries and vasa recta into the tubular lumen

Excretion: Solute in urine due to filtration, secretion, reabsorption (sum of 3 processes)

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13
Q

Where does most of the reabsorption of glucose, bicarbonate, and amino acids occur?

A

In the proximal convoluted tubule (PCT), almost all glucose, bicarbonate, and amino acids are reabsorbed.

2/3 of sodium is reabsorbed in the PCT, while chloride and water are reabsorbed passively.

In the PCT, organic acids and bases are actively secreted into the tubule.

The PCT is the site of action for acetazolamide (inhibition of carbonic anhydrase) and parathyroid hormone (promotes excretion of phosphate).

NOTE: Parathyroid hormone also acts at the distal convoluted tubule.

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14
Q

How much of renal blood flow gets filtered through Bowman’s capsule?

A

20% of all renal plasma flow enters Bowman’s capsule to begin the filtering process.

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15
Q

What are the mechanisms by which the kidneys regulate serum acid-base content?

A

The kidneys regulate serum acid-base content through reabsorption of filtered HCO3- and excretion of fixed H+ as either H2PO4- (titratable acid) or NH4+.

In the proximal convoluted tubule cells, H+ and HCO3- are produced from CO2 and H2O in a reaction catalyzed by carbonic anhydrase: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

The H+ is secreted into the tubular lumen by an Na+/H+ exchanger, while the HCO3- is reabsorbed into the interstitium.

NOTE: Here, there is NO net excretion of H+.

Rather, the secreted H+ is paired with another luminal HCO3- to reform CO2 and H2O bybrush border carbonic anhydrase, and brought back into the proximal tubule cells to restart the cycle.

Fixed H+, also generated by mechanism outlined above, is secreted into the tubular lumen by an H+-ATPase, to be excreted either by combining with filtered HPO42- to form H2PO4-or with NH3, generated from glutamine in proximal tubule cells, to form NH4(ammonium). This process may be enhanced by the action of aldosterone on the H+-ATPase.

NOTE: In this process there IS net excretion of H+.

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16
Q

What is reabsorbed in the descending loop of henle?

A

The descending loop of henle enters the deeper portions of the kidney, where the interstitial osmotic gradient increases, causing the reabsorption of water and the concentration of fluid in the tubule.

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17
Q

The unfiltered blood that exits the glomerulus drains into what blood vessel?

A

Unlike most other capillary beds, the glomerulus drains into an efferent arteriole rather than a venule.

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18
Q

Name some of the endocrine functions of the kidney (try to name four).

A

The kidney also has several endocrine functions including the production of:

  1. EPO - involved in increasing red blood cell production
  2. 1-α-hydrolyase - stimulated by PTH, catalyzes reaction forming active Vitamin D
  3. Prostaglandins - local vasodilatory function
  4. Renin - involved in triggering the renin-angiotensin-aldosterone system
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19
Q

What percentage of cardiac output supplies renal blood flow?

Which part of the kidney receives most of the total renal blood flow – the cortex or the medulla?

A

RBF (renal blood flow) is normally ~20% of cardiac output.

The renal cortex receives ~90-95% of total RBF.
The renal medulla receives ~5-10% of total RBF.

To reach the kidney, arterial blood leaves the descending (abdominal) aorta to enter the renal artery. Note: the renal artery emerges from the descending aorta at the level of L2(second lumbar vertebra).

From the renal artery, blood travels through a series of named vessels, in sequence:

Renal artery → segmental artery → interlobar artery → arcuate artery → interlobular artery → afferent arteriole → glomerular capillaries → efferent arteriole → peritubular capillaries → interlobular vein → arcuate vein → interlobar vein → renal vein → IVC (inferior vena cava) → right atrium

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20
Q

To what extent is water reabsorbed in the distal convoluted tubule?

A

The cells of the distal convoluted tubule (DCT) actively reabsorb NaCl, however they areimpermeable to water, making the tubular fluid hypotonic.

Increased sodium reabsorption in the DCT is mediated by aldosterone.

Calcium is reabsorbed in the DCT under the influence of parathyroid hormone.

The NaCl channels in the DCT are the targets for thiazide diuretics.

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21
Q

What is the physiological function of buffers?

A

Buffers minimize changes in pH upon the addition or removal of H+.

Buffers consist of a solution containing:

Either a weak acid and its conjugate base

Or a weak base and its conjugate acid

The major extracellular buffer is HCO3- (pKa 6.1).

Carbonic anhydrase mediates the following reaction, converting CO2 and H2O to H+ and HCO3- (bicarbonate):
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-

The minor extracellular buffer is phosphate. The concentration of phosphate in the blood is so low that it is relatively unimportant. But, because the concentrations are higher in the urine, this is the most important urinary buffer, aiding in the excretion of H+ as H2PO4-(titratable acid).

Hemoglobin, specifically deoxyhemoglobin, is the major intracellular buffer. The greater ability of deoxyhemoglobin to form carbaminohemoglobin explains why deoxygenated blood is better than oxygenated blood at carrying CO2, which is the Haldane effect.

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22
Q

Other than the aortic arch and carotid body chemoreceptors, what organ system is responsible for maintenance of:

  • arterial PCO2?
  • HCO3-?
A

Arterial PCO2 is primarily maintained by the lungs, while plasma HCO3- is primarily maintained by the kidneys.

23
Q

The afferent arteriole that supplies blood to the glomerulus is a branch of which artery?

A

The afferent arteriole that supplies the glomerulus is a branch of an interlobular artery in the cortex.

Abdominal aorta → renal artery → lobar artery → interlobar artery → arcuate artery → interlobular artery → afferent arteriole → glomerulus → efferent arteriole → peritubular capillaries → → → renal vein → inferior vena cava

24
Q

How does the respiratory system regulate acid-base content?

A

The respiratory system regulates acid-base content by alterations in ventilation. Because CO2 is lipid-soluble, it crosses cell membranes rapidly, allowing for quick changes in pH with changes in respiration.

Respiratory regulation is finely tuned at central and peripheral chemoreceptors that monitor and respond to changes in arterial PCO2.

The signal from chemoreceptors is then sent to the respiratory center at the medulla, where alterations in minute ventilation are controlled.

25
Q

A patient with a ureteral stone develops oliguria. The decreased glomerular filtration rate (GFR) in this individual is the result of:

A Decreased glomerular capillary hydrostatic pressure

B Increased glomerular capillary oncotic pressure

C Increased Bowman’s space hydrostatic pressure

D Increased bowman’s space hydrostatic pressure and oncotic pressure

E Decreased bowman’s space oncotic pressure

A

Increased Bowman’s space hydrostatic pressure

The driving force for glomerular filtration is the net ultrafiltration pressure across the glomerular capillaries:
GFR = Kf [(HPgc – HP bs) – (OPgc – OP bs)]

HPbs – Bowman’s space hydrostatic pressure
Constriction of ureters will increase HP bs. In addition to decreased GFR, fraction fraction is also decreased with occlusion of the ureters.

Another way to express GFR is through use of Starling equation:
GFR = Kf [(HPgc – HPbs) – (OPgc – OPbs)]

Where:

Kf – filtration coefficient of glomerular capillaries

HPgc – glomerular capillary hydrostatic pressure, which is constant along the length of the capillary

HPbs – Bowman’s space hydrostatic pressure

OPgc – glomerular capillary oncotic pressure

OPbs – Bowman’s space oncotic pressure

The driving force for glomerular filtration is the net ultrafiltration pressure across the glomerular capillaries.

OPgc decreases by decreases in capillary protein concentration, such as in cirrhosis or nephrotic syndrome. This results in an increased GFR.

The value of oncotic pressure in Bowman’s space is usually zero since only a small amount of protein is filtered.

26
Q

Where does the most reabsorption happen in the glomerulus?

A

the proximal tubule - 67% of water and solutes are returned to the bloodstreem by peritubular capillaries

Glomerular capillaries are high pressure, allowing filtration of solute and water out of the systemic bloodstream and into the urine.

Peritubular capillaries are low pressure, allowing reabsorption of solute and water from urine into the systemic bloodstream.

27
Q

What is the difference between glomerular and peritubular capillaries?

A

Glomerular capillaries are high pressure, allowing filtration of solute and water out of the systemic bloodstream and into the urine.

Peritubular capillaries are low pressure, allowing reabsorption of solute and water from urine into the systemic bloodstream.

28
Q

What are the starling forces that control water movement regarding the peritubular capillaries?

Which force is the driving force for water movement in the peritubular capillaires and why?

What force is missing and why?

A

•3 Starling forces that control H2O movement

  1. Plasma oncotic pressure in peritubular capillary (πPC)
    - driving force for reabsorption - b/c of high [protein]
  2. Hydrostatic pressure in peritubular capillary (PPC)
    - force that prevents water from entering capillary
  3. Hydrostatic pressure in interstitial space (Pi / Po)
    - H2O follows solutes – increase pressure – forces H2O into capillary

The oncotic pressure in the interstitial is missing because there should not be protein there (πpi).

  • Pulling out of the lumen and back into the capillary network, starling forces help control the movement
  • Hydrostatic forces push water and fluid away and here it prevents water from being reabosorbed into the capillary
29
Q

What do the peritubular capillarilies run along side?

A

the proximal and the distual run along side the convoluted tubules (the epithelium section of the nephron)

the convoluted portion of the vertebrate nephron that lies between Bowman’s capsule and the loop of Henle and functions especially in the resorption of sugar, sodium and chloride ions, and water from the glomerular filtrate

30
Q
  1. How does solute move in the nephron?
  2. Where is the only place you’ll find flitration?
  3. Where does reabsorption/secretion happen & what is moving where?
    1. Proximal tubule?
    2. Descending loop of henle?
    3. Ascending loop of henle?
    4. Distal tubule?
  4. Where is concentration and dilution happening?
A
  1. Into afferent arteriol and out through the effernt arteriole
  2. Filtration happens in the glomerular capillaries into the bowmans space (filtered ultra filtrate)
    1. Proximal tubule -reabsorption of solutes you want to keep (Na+, K+, urea, H20) & Secretions of solutes you don’t want to keep into the lumen for secretion (Creatinine, PAH)
    2. Descending loop of henle - pearmeable to water & impearmeable to solutes - water is reaabsorbed which causes a concentration of solutes
    3. Ascending loop of henle - is reabsorption of solutes only - water impearmeable - dilution of solutes b/c they are leaving
    4. Distal tubule reabsorption and secretion “early portion” impermeable to water and only absorbs solutes. “Late protion” is pearmeble to solutes and water if dehydrated.
31
Q

What is the only solute that can be absorbed or secreted anywhere in the nephron?

A

Potassium

32
Q

What happens during afferent arteriole constriction?

What happens during effernt arteriol constrction?

A

Afferent arteriole constriction: glomerular hydrostatic pressure decreased, decreasing filtration → decreases GFR

Efferent arteriol costriction: Glomerular hydrostatic pressure increases, increasing filtration → increases GFR

33
Q

Why does GFR need to stay balanced?

A

If too high, needed substances can’t be reabsorbed quickly enough and are lost in urine

If too low, reveryting is reabsorbed, including wastes that are normally disposed

34
Q

How is GFR autoregulated?

A

The GFR and RBF likes to stay at a constant rate of 80-180 mmHG.

Regulation happens with Myogenic Repsonse and Tubuloglomerular feedback.

  1. Myogenic response: Increased arterial pressure stretches in smooth muscles in blood vessel walls induces constriction of afferent arteriole and increases GFR.
    • Increased blood pressure → Increased afferent arteriol stretch → opens Ca+ channels → afferent arteriol contraction
  2. Tubuloglomerular Feedback: Involves macula densa and vasoactive substances (adenosine, kinins, PGs) to constrict afferent/efferent arterioles.
    • Sends signal to juxtaglomerular cells located next to the mascula densa that NaCl is low (b/c of low blood flow) and renin is released
  • Macula densa cells part of juxtaglomerulus apparatus that sense tubular flow and GFR and send feedback signals to afferent or efferent arteriole to constrict/dilate to keep GFR at normal levels
35
Q

Decribe the process of sodium transport in the early proximal tubule.

What is mainly absorbed?

A

NaHCO3 REABSORPTION

Most essential solutes are reabsorbed with Na+: (Glucose, amino acids and HCO3-)

Cotransport mechanisms: Na+ reabsorbtion is coupled with uncharged molecules (glucose; amino acids, phosphates, lactate, citrate)

– accounts for 10% Na+ reabsorption; H2O follows

Countertransport/Exchanger: Na+ /H+ antiport allows H+ secretion for HCO3- reabsorption; HCO3- is the anion reabsorbed with Na+

–accounts for 20-25% Na+ reabsorption

36
Q

Describe what’s absorbed in the late proxima tubule.

A

LATE PROXIMAL TUBULE = NaCl REABSORPTION

Cellular component: Na+ /H+ antiporter coupled to Cl- reabsorption and formate secretion

  • accounts for ~35% Na+ reabsorption

Paracellular component: Passive reabsorption of Na+ and Cl-

37
Q

Describe the absorption of the thick ascending limb of the loop of henle.

A

Cellular mechanism: Na+ /K+ /2Cl- cotransporter

Energy is derived from Na+ gradient with reabsorption of Na+ K+ 2Cl

Na+ /H+ antiporter to allow for HCO3 - reabsorption

Accounts for 25% Na+ reabsorption

38
Q

Describe the absorption in the early distal tubule.

A

Cellular Mechanism: Na+ - Cl- cotransporter

Energy is derived from Na+ gradient with reabsorption of Na+ and Cl

Accounts for 5% Na+ reabsorption

39
Q

Describe the absorption in the late distal tubule & collecting duct.

A

2 cell types interspersed

  1. Principal: Involved in Na+ reabsorption and K+ secretion
  2. a- Intercalated: Involved in K+ reabsorption and H+ secretion

Mechanism: Na+ Channels Na+ diffuses through the channels down its electrochemical gradient

Accounts for 3% Na+ reabsorption

Fine adjustments to Na+ excretion Hormonally regulated by aldosterone

– synthesizes Na+ channels to increase Na+ reabsorption

40
Q

What does renin do?

A
  • Secreted by the juxtaglomerular cells (JG) of the afferent arterioles in response to low renal arteriole pressure
  • catalyzes conversion of plasma protein, angiotensinogen, to Angiotensin I eventually giving Angiotensin II
  • The macula densa cells located in the distal tubules stimulate the JG cells to release renin in response to decreased NaCl concentration in the tubules
41
Q

What does Angiotensin II do?

A

Angiotensin II: Potent arteriole vasoconstrictor, increases Na+ reabsorption in proximal tubule, stimulates thirst, stimulates aldosterone secretion from adrenal cortex

(effernt arterial → helps get GFR back to normal)

42
Q

What does aldosterone do?

A

Aldosterone: Increases Na+ reabsorption and K+ secretion by principal cell in late distal tubule and colleting duct

secreted in response to Angiotensin II, hyperkalemia (high blood [K+]), hyponatremia (low plasma [Na+])

43
Q

How is sympatheic stimulation activted in reponse to deceased arterial pressure?

A

Nerves decreases Na+ excretion in 3 ways:

  1. Decreases GFR and RBF ⇒ decreased filtered Na+ load for excretion
  2. Direct stimulatory effect on Na+ reabsorption by renal tubules
  3. Causes renin release ⇒ increases angiotensin II and aldosterone levels for reabsorption
44
Q

How does atrial natriuretic peptided (ANP) increase sodium and water excretion?

Who does it respnd to high blood pressure?

A

Secreted by atria in response to increase In ECF volume

  • Increases GFR (dilate afferent / constrict efferent arterioles)
  • Inhibits reabsorptive mechanisms along tubule – Inhibits Na+ reabsorption at collecting duct

– Inhibits renin secretion by juxtaglomerular cells in kidney  inhibits RAA system

– Inhibits aldosterone secretion by adrenal gland – Inhibits ADH secretion

– Inhibits adenylate cyclase in target tissues

• Increases Na+ and H2O excretion

High blood pressure stretches the heart chambers, and in response, atrial natriuretic hormone is secreted by the right atrium

• Inhibits reabsorption of Na+ and water - stimulates Na+ and water excretion  blood volume is lowered and decreases blood pressure

45
Q

What does anti-diuretic hormone (ADH) do?

What secretes it?

What stimulates it?

What is it’s function?

A

ADH is also called Vasopressin - Involved in the regulation of body water content

  • Secreted by posterior pituitary
  • Allows formation of water channels in the late distal and collecting duct increasing reabsorption of water
  • Secretion stimulated by:
  1. Plasma osmolarity rises 1 mOsm/L (normal = 280-295 mOsm/L)
  2. Hypovolemia >8%

• Functions: Reabsorbs H2O - Increases urine osmolarity and decreases urine flow volume

46
Q

Describe the following:

  1. Acidema
  2. Acidosis
  3. Alkalemia
  4. Alkalosis
A
  1. Acidemia - Low arterial pH (<7.35)
  2. Acidosis: Process leading to a reduced pH
  3. Alkalemia - High arterial pH (>7.45)
  4. Alkalosis: Process leading to an increased pH
47
Q

What are 3 defenses against changes in [H+]?

A

3 primary systems to regulate H+:

  1. Buffering systems of body fluids:
    * IMMEDIATELY combines with acid/base to prevent large changes in [H+]
  2. Respiratory Response:
    * Within minutes to eliminate CO2 (H2CO3) from body
  3. Renal Response:
  • Slowest - hours/days to eliminate excess acid/base
  • MOST POWERFUL REGULATORY SYSTEM
48
Q

What is a buffer?

How can they regulate pH?

A

Buffer: Any substance that can reversibly bind H+

HA ⇔ H+ + A-

(Mixture of a weak acid and its conjugate base OR a weak base and its conjugate acid)

i.e. H2CO3 ⇔ H+ + HCO3-

  • FIRST line of defense against pH changes (Regulate by accepting or givng H+ ion in solution)
  • Buffered solution MINIMIZES A CHANGE IN pH but does not prevent it
  • Several buffering systems (ECF and ICF) and the sum = 7.4
49
Q

What are some ECF and ICF buffers?

A

Extracellular Buffers:

Blood proteins

Inorganic phosphates (H2PO4/HPO4-)

Intracellular Buffers:

Hemoglobin

ATP

ADP

glucose-phosphates

50
Q

Explain the HCO3/CO2 buffer system Is the most important extracellular system.

A

MOST IMPORTANT ECF BUFFER

  1. [HCO3-] is higher (24 mEq) than HPO4-2 (1-2 mM/L) and can be adjusted by kidney
  2. CO2, acid form of buffer is volatile and can be expired by lungs
  3. pK is 6.1..close to ECF pH

It’s the first line of defense!

51
Q

How the pulmonary system regulates pH?

A

Respiratory Response:

- Within minutes

- Control centers respond by increasing/decreasing ventilation to keep Pco2 near 40 mmHg

  • Acts rapidly to prevent large changes in [H+] until kidney response
  • Doesn’t return [H+] all the way to normal: effectively gains 1-3 pH units within 3-12 minutes…but 1-2x greater buffering power than ECF buffers combined
  • With abnormalities: Compensates for changes in [HCO3-]
  • PaCO2 = 40mmHg with normal [HCO3-]; pH= 7.4 if decrease [HCO3-] will compensate by decreasing PaCO2 (hyperventilating) which returns pH to normal
  • Compensation…same direction but never completely returns pH to normal
52
Q

How can you regulate [H+] in ECF?

A

Regulate ECF H+ concentration through 3 mechanisms:

A. Secretion of H+

B. Reabsorption of filtered HCO3-

C. Production of new HCO3- (via ammonia/titratable acid excretion)

53
Q

What are the metabolic and respiratory acid­-base disturbances.

A

METABOLIC DISTURBANCES: primary disorder with [HCO3-]

  1. Metabolic acidosis: ⬆️ [H+] and ⬇️ [HCO3-] – more buffering
  2. Metabolic alkalosis: ⬇️ [H+] and ⬆️ [HCO3-] – loss of H+ /gain of HCO3-

RESPIRATORY DISTURBANCES: primary disorder of CO2

  1. Respiratory acidosis: hypoventilation/ ⬆️PCO2
  2. Respiratory alkalosis: hyperventilation/ ⬇️ PCO2

MSAP 2015 (10 decks)

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