Exam 4 Flashcards

Question 1

Q

1-major function of kidneys

2-Na content affecting extracellular fluid volume

Answer

A

1-regulate volume & composition of the extracellular fluid (ECF)

2-Pna= Total Body Na content (mEq)/ ECF volume

Na and its anions (Cl, HCO3) are primary solutes in the extracellular fluids and are determinants of plasma osmolality
if Na content inc, Total body water increases to compensate (via thirst)
if Na content dec, total body water dec to keep plasma osmolality constant (kidney will excrete h20)
–to maintain extracellular fluid volume, the kidneys must match daily output of Na w/ intake of Na

Question 2

Q

1-Na Balance

2-hyperaldosteronism

Answer

A

1-Balance: output= input

neg Na balance (loss of body Na content)= dec in ECF (ECF contraction)
pos Na balance (gain of body Na content)= inc in ECF (ECF expansion)

-problems w/ sodium balance typically manifest as altered extracellular fluid volume

2-elevated aldosterone release from adrenal cortex—> kidney reabsorbes excess amts of sodium—> plasma osmoallity inc slightly so H20 consumption (thirst) & H20 conservation at kidney inc—> ECF vol inc—> patient becomes hypertensive due to ECF expansion

Question 3

Q

1-transport mechanisms used by the kidney

types of facilitated diffusion in the kidney tubule
2-symport

3-antiport

4-imp role of Na/K ATPase in tubule cell

5-H20 movement

Answer

A

1-solute movememnt (electrolytes, glucose, proteins) may be passive or active)—(active=ATP)
-Diffusion: solute goes down its electrochemical gradient:
—transcellular= through cell membrane
—paracellular= between cells
Facilitated Diffusion= movement of solute depends on interaction w/ specific protein in the membrane

2-coupled transport of 2 solutes in the same direction. process= co-transport & protein called transporter or symport

3-couple transport of 2 or more solutes in opposite direction. processs= exchange & protein called exchanger or antiport

4-conc gradient for Na to move into cell from tubule lumen is maintained by active transport of Na out of the cell by Na/K ATPase

5-H20 movement is passive, dirven by osmotic pressure gradients caused by reabsorption of Na & other solutes

Question 4

Q

1- solvent drag

2-aquaporins

3-Tm Limited Transport

Answer

A

1-when reabsorbed, solutes dissolved in H20 are carried along

how solutes can be reabsorbed by kidney via paracellular route
H20 goes through transcellular & paracellular paths in tubular segments that are permeable to H20

2-transcellular movement of h20 in response to osmotic pressure in prox tubule= high bc of water channels
-Aquaporin 1= proximal tubule—present in collecting duct but those are called Aquaporin 2 and are controlled by vasopressin

3-when transported is involved in movign a solute theres a max rate of transport for that solute
—# of sites x’s rate of transport/site
Tm= transport max, expressed in mg/min
===secretion & reabsorption

Question 5

Q

1-Tm limited reabsorption

2-Tm limited secretion

3-clinical relevance

Answer

A

1-if reabsorption is Tm limited—if filtered load exceeds Tm the solute will appear in urine
—if filtered load is less than Tm, the urine will be devoid of solute

2-secretion= transfer from peritubular capillaries to the tubule fluid
-if delivery of solute to peritubular capillaries exceeds the Tm secretion rate, then some solute will be returned to circulation via renal vein
-if deliver of solute is less than Tm, then no solute will appear in renal venous blood
Ex= PAH, penicillin, bile acids, creatinine, urea —all are secreted by Tm limited mechanisms

3-co-admin of drugs that compete for the same transporter can inc plasma conc of both drugs…probenecid w/ penicillin will inc plasma half life of penicillin by competing for the same renal transporter

Question 6

Q

1-electrolyte reabsorption & secretion along nephron

Answer

A

1- Na transporters are site of diuretic action…esp in proximal tubulue, site of acid-base regulation
K secretion in principal cells = safe plasma K in blood
-most of filtered Na is reabsorped in proximal tubule, followed by loop of henle…distal tubule & collecting duct “fine tune” the excretion of Na while Cl is reabsorbed
-proximal tubulues reabsorb LOTS of solute, then the loop then small amounts in the distal tubule.
-K is secreted from prinicpal cells whenever theres normal/elevated intake of K

PTH enhances tubular Ca reabsoprtion
PTH reduces Pi reabsorption by tubular cells

Question 7

Q

1-early proximal tubule & Na Linked Transport

2-why is Na/K atapase more imp in proximal tubule

3-Na-H antiport

4-Na-solute symport

Answer

A

1-proximal tubule, the reabsorption of every substance (even H20) is linked bc of Na-K ATPase pump

2-movemnt of solutes is linked to passive movememnt of Na into the tubule cell down its electrochemical gradient, the accum of solute in the interstitial space drives the passive movement of H20

3-secretion of H ion is imp renal mechanism for removing acid from blood
-results in bicard reabsorption in 1 for 1 exchange w/ H

4-Na-glucose—SGLT 1&2

Na-amino acids
Na other solutes (phosphate & lactate)

glucose & AA are cleared form tubule fluid by end of proximal tubule

Question 8

Q

1-late proximal tubule Na reabsorption

2-prox tubule summar

3-diuretics

4-natriuesis

5-kaliuresis

6-diuretics inhibiting Na reabsorption

Answer

A

1-little Cl was reabsorbed in early proximal tubule

late proximal tubule, Cl is avidly reabsorbed due to passive diffusion of Na, Cl, via paracellular path
operation of parallel Cl/Anion & Na/H antiporters reabsorb NaCl via transcellular route

2-Na is reabsorebed in prox tubule by

–Na/H antiport, Na/solute symport, passive diffusion w/ Cl, solvent drag w/ H20
all glucose + AA are reabsorebed here
large amts of Ca & P are reabsorbed
H20 reabsorbed
by the end of the tubule, tubular fluid= isoosmotic to plasma bc of the osmotic movement of H20

3-inc excretion fo both Na & H20

4-inc in Na excretion

5-inc in K excretion

6-diuretics dec ECF volume…reduction initiates compensatory mechanisms that enchance Na reabsorption in tubules so the patient returns to Na balance of input=output, but at a lower level of total body Na & steadstate ECF

Question 9

Q

Diuretics & prox tubule

1-osmotic diuretics

2-carbonic anhydrase inhibition

Answer

A

1-osmotic diuretics are unresorbable solute that slows osmotic movement of H20 from lumen to the interstitial space
—dec in H20 reabsorption = less Na reasborption via paracellular solvent drag
—excess gluocse in prox tubule (filtere load> Tm) = diuretic…ppl w/ untreated diabetes= polyuria
(manitol= diuretic)
—osmotic diuretics arent ised in control of arterial hypertension= acute fluid overload

2-acetazolamide= inhibitor of enzyme carbonic anhydrase. inhibition of CA slows the Na-H exchanger= inc in Na & H20 excretion…H20 accompanies extra Na in lumen

–Ca inhibitors arent used for hypertension
–Ca inhibitors can alter acid base balance—make it more ifficult for body to excrete acid & easier to lose bicarb in urine…so CA inhibitors can be used to treat alkalotic condition= promote metabolic acidosis

Question 10

Q

Na reabsorption in the loop of henle

1-thick ascending limb

2-thin descending limb

3-thick ascending limb of the loop of henle TALH

Answer

A

1-Na reasborption occurs—25% of filtered load of Na

2-doesnt reabsorb that much—H20 reabsorbed bc of inc osmotic gradient

3-reabsorption of Na, K & Cl bc of basolateral Na/K ATPase—-apical transported called Na-K-2Cl symport

blocked by diuretic furosemide—loop diuretic
loop diuretic= powerful, treat acute pulm edema & to control edema in patients w/ congestive heart failure
Na/H antiport= reabsorbs Na
tubule segment is impermeable to H20
positively charged lumen drives passive paracellular reabsorption of cations—Na, K, Ca, Mg…some K returns to tubular lumen via sep apical K channel, reasonw hy tubular lumen +3-10mV to peritubular fluid
Na reabsorption in loop of henle occurs via paracellular route via facilitated diffusion

Question 11

Q

1-early distal tubule

2-late distal tubule & collecting duct

3-aldosterone & principal cell

Answer

A

1-Na-Cl symporter = reabsorb Na in early distal tubule

early distal tubule reabsorbs Ca & Pi
located in cortex, is impermeable to H20
Na-CL symporter is blocked by thiazide diuretics…treat hypertension & congestive heart failure

2-principal cells & intercalated cells

principal cells= reabsorbe Na & secrete K
intercalated= secrete H or HCO2 & reabsorb K (imp for acid base)

3-aldosterone= adrenal mineralocorticoid—stimulates Na reabsorption in thick ascending limb TALH, early distal tubule & in principal cells of late distal tubule

inc Na/K ATPase protein abundance
Aldosterone also inc the amt of apical Na/K/2Cl symporters (TALH) and Na-CL symporters (early distal tubule)
*-primary site of aldosterones action in principal cell in the late distal tubule & collecting duct= Na reabsorption & K secretion**
alters protein synthesis by acting w/ nuclear DNA
–release is stimulated by angiotensin 2, high plasma K, & plasma acidosis

Question 12

Q

1-epithelial Na channel (ENaC) for Na reabsorption in principal cell

2-aldosterone inc Na Reasborption by

3-aldosterone inc K secretion by

Answer

A

1-Na enters principal cell through epithelial channel that is blocked by diuretic amiloride.

can be be slowed by aldosterone recep. antagonists
tubule lumen is neg compared to peritubular fluid, lumen negativity helps K secretion down gradient
Cl is reabsorbed via paracelullar pathway by lumen neg voltage
Cl is reabsorbed via paracellular pathway, driven by lumen neg voltage
H20 permeability is dependent on action of ADH (vasopressin)

2-inc permeability to Na by inc number of active ENaC’s by stimulating synthetsis & insertion of new ENaC’s into apical membrane

inc activity & # of Na/K ATPases in basolateral membrane
–principal cell= site of renal tubular K secreton

3-stimulating Na reabsorption
-inc number of open apical K channels

Question 13

Q

1-kidney & maintaining K homeostasis in the body

2-insulin

3-epinephrine

4-aldosterone

Answer

A

1-maintenance of plasma K w/in narrow limits is imperative. REnal excretion of K takes longer but is regulated…rapid movement of K into cells is regualted by 3 hormones
-hormones stimulate activity of Na/K ATPase, Na/K/2Cl symporter, and Na/Cl symporter in skeletal muscle liver, bone, & RBC

2-move K into cells w/in min. Insulin infused IV to rapidly correct hyperkalemia

3-stimulation of alpha adrenoceptors releases C from cells & stimulation of beta-2 adrenoceptors promotes uptake of K…w/in min

4-peripheral action to promote cell uptake of K= a hour. chronic elevation of aldosterone (adrenal tumor)= hypokalemia bc of inc excretion of K via kidney & via uptake of K into cells

Question 14

Q

1- K reabsorption along the nephron

Answer

A

1-major role in regulating K balance in body, unlike Na, K can also be secreted into the tubule—secretion & reabsorption of K can happen in late distal tubule/collecting

secretion= principal cell, reabsorp=intercalated cell
secrete K on a normal K intake
high dietary intake, secretion inc greatly
low dietary intake, reabsorption of K = reduce excretion to 1% filtered load
–plasma K & aldosterone = physiologic regulators of K secretion, w/ aim of maintaing normal K balance

Question 15

Q

1-aldosterone & K secretion

2-plasma & K secretion

Answer

A

1-normal circulating levels of aldosterone regulate K loss via principal cells

further inc in aldosterone further stimulate K secretion, hyperaldosteronism= hypokalemia
lack of aldosterone = difficult to remove extra K from body…low aldosterone= hyperkalemia
plasma K regulates aldosterone release

2-inc in plasma K= inc renal secretionof K

dec in plasma K= dec renal secretion of K
effects= direct effect of plasma K on principal cells & indirect effect = modulation of aldosterone release

Question 16

Q

1-K-sparing diuretics works at principal cells

Answer

A

1-principal cell= site of action for 2 diff types of diuretics

first type is ENaC channel blockers= amiloride, block Na from using ENaC
2nd type= aldosterone receptor antagonist= spironolactone—block from interacting w/ intracellular
K secretion from prinicpal cell dec when principal cell based diuretics are used…K sparing diuretics
other diuretics–osmotic, loop, thiazides, all inc K excretion by the kidney—K losing diuretics…bc of enhanced delivery of Na to principal cells

K SECRETION DEC WHEN NA REABSORPTION SLOWS DOWN

Question 17

Q

1-water balance

2-sensed

3-sensor

4-effector

5-affected

6-clinical Dx

Answer

A

1-lose water via sweat glands, respiration, fecal route, urinary route, vomiting

water intake= oral and is variable
kidney regulates water loss via conc or dilution of urine
kidney excrete urine that varies from 50-1200 mOsm/kg H20
amt of H20 lost from body affects plasma osmolality

2-ECF vol= effective circulating volume
Plasma Osmolality=plasma osmolality

3-ECF vol= arterial & cardiac barorecptors
plasma osmolality= hypothalmic osmoreceptors

4-ECF Vol= ANg 2/aldosterone/SNS/ANP
plasma osmolality= ADH

5-ECF Vol= urine Na excretion
plasma osmolality= urine osmolality (H20 output) & thirst (H20 intake)

6-ECF vol= bedside Exam of ECF volume
plasma osmolality= lab test plasma osmolality

***problems w/ Total body water= altered plasma osmolality, reflected as alteration in plasma Na
***problems w/ total body Na= manifest as altered ECF vol

Question 18

Q

1-Antidiuretic hormone & control of renal H20 excretion

2-ADH

3-osmotic regulation of ADH

Answer

A

1-normal plasma osmolality= 275-295 mOsm/Kg H20

diuresis= excretion of a large amt of urine
antidiuresis= excretion of a small amt of urine
during diuresis the urine = hypoosmolar or dilute(Uosm < Posm)
during antidiuresis, urine is hyperosmotic or concentrated (Uosm>Posm)

2-same hormone as vasopressin or AVP

release from posterior pituitary is inc or suppressed depending on neural signal from hypothalamic osmoreceptors or from signals arising from arterial & atrial baroreceptors
ADH inc H20 reabsorption in late distal tubule & collecting duct, regualtes how much H20 leaves in urine

3-cells in hypothalamus sense changes in plasma osmolality

osmoreceptors then send a signal to hypothalamic neuronal cells to either suppress or inc ADH release
neural cells synthesize ADH & then secrete ADH from nerve terminals in posterior pituitary
when osmolality is <280 or so, ADH secretion= zero
sensitive to small inc in osmolality above this point

Question 19

Q

1-low plasma osmolality

2-high plasma osmolality

Answer

A

1-sensed by hypothalmic osmoreceptors (dec firing rate)

reduced stimulation of vasopressin neurons, dec secretion of vasopressin
dec plasma vasopresisn, reabsorption of H20 in collecting duct dec, amt of H20 in urin inc
return of plasma osmolallity towards normal

2-sensed by hypothalmic osmoreceptors (inc firing rate)

enhanced stimulation of vasopressin, inc secretion of vasopressin
inc plasma vasopressin, reabsorption of H20 in collecting duct inc, amt of H20 in urine dec
conservation of plasma H20…return to nromal plasma osmolality requires intake of fluid

Question 20

Q

1-ADH & aquaporins

2-overview of conc & dilution

3-conc & dilution occur bc

Answer

A

1-ADH inc H20 permeability in collecting duct, so ADH dec urine flow rate & inc urine osmolality

in principal cells of kidney, ADH binds to vasopressin 2 receptor—V2 receptor inc cAMP levels that will trigger a cascade that causes insertion of aquaporins into apical membrane
aquaporin channels are H20 channels & are selective…allow H20 but not electrolytes
when ADH levels dec, the aquaporins zip back into interior of cell…dec H20 permeability in the cells

2-in prox tubule, water follows solute reabsorption= isoosmolar fluid by end of proximal tubule

kidney is capable of disengaging H20 from solute reabsorption…only in this way can the kidney regulate H20 & solute balance separately
disengagement is found in processes of conc & dilution

3-parts of nephron are impermeable to H20 yet transport solute (loop of henle, early distal tubule)

parts of nephron have a H20 permeability that is dependent on level of ADH (late distal & collecting)
medullary interstitium is hyperosmotic, & level of tonicity can be altered

Question 21

Q

1-cortical & medullary osmolality

2-what creates medullary interstitial osmotic gradient

Answer

A

1-ADH alters the tubule permeability to H20

H20 will only move when there is a conc difference between tubule fluid & interstitial fluid
medullary interstitium has graded levels of hyperosmolality
hyperosmlality is critical for formation of hyperosmotic (conc) urine

2-solutes that are reabsorbed by thick ascending limb & collecting ducts—particularly NaCL & urea provides osmoles for interstitial gradient
-unique anatomic arrangement of loop of henle + collecting—contributes to medullary interstitial gradient= countercurrent multiplication= porgressive inc in osmolality as loop dips deeper into medulla

Question 22

Q

1-overview of dilution of urine

2-dilution steps

Answer

A

1-dependent on thick ascending limb of loop of henle

solutes are reabsorbed here w/o water
impermeable to water—if you remove solute but not H20, tubule fluid= more dilute
ADH must be low to keep tubular fluid dilute as collecting duct moves through the medullary interstitial osmotic gradient on way to papilla of kidney

2-iso-osmolar tubular fluid enters thin descending limb

water is removed & tubular fluid= hyperosmotic at end of loop
thin ascending limb, NaCl moves out but H20 cant leave…dilution starts
thick ascending limb, Na-K-2Cl symport removes solute, but water cant elave, tubular fluid becomes hypo-osmolar
distal tubule & cortical collecting duct continues to reabsorb NaCl…in absence of ADH, Water perm= low and tubular fluid osmolality is 100 water
medullary collecting duct, some NaCl is reabsorbed…absence of ADH, H20 permeability is low…final urine can be hyp-osmolar as 50 w/ minimal amts of NaCl

Question 23

Q

1-concentration step by step

2-key pt

3-imp role of urea in medullar osmolality

Answer

A

1-same steps from proximal tubule through early distal tubule

then if ADH is present, H20 perm inc in late distal tubule & collecting
H20 leaves the tubule & the tubule fluid equilibrates w/ surrounding hyperosmotic medullary interstitial fluid
end of collecting duct, urin has an osmolality of 1200 or whatever the level is in the medulla

2-transport of NaCl out of ascending thick limb= impaired, renal concentrating power will dec bc max medullary interstitial osmolality will be lower than usu

3-urea= byproduct of protein metabolism

important solute in inner medulla interstitial fluid
collecting duct = permeable to urea only in inner medulla & permability inc w/ ADH
ADH does this by phsophorylating urea transporters in apical membrane of the inner medullary collecting duct cells
chronic H20 restriction, ADH stimulate production of additional transporters
urea moves out of tubule along its conc gradient & accumulates in interstitium
antidiuresis is max about 600 of total medullary osmolality is attributabe to NaCl & about 600 is attributable to urea

Question 24

Q

1-when ADH levels are suppressed

2-key pt

Answer

A

1-urea perm in inner medulla dec
but theres still urea perm in absence of ADH
-some of urea will reenter the tubule & thin ascending limb through a urea transporter
-recycling of urea in kidney facilitates accum in interstitium
-permeability of loop of henle to urea= less than the permeability in inner medulla

2-accum of urea in the interstitium is necessary to reach max renal conc power

—animals w/ defect in renal ureal transporters= reduced urinary conc ability…low protein diet can cause a dec in urinary conc ability while a high protein diet can enhance max conc power

Question 25

Q

1-vasa recta & medullary washout

2-why isnt max medullary osmolality 1200 during diuresis

3-vasa recta also supple O2 to medullary segment of nephron

Answer

A

1-vasa recta capillary loop arouns the tubules & pick up excess H20 & solute deposited in the interstitium by tubules..solute & H20 are returned to the systemic circulation via renal venous
-if vasa recta flow inc, high blood flow will wash out the gradient by picking up more solute—conc ability will be decreased until gradient can be reestablished

2-medullary osmolality isnt maximal during diuresis bc Vasa recta blood flow is higher than usual= helping to wash out solute
& urea content in intersitium is low= isnt much urea moving out of collecting duct into interstitium= lower medullary osmotic gradient bc ADH is low during diuresis & low ADH will dec urea permeability

3-if vasa rec dec (hemorrhage/ischemia), medulla will be starved of O2. so NaCl reabsorp by loop will be impaired (ATP process) and medullary intersitial osmotic gradient will dissipate & will be conc ability

Question 26

Q

Summary
1-rate of active Na reabsorption in thick ascending

2-permeability of late distal/collecting duct to H20

3-vasa recta blood flow

4-protein content of diet

Answer

A

1-high rate of Na reabsorption enahnces medullary interstitial osmotic gradient
low rate of Na reabsorption reduces medullary interstitial osmotic gradient

2-higher the plasma ADH, greater the rate of H20 reabsorption, assuming cells respond to ADH

3-low flow= high medullary interstitial osmolality
-high flow= washout (reduction of the gradient)

4-inc protein diets = enhance conc power
while low protein diets reduce conc power by modifying urea content of medulla

Question 27

Q

1-H20 balance and the kidney

2-urine osmolality & conc & dilution of urine

3-quantitiating amt of free water the kidney generates

4-minimum urine vol per day

Answer

A

1-kidney adjusts the amt of H20 in the plasma by regulating how much H20 leaves the body in urine

plasma osmolality is too high= kidney conserves H20…more H20 than solute is returned to circulation
plasma osmolality is too low= kidney dumps excess H20 …more solute than H20 is returned to circulation

2-hypoosmolar= Uosm\< Posm (dilute urine)---dissolving solute in large vol of H20
iso-osmolar= Uosm = Posm 
hyperosmotic= Uosm\> Posm (conc urine)--- dissolving solute in small vol of H203-

3-free water clearance= amt of water that was either added to the urine to make the urine dilute
or taken out of the urine to make the urine conc
—neg free water clearance= tubular conservation of water
-free water clearnce is + when urine is dilute (plasma water is lost in excess of solute, extra water in urine)
-free water clearance is - when urine is conc (plasma water is retained in excess of solute, extra water taken out of urine
-free water clearance is 0 when urine has same osmolality as plama

4-generate abotu 600 mmol of excess sol per day
-mac concentrating power of kidney=1200, minimum urine output is 600/1200 or .5 l/day
most people generate 1-2 L/day
oliguria= urine output <400 ml day
anuria= urine output <50ml day

Question 28

Q

1-hyponatremia

2-pseudohyponatremia

3-isotonic or hypertonic hyponatremia

4-hypotonic hyponatremia (true)

hypotonic

5-hypovolemic

6-euvolemic

7-hypervolemic

Answer

A

1-normal plasma Na= 135-145

hyponatremia most common disorder of electrolytes encountered in clinical practice—acutely or chronically hospitalized patients
hyponatremia= typically the result of H20 retention in excess solute but doesnt necessarily mean patient is hypervolemic…hyponatremia= euvolemic

2-Na in plasma water is normal, Na in total plasma fraction is low bc of hyperlipidemia & hperproteinemia

3-presence of unmeasured effective osmoles initiating fluid shift from ICF to ECF—hyperglycemia, mannitol, & radiograph contrast signs

4-effective osmolality of plasma= low

5-signs of vol depletion, orthostatic intolerance, dry mucous membranes, dry axillae, dec skin turgor, low spot urine, infusion of normal saline

6-modest diff in ECFV cant be detected

absence of clinical or biochemical signs of volemia
spot urine greater than 30

7-clinical signs of vol expansion
-subcutaneous edema, ascites, pulm edema, elevated BNP, spot urine under 30

Question 29

Q

1-hyponatremia cont

2-pseudohyponatremia

3- isotonic or hypertonic hyponatremia

Answer

A

1-if plasma osmolality dec, plasma ADH would dec & free H20 clearnce would inc dramatically to correct imbalance, so hyponatremia must be secondary to a defect in renal H20 excretion
-exceed normal kidneys ability to excrete free H20…can occur if water is ingested so rapidly that it exceeds ablity to exrete H20 per hour

2-when Na levels are measured in total plasma, but Na levels are normal if only plasma water is sampled
-directly measured plasma osmolality is measured

3-normal or elevated plasma osmolality…bc another effective osmole has been added to plasma either endogenous like glucose or exogenous like radio contrast agents
-additional osmoles draw H20 osmotically from ICF to ECF & dilute plasma Na…removal of additional effective osmoles will result in correction of dilution hypnatremia

Question 30

Q

1-syndrome of inapprorpiate ADH

2-patients w/ SIADH present w/

3-hypnatremia w/ SIADH treated w/

Answer

A

1-SIADH- common cause of hyponatremia—euvolemic

patients dont show sign of either hypo/hypervolemia
plasma ADH is too high compared to plasma osmolality
may be bc of persistent secretion from pituitary or ectopic tumor or bc of reset osmostat for release of ADH
must be intake of H20 sufficient to overwhelm reduced renal capacity to excrete free H20

-some drugs stimulate ADH release like antidepressents & morphine…causing SIADH= postsurgery, aggressive post surgical fluid replacement & enahnced ADH release bc of morphine admin

2-hypnatremia

urine osmolality that is greater than 100 and may exceed plasma osmolality
free water clearance may be neg

3-water restriction—-onset was gradual & patient shows minimal signs
pharmacological blockades of action of ADH at collecting duct

Question 31

Q

1-hypernatremia

2-diabetes insipidus

3-central diabetes insipidus

4-nephrogenic diabetes insipidus

5-patients w/ both types of DI

Answer

A

1-hypernatremia is Pna>145

hyperosmolality
unreplaced H20 losses
less common is hypernatremia= induced by infusion of IV solution of hypertonic saline
defense against H20 loss is ADH & thirst
H20 intake is the ultimate defense against hypernatremia

2-excretion of large volumes (polyuria) of hypotonic urine due to defect in ADH fucntion or release

3-dec in production or release of ADH from pituitary: stroke, tumor, drug induced, genetic

4-kidney is unable to respond to ADH- drug induced lithium carbonate, defect in V2 recetor or aquaporin

5-at risk for developing hypernatremia—risk is inc if access to fluids is restricted

Question 32

Q

Testing Renal Concentrating Ability in cases of suspected DI

Answer

A

test ability of kidney to concentrate urine via water deprivation test
normal osmoregulation, ADH will be released as plasma osmolality inc due to lack of water ingestion—result = urine conc (Uosm>Posm)
–patient w/ compelte central DI, little change in urine osmolality even as plasma osmolality rises…urine osmolality will remain below plasm osmolality
not test ability of kidney to respond to ADH by giving exogenous ADH—if you give ADH & urine osmolality doesnt inc then the kidney cant respond to ADH or kidney is already responding max to endogenous plasma ADH
–if Uosm begins low & stays low after giving exogenous ADH then patient has completel nephrogenic DI
–if urine osmolality is very high before giving endogenous ADH as will happen in response to H20 deprivation in patient w/ normal osmoregulation—kidney reached max physiologic capacity to concentrate urine even if more exogenosu ADH is provided it cant go any further
w/ primary polydipsie= little response to exogenous ADH—diff between normal condition & primary polydipsia would be level of urine conc reached

-using both tests distringuish between polyuria due to central DI, nephrogenic DI & psychogenic polydipsia

Question 33

Q

1-regulation of ECF vol and osmolality are interrelated

2-ADH system responds to acute changes in plasma osmolality

Answer

A

1-ECF regulating system operates w/in osmoregulatory system & w/o ECF regulatory system
-operation of osmoregulatory system could result in excessive ECF expansion or contraction in response to changes in dietary Na intake

2-change in Na intake/output can cause change in plasma osmolality…body alters water intake & renalw ater reabsorption to maintain isotonic ECF…osmolality is maintained at expense of ECF volume

–dec Na intake—> neg Na balance (dec body Na)—>eventual ECF contraction
–inc Na intake—>pos Na balance (inc body Na)—>eventual ECF expansion
ECF returns to normal when body Na is either lost from body or regained via eating/drinking

-acute change in water intake or output= acute change in plasma osmolality…modulation of ADH levels= excretion of excess H20 or renal retention of H20 to return plasma osmolality to normal levels at euvolemia

Question 34

Q

1-changes in body Na content are reflected in changes in ECF

2-renal response to changes in ECF

3-Renal Sympathetic Nerve Activity

Answer

A

1-changes in ECF volume alter BV & BP…hemodynamic alterations are detected by arterial baroreceptors, atrial receptors & kidney
-change Na & H20 reabsorption to return ECF volume towards normal…return BP towards normal

2-4 effector:

renal symp nerve activity (renal SNA)
renin-angiotension aldosterone system (RAA)
ADH (vasopressin)
Atrial Natriuretic Peptide (ANP)

3-inc renin release via beta-1 receptors, activates RAA system

directly inc Na reabsorption in proximal tubule
–Na reabsorptive effect is present at basal levels of renal symp nerve activity
inc RSNA plays imp role in conserving Na durign Na deprivation and may play role in disorders of body fluid volume regulation
normal conditions, suppression of basal RSNA= natriuresis but effect is small

Question 35

Q

1-renin angiotensin aldosterone system

Answer

A

1-angiotensin 2 effects=

inc Na reabsorption via At1 receptors—enhances Na reabsorption in prox tubule, via inc Na-H antiport insertion into apical membrane
stimulates aldosterone synthesis & release- from adrena cortex (aldosterone enhances Na reabsorption)
inc filtration fraction (keeps GFR from going too low) by constricting efferent arteriole
systemic arteriolar vasoconstriction(raise BP via inc in TPR)
inc H20 retention & intake (stimulates ADH release & thirst center in brain)
neg feedback effect on renin release

—hormonal control of BP the RAAS

Question 36

Q

1-ADH (vasopressin) stimuli for release

2-atrial natriuretic peptide (ANP)

Answer

A

1-osmolality= affects ADH release from pituitary

–inc ADH release as plasma osmolality inc above threshold
–ADH release is suppressed if plasma osmolality dec
nonosmotic stimuli= angiotensin 2 &&&cardiac (atrial) and arterial baroreceptors (dec stretch)
–activated when ECF volume and/or BP dec

2-ANP is a peptide released from heart…inc Na exretion so H20 excretion too
-release of ANP is stimulated w/ hypertension and/or expanded ECF volume…doesnt appear to be very important in controlling daily Na balance under normal conditions—-but release of ANp from heart is heightened when ECF volume is expanded

–ANP inc Na excretion by—inc GFR (inc filtered load of NA)
reduction in proximal tubule Na reabsorption
reduction in tubular Na reabsorption in collecting duct system

Question 37

Q

1-High ECF volume

2-Low ECF volume

Answer

A

1–inc GFR which inc filtered load of Na & H20

dec Na reabsorption in proximal tubule
dec Na reabsorption in collecting duct (principal cell)
inc H20 excretion (dec H20 reabsorption)
—-excretion of excess Na & H20, maintain isotonicity of plasma

2–Dec GFR which dec filtered load of Na & H20

inc Na reabsorption in prox tubule
inc Na reabsorption in collecting duct (principal cell)
dec H20 excretion (inc H20 reabsorption)
–intake of H20 & Food

Question 38

Q

Normal
1-pH
2-PCO2
3-HCO3

Mass Action-effect of PCO2 on HCO3
4-inc PCO2 of 10mm
5-dec PCO2 of 5 mm
6-dec PCO2 of 10 mm

7-anion gap

8-procedure to evaluate acid-base imbalances

Answer

A

1-7.35-2.45

2-35-45 mmHg

3-22 to 26 mEq/L

4-= inc HCO3 by 1

5-= dec HCO3 by 1

6-=dec HCO3 by 2

7-8-16 mEq

8-check pH, acidotic or alkalotic?

acidosis= metabolic dec HCO3 or resp inc PCO2
alkalotic= metabolic inc HCO3 or resp dec PCO2
is it bc of mass action

Question 39

Q

1-acid base intro

2-why H ion conc is important

3-pH scale

4-Henderson Hasselbalch equation

Answer

A

1-regulates CO2 concentration

ventilation reduced, CO2 accumulates combines w. H20 and forms carbonic acid
2nd component is metabolism
diet & anaerobic metabolis add acid to the body—acids are buffered by bicarb so bicarb must be replaced
kidneys = homeostasis for acid base

2-H ions are highly reactive and can alter a proteins charge

change molecular configuration & activity of protein
activity of pH sensitive enzyme is refuced when pH dec …pH must be tightly regulated
extracellular Na conc= regulated w/in .01 M
extracellular H conc regulated w/in .0000000001m

3-normal extracellular H2 ion conc ranges from pH 7.35-7.45

35 pH has H ion conc of 45 vs basic 7.45 which has ion conc of 35…lower numbers= acidic…dec in pH scale of .3 is equivalent to doubling of H ion concentration
- change in pH of 1.0 is 10x change in H ion conc (logs)

4-utilizes the pKa dissociation constant for bicarb & neg log scale to account for pH scale…CO2 conc is calc w/ solubulity constant of (0.03 mM)
pH= pKa + log { [HCO3]/ (0.03 * PCO2) }

Question 40

Q

1-henderson-hasselbalch equation

Answer

A

1-using arterial values, HCO3 conc of 24 mEq, PCO2 of 40 mmHg, a CO2 solubility constant of 0.03 and equilibrium constant (pKa) of 6.1 at body temp…pH of arterial blood= 7.4

HCO3:PCO2 ratio of 20:1…generates normal pH of 7.4
pH is function of ratio of plasma bicarb to dissolved CO2
pH maintained by—kidneys ability to regulate plasma bicarb conc
–lungs ability to regulate plasma CO2 conc
used to measure the equilibrium constant using known conc of HCO3 & PCO2 and measuring pH

pH= ( [HCO3]* Base )/ ([CO2] * Acid)

Question 41

Q

1-buffers

Answer

A

1-reversibly bind & release H, they stabilize pH

buffers minimize changes in pH and dont prevent changes in pH
buffers in body are located in extracellular & intracellular fluids & bone
ability of a buffer to maintain pH is proportional to its conc & disassociation constant
pKa of buffer refers to pH at which dissociated & associated forms of buffer system are in equal conc
–buffers are most effective in solutions where desired pH of solution is close to pKa of buffer…normal blood pH is 7.4 the ideal buffer should have a pKa close to 7.4

Question 42

Q

1-blood buffers

Answer

A

1-bicarb bugger system is most important buffer in blood & accounts for 53% of blood buffering capacity despite pKa= 6.1

CO2/HCO3 buffering system= effective in buffering blood pH bc of high HCO3 conc & combined regulation of its conc by lung & kidney
Hemoglobin accounts for 35% of buffering—7.85 deoxy & 6.6 when oxy—buffering action is greatest in venous blood
acidic environment oat tissue promotes dec in Hb-O2 affinity and O2 unloading (bohr) promote CO2 binding to H2, prevents production of H from CO2 & free Hb facilitates buffering H
plasma proteins have ideal pKa 7.4—but conc in blood is low
phosphate accounts for 5% of bloods buffering
buffers reversibly bind & release H as H conc changes

Question 43

Q

1-bone buffers

2-intracellular buffers

Answer

A

1-in response to an inc in plasma H2 ion conc, excess H2 ions are echanged w/ Ca, Na, & K associated w/ carbonate on the bone surface

during chronic metabolic acidosis, osteoclasts in bone are also activated…that release additional Ca carbonate & Ca phosphate into extracellular fluid
buffering H ions by bone contribute up to 40% of total buffering capacity during chronic acidosis
oral health of your loss & poor fitting dentures..bone diseases liek rickets, osteomalacaia

2-excluding RBCs, primary intracellular buffers are proteins & organic/inorganic phosphates

due to their high intracellular concentrations
importantly intracellular bicarb conc is very low & therefore is not an effective intracellular buffer

Question 44

Q

Systemic Buffering for Metabolic vs Respiratory Acidosis

1-buffering for metabolic acidosis

2-buffering for resp acidosis

Answer

A

1-diarrhea can induce metabolic acidosis by loss of HCO3…aprrox half of excess H will be buffered by remaining extracellular buffers

remaining H will enter cells or exchange cations on bone
buffering extracellular bicarv occurs w/in min
entry & neutralization of H in cells or bone will take 2-4 hours
resp system will compensate by inc ventilation & reducing PCO2

2-COPD may lead to resp acidosis…resp based acid-base imbalances are complicated bc extracellular bicarb is no longer an effective buffer bc mass action effect of elevated CO2 drives reaction ot the right to create H & HCo3…bc of conc gradients, H will not recombine w/ HCO3 to reform H2CO3
-so excess H will be buffered by intracellular buffers…2-4 hrs

–renal system will compensate by creating new bicarb
–compensation occurs by opposite system

Question 45

Q

transcellular exchange of ions
1-ion exchange due to diff H conc

2-ionc hange due to diff K conc

Answer

A

1-when there is an inc in H ion conc in extracellular fluid, H ions will enter cells down their conc gradient

in order for cell to maintain electroneutrality a cation but leave…involves exit of a K ion
transceullar ion exchange during acidosis= K efflux which may alter K balance and result in potential fatal elevation in plasma K conc
reverse exchange of ions iwll occur during alkalosis
transcellular excahnge occurs systemically, renal cells respond to alterations in intracellular H ion conc by changing expression of carbonix anhydrase & activity of glutaminase…alters rate of bicarb recovery & production of new bicarbonate

2-transcellular ion exchange can be induced by elevated levels of K…when plasma K is elevated, K moves into cells in exchange for H

Question 46

Q

1-Mass Action

2-resp acidosis -inc PCO2

3-resp alkalosis- dec PCO2

Answer

A

1-rate of reaction is proprotional to product of participating molecules

an inc in CO2 conc will inc production of HCO3
response isnt linear & favors loss of HCO3
concept is essential in order to determine whether a change in bicarb is due to the initial resp imbalance or whether renal comp has occured

2-for ever 10 mmHg inc in PCO2 from 40 mmHg, mass action will inc plasma HCO3
PCO2: 40-50mmHg will inc HCO3 from 24 to 25

3-for ever 10 mmHg dec in PCO2 from 40 mmHg mass action will dec plasma HCO2 by 2mEq
-PCO2 40-30 will dec HCO3 from 24 to 22

Question 47

Q

1-acid base balance & kidneys

2-carbonic acid

3-non carbonic acid

4-clinical

Answer

A

1-intake of acid in normal diet combined w/ cellular metabolism of proteins & phospholipids generates 5070 of acid/day for an avg adult…2 types of acid contribute to daily acid load= carbonic acid & non carbonic

2-metabolism of carbs & fats produces CO2 which combines w/ H20 in RBCs to form carbonic acid—facilitated by enzyme carbonic angydrase

carbonic acid disassociates to form H & HCO3
at lung bc of low PCO2, chemical reactions reverse & carbonic acid is removed as CO2 in expired gas

3-metabolism of proteins and intake of foods w/ phosphates & suplhates lead to daily acid production

metabolism of cysteine & methionine generate sulfuric acid while metabolism of lysine produces HCl
metabolism of glutamate generates a base but net effect of our diet is acid production

4-w/o buffering, acids would reduce body pH to 3
extracellular pH is maintained bc acids are 1) buffered by blood bicarb and other buffers to produce H20 & CO2
2) lungs remove CO2 from body
3) kidneys filtered bicarbox is recovere and an equivalent 50-70 mEq of new bicarb is created

Question 48

Q

Global Renal Overview

Answer

A

1-Acid production= non aerobic metabolism will produce lactic acid along w/ sulfuric, phosphoric & organic acid
-acid is buffered by blood (bicarb, Hb, & plasma proteins), tissue, proteins & bone
-CO2 generated from tissues…converted to carbonic acid in RBC by carbonic anhydrase…acid dissociates into bicarb & H which is buffered by deoxy Hb
-at lungs, low PCO2 shifts this equation to left…overally carbonic acid leaves body as CO2
-bc bicarb is consumed by noncarbonic acids…must be replenished…filtered bicarbs ISNT reabsorbed but bicarb recovery & creation of new bicarb exist
-in proximal tubule cell, CO2 & H20 are converted to bicarb & H w/ enzyme carbonic anhydrase.
the H is secreted into lumen & bicarb is recovered by circulation…secreted H is neutralized by filtered bicarb in early portion of nephron so bicarb is recovered by its production & loss in proximal tubule
-new bicarb if formed by 2 mechanisms
——-proximal tubule—Glutamine is metabolized to form new bicarb & ammonium, new bicarb added into circulation
—–medullary collecting duct, carbonic anhydrase produces new bicarb…imp, the secreted H is neutralized by non bicarb buffers…production of bicarb and use of nonbicarb buffer leads to new bicarb

***acid & CO2 productions are buffered & removed and bicarb is recovered & created to maintain acid base balance

Question 49

Q

1-renal bicarb regulation

2-bicarb recovery—high capacity, low gradient

Answer

A

1-glomerular filtration rate is 180 L/day

less than 50 g of fluid moving through kidneys per day, w/ a plasma bicarb concentration of 24 approx 4300 mEq of HCO3 is filtered out of plasma and into nephron
maintain normal pH, filtered bicarb must be returned to circulation
filtered bicarb isnt reabsorbed but is recovered
80% of bicarb is recovered in early proximal tubule…10% in thick ascending limb
6% in distal tubule, 4% in collecting ducts…no bicarb in urine
80% bicarb is recovered in early prox, not resabsorbed in kidney but is recovered

2-combo of CO2 & H20 to form H & HCO3 inside renal tubular cells

Question 50

Q

1-proximal tubule

Answer

A

1- start= formation of H & HCO3 via carbonic anhydrase in renal tubular cells
-H secretion= 2/3 of H secretion is mediated by Na-H exchanger…Bc of high Na conc in proximal tubule= high capacity system
1/3 of H is transported w/ ATP dependent pump
-Buffering= secreted H is buffered by filtered bicarb, resulting carbonic acid is converted to CO2 and H20 by luminal carbonic anhydrase —luminal carbonic anhydrase keeps H conc low, optimizing gradient for additional H secretion, contributes to high capacity, low gradient & high rate of bicarb recovery in prox tubule
-bicarb production= inside proximal tubular cells, bicarb transported across membrane & into interstitial fluid by 3HCO3—1 Na cotransporter (high capacity)…cotransporter is assisted by electroneg potential generated by Na/K ATPase pump…bicarb transpoted into interstitial fluid by Cl ion exchange
-Net effect= 1:1 recovery—high capcity, low gradient 1:1 recovery system for bicarb

Question 51

Q

1-new bicarb

2-new bicarb via glutamine metabolism

Answer

A

1-sodium bicarb is consumed in the buffering process & lungs remove CO2 bc our diet & metabolism generate approx 50-70 an equal amt of bicarb must be replenished

2-start= proximal tubular cells are efficient at transporting the AA glutamine & cotransporting Na & glutamine into cells

Glutamine Metabolism= glutamine is broken down by glutaminase deaminated & then oxidized to produce 2HCO3 & 2NH4
New Bicarb- retention of new bicarb is dependent upon ammonium excretion by Na exchange, NH4 were returned to the circulation it would be metabolized by the liver to form urea & H…production of H would engate new bicarb formation
Ammonium Handling= pos charge of ammonium prevents reabsorption in proximal tubule—ammonia & diffusion trapping= ammonia is filtered & can buffer H secreted into tubular lumen to produce NH4 bc NH4 is trapped in tubular lumen, process= diffusion trapping, allows for excretion of large quantities of H w/ little change to tubular fluid pH

***ammonium secretion in proximal tubule inc in chronic acidosis—bc glutaminase activity is stimulated by acidosis…NH4 excretion can inc from normal value to over 300 in response to severe acidosis…glutaminae acitivty is also affected by K balance w/ hyperkalemia suppressing activity of enzyme

Question 52

Q

1-new bicarb via non bicarb buffers (low capacity, high gradient)

2-quick renal bicarb summary

Answer

A

1-start= medullary collecting tubulue, H & HCO3 made my carbonic anhydrase

type A cells= new HCO3 is transported into interstitial fluid by chloride ion exchange…in this part of nephron H secretion is dependent upon active transport by H-ATPase
non bicarb buffers= very little filtered bicarb is left in distal nephron, secreted H is buffered by nonbicarb buffers…primary non bicarb buffers are disodium phosphate, creatinine, & uric acid…production of new bicarb by carbonic anhydrase & neutralization of H via a non bicarb buffer results in net gain of new bicarb
limitations as availability of Na2HPO4 is regulated to maintain phosphate balance vs acid base balance

2-generation of H & HCO3 inside renal tubular cells is catalyzed by carbonic anhydrase

H is secreted into lumen of renal tubule, HCO3 is transported out of cells & into systemic circulation
recovery of filtered HCO3 occurs when secreted H ion binds to filtered HCO3 which is converted to H20 & CO2 no net gain of HCO3
creation of new HCO3 occurs w/ glutamine metabolism & secretion of NH4 into lumen of collecting duct, net gain of HCO3
creation of new HCo3 occurs when a secreted H binds to a nonbicarb buffer in the tubular lumen, net gain of HCO3

Question 53

Q

1-renal H & HCO3 secretion

2-mechanisms regulation H Secretion PCO2

3- “ “ HCO3

4-acidosis stimulates expression & activity of carbonic anhydrase

Answer

A

1-recovery of bicarb & production of new bicarb depend upon H ion secretion & eventual excretion

2-effects of PCO2- partial pressure of CO2 in extracellular fluid determines rate of CO2 diffusion into renal cells

subsequent conc of intracellular CO2 establishes rate of H production by carbonic anhydrase
inc Plasma CO2= inc intracellular CO2= inc H production= inc H secretion
resp acidosis will inc H excretion…oppsoite occurs when PCO2 dec

3-conc of HCO3 in extracellular fluid influences the rate of bicarb transport out of renal tubular cells & rate of H secretion

dec extracellular HCO3 conc—>facilitates HCO3 transport out of renal cells—> reduced intracellular HCO3 in renal cells facilitates production of H—> inc H secretion
–metabolic acidosis will facilitate H excretion…opposite occurs when extracellular HCO3 conc are inc

4-expression & activity of carbonic anhydrase is regulated by H conc
w/ acidosis the inc in carbonic anhydrase enzymes & inc in activity favors the production of HCO3 & H production—> H secretion & H excretion…opposite w/ alkalosis

Question 54

Q

1-reciprocal relationship between plasma K & HCO3

2-limitations to H secretion

Answer

A

1-consider effects of hyper & hypokalemia on transcellular exchange of H ions in renal cells

hyperkalemia leads to K influx & H efflux
inc in intracellular pH will reduce the expression of carbonic anhydrase
it will reduce bicarb recovery—an inc in plasma K will reduce HCO3 recovery—-opposite w/ hypokalemia

2-substantial quantities of buffer int ubular fluid—only limitation to H secretion is H production in renal tubular cells

as concentration of buffer is reduced, tubular fluid becomes more acidic
pH approaches 4.4 the H conc gradient exceeds capacity of H ATPase to transport H ions into lumen

Question 55

Q

Renal H secretion
1-H secretion is inc when

2-H secreted is dec when

3-mechanisms regulating bicarb ion secretion

Answer

A

1-inc partial pressure of CO2

dec extracellular HCo3
inc activity of carbonic anhydarse
dec lumen H= inc lumen pH

2-dec partial pressure of CO2

inc extracellular HCO3
dec activity of carbonic anhydrase
inc lumen H= dec lumen pH

3-during periods of chronic metabolic alkalosis…type B cells in cortical collecting duct will transport HCO3 into tubular fluid & transport H ion into interstitial fluid

once bicarb is in tubular lumen it will associate w/ available cation usually Na
NaHCO3 is then excreted in the urine eliminating bicarb from body—mirror image of type A found w/in medullary collecting duct

Question 56

Q

1-visualization of acid base balance w/ davenport diagram

2-mass action

3-uncomensated change= pure

4-metabolic acid base imbalance

Answer

A

1-davenport diagram isnt used clinically, but visually explains what happens w/ mass action
middle of diagram…normal pH= 7.4
HCO3= 24
and PCO2= 40

2-change in PCO2 will result in changes in HCO3 conc via mass action and will follow the mass action line

inc in PCO2 of 10 results in 1 inc in HCO3
dec in PCO2 of 10 willr educe HCo3 by 2

3-pure acid base disturbance occurs before the other system can compensate
-pure metabolic disruption will follow PCO2 line of 40 and pH will change accordingly w/ no change in PCO2…pure resp disruption will follow mass action line

4-compensation

change in extracellular HCo3 will induce equal equilibration of HCO3 in CSF
metabolic acidosis can be induced by dec in extracellular HCO3= dec in CSF, shift in conc leads to inc H conc
extra H will diffuse into extracellular fluid surroundign chemosensitive neurons, activate them & inc signaling to pre Botz complex= inc in ventilation, inc in ventilation reduces PCO2 and brings pH closer to normal at expense of further reduction in HCO3
alkalosis induced by inc in HCO3 will also inc Cerebral HCO3, reduce H concentrations, reduction in H diffusion will reduce chemoreceptor signaling for ventilation which will inc PCO2

Question 57

Q

1-compensation for metabolic acidosis

2-numbers fo pH, HCO3, & PCO2

3-compensation for metabolic alkalosis

4-numbers for pH, HCO3, & PCOr

Answer

A

1-metabolic acidosis caused by a reduction in HCo3, compensation is directed toward a dec in PCO2 to return the HCO3: CO2 ratio to 20:1. compensation is the same direction as the causative factor…direction of compensation is the same direction as causative factor…CO2 will be reduced which will further reduce bicarb concentration

2-uncompensated pH= 7.25
compensated pH= 7.33

uncompensated HCO3= 17
compensated HCO3=16

uncompensated PCO2= 40
compensated PCO2=30

3-caused by inc in HCO3. compensation is directed towards inc PCO2 to return the HCO3:Co2 ratio to 20:1. Co2 will inc by slowing resp rate

4-uncompensated pH= 7.5
compensated pH=7.46

uncompensated HCO3= 30
compensated HCO3=31

uncompensated PCO2=40
compensated PCO2=45

Question 58

Q

1-Resp Compensation is limited

2-resp acid base imbalance-mechanism for compensation

Answer

A

1-resp compensation is only able to acheive partial compensation

return of plasma pH to normal value by changing the respiration rate is very rare & generally occurs w/ artifical ventilation
metabolic acidosis, resp compensation is limited by resp workload and has lower limit of PCO2= 10-15
metabolic alkalosis, resp compensation is limited by hypoxemia, w/ upper limit for PCO2= 60…so if metabolically induced acid base imbalance, resp compensation= partial

2-inc in extracellular CO2 will also inc Co2 conc w/in renal tubular cells—inc in CO2 will stimular carbonic anhydrase and inc production & secretion of H into tubular lumen & production & transport of HCO3 into circulation

in proximal tubule, glutamine metabolism is stimulated by acidosis…promotes formation of new HCo3 and loss of H via NH4 diffusion trapping
medullary collecting tubule, secretion of H & buffering by non bicarb buffers = new bicarb= elevate plasma HCO3 to compensate for inc in plasma CO2

Question 59

Q

1-compensation for resp acidosis

2-numbers for pH, HCO3, PCO2

3-compensation for resp alkalosis

4-numbers for pH, HCO3, PCO2

Answer

A

1-resp acidosis caused by inc in CO2. compensation is directed toward an inc in HCo3 to return the HCo3, CO2 ratio to 20:1. direction compensation is dame direction as causative. CO2 inc, plasma HCO2 will inc bc of mass action…mass action effect isnt compensation. compensation occurs when kidneys elevate plasma HCO3 beyond effect of mass action

2-uncompensated pH= 7.32
compensated pH=7.4

uncompensated HCO3= 25
compensated pH= 30.5

uncompensated pH= 50
compensated pH= 50

3-caused by dec in CO2, directed towards a dec in HCO3 to return the HCO3: CO2 ratio to 20:1.

direction of compensation is same direction as the causative factor
when CO2 dec, plasma HCO3 will dec bc of mass action
compensation occurs when kidneys dec plasma HCO3, beyond effect of mass action

4-uncompensated pH= 7.54
compensated pH= 7.4

uncompensated HCO3=22
compensated HCO3=15

uncompensated PCO2=30
compensated PCO2=30

Question 60

Q

1-metabolic acidosis

2-metabolic alkalosis

3-respiratory acidosis

4-respiratory alkalosis

Answer

A

1-problem= dec HCO3 compensation= dec CO2 = inc respiration

2-problem= inc HCO3 compensation= inc CO2= dec respiration

3-problem= inc CO3 compensation= inc HCO3= bicarb new synthesis

4-problem= dec CO3 compensation= dec HCO3=dec recovery & inc secretion

Question 61

Q

1-Electroneutrality Principle

2-Na

3-HCO3

4-Cl

5-anion gap

Answer

A

1-in an electrolye solution, conc of pos ions & neg ions = neutral solution
-built up of a charge inhibits further breakdown of salt
-total charge ofc ations= total charge of anions
charge for Na, K, Mg, Ca (all +) = charge for Cl, HCO3, H2PO4 HSO4 (all -)

2-140 mM

3-24 mM

4-104 mM

5-cause & potential treatment for metabolic acidosis
-to calculate, determine diff between Na conc & sum of Cl and HCO3 conc [Na - (Cl + HCO3)]
usually between 8-16 mEq

Question 62

Q

1-normal anion gap

2-wide anion gap

Answer

A

1-excess H = inc anions
-if acid is HCL then an inc in Cl conc will occur and H will be buffered by bicarb (loss of HCO3)—patient has metabolic acidosis w/ normal anion gap = hyperchloremic acidosis…
major causes= GI loss of HCO3 bc of diarrhea, renal failure leading to reduced bicarb recovery or dec excretion of H by kidney

2-production of a patholgic acid (non HCL) leads to similar loss of HCO3 due to buffering

however conc of unmeasured anions will inc = wide anion gap
most common cause of metabolic acidosis w/ widened anion gap= diabetic ketoacidosis—this case= uncontrolled diabetes= inc in ketoacids
metabolic acidosis w/ a widened gap= lactic acidosis, ingestion of methanol, ethylene glycol, inhalation of toluene & renal failure

—anion gap helps determine potential causes & treatments

Question 63

Q

1-role of proteins in anion cap

2-compensatory changes in ion conc

3-wide anion gap

4-narrow anion gap

Answer

A

1-neg charge proteins= majority of unmeasured anions
-if patient gets hypoalbuminemia= retention (inc) in other neg charged ions like Cl & HCO3
= false narrowing of anion gap bc of low plasma protein levels
-correct anion gap calc by 2.5 for ever 1 gm change

2-unmeasured anions such as phsophate are inc, to maintain electrical neutrality, measured cations inc Na and/or measured anions dec (Cl & HCO3) =s wide anion gap

3-hyperalbuminemia= severe dehydration
hyperphosphatemia= low parathyroid hormone

4-hypoalbuminemia= liver disease, burn injury, & inc vascular perm

excess K, Ca, Mg, and Li
excess paraprotein w/ cancer of plasma cells
excess bromide ingestion—it should widen anion gap but isdetexted by chloride analyzer w/ a 3+ error causing a narrow anion gap

Question 64

Q

Answer 64

A

1-check pH= acidotic or alkalot?
-metabolic or resp?
-if resp imbalance, determine whether change in HCO3 is bc of mass action or if compensation occured
-if compensation is present, it it partial or complete
if pH in norm range but PCO2 & HCO3 arent then complete compensation occurred

2-pH is a function of the ratio of plasma bicarb (acid) to dissolved carbon dioxide (acid)

ratio of 20:1, the pH is 7.4
alkalosis= inc in base HCO3 or dec in acid=CO2
–HCO3/CO2 >20
acidosis= dec in base HCO3 or inc in acid CO3
–HCO3/CO2 <20

3-mass action= effect of changes in PCO2 on HCO3
-a change in PCO2= change in HCO3
for every 10 of CO2 above 40 bicarb will inc by 1
for every 10 below 40 bicarb will dec by 2

4-mass action will inc HCO3 from 24 to 25.5 so any wariations w/in that range= mass action
any value above the range would be bc of renal compensation…compensation tries to retun pH to normal at expense of further deviation in HCO3 conc

Answer 65

A

1-if buffering capacity of body cant maintain normal pH, compensation will occur

body will compensate using system that ISNT causing imbalance
achieved by adjusting plasma HCO3 or CO2 towards normal 20:1 ratio
renal failure leading to reduction in plasma bicarb & metabolic acidosis will be compensated for by dec PCO2 via inc resp rate(min to hours)
so a change in plasma CO2 = acid base disturbance will be compensated for by changign plasma HCO3 conc…(hours to days)

2-partial & complete compensation return pH to normal levels at expense of deviation from norm bicarb or CO2 values
correction- occurs when cause of acid base imbalance is corrected and all values are returned to normal

3-high CO2, correction= inc ventilation rate to retun CO2 to normal values

4-low CO2, correction= dec ventilation rate to retain CO2 & return CO2 to normal

5-low HCO3, correction= kidneys make additional HCO3 & return HCO3 to normal

6-high HCO3, correction= kidneys would inc HCO3 excretion and dec H secretion to return HCO3 to normal values

Answer 66

A

1-dec HCO3, normal PCO2

2-dec HCO3, dec PCO2 pH<7.35

—completely compensated metabolic acidosis doesnt happen

3-inc PCO2, normal HCO3

4-inc PCO2, inc HCO3, pH<7.35

5-inc PCO2, inc HCO3, pH normal

6-pH<7.35 inc PCO2 but usually dec HCO3

Answer 67

A

1-inc HCO3, normal PCO2

2-inc HCO3, inc PCO2, pH >7.45

***completely compensated metabolic alkalosis doesnt happen

3-dec PCO2, normal HCO3

4-dec PCO2, dec HCO3, pH >7.45

5-dec PCO2, dec HCO3, pH = normal

6-pH>7.45, dec pCO2 , usually inc HCO3

Answer 68

A

1-due to dysfunction or to tissue damage or combo

dysfunction can lead to path and path can lead to dysfunction
disease process or dysfunction is transient & reversible…others= progressive & perm reduction in renal function= hallmark
secondary manifestations of systemic illness, like renal disase= autoimmune disorders = arterial hypertension
kidney responsible for regulating volume and comp of ECF & as endocrine organ…effects eryhtropoesis & Ca metabolism
renal disease can affect electrolyte & water balance, plasma protein conc, acid base balance & cardiovascular function

2-prerenal, intrarenal, & postrenal causes of renal disease or dysfunction

Answer 69

A

1->90 ml/min —normal/elevated GFR

2-60-90 ml/min—mild dec GFR

3-30-60 ml/min—moderate dec GFR

4-15-30 ml/min—severe dec GFR

5-failure—<15 or on dialysis

6-GFR decreases w/ age y

Answer 70

A

1-renal failure= from inadequate perfusion to kidney

causes reduction in GFR & reduction in O2 & fuel delivery to renal tubular cells
result in 2ndary damage to renal tubular cells= acute tubular necrosis (death of cells)
–causes= low BV, renal artery obstruction, renal vasoconstriction, systemic hypotension
i.e.= common consequence of hemorrhage= acute renal injury bc of prolonged reduction in blood flow to kidney
second example= GFR/RBF 2 lecture is NSAID induced renal arteriolar vasoconstriction & reduction in GFR
third example= GFR/RBF2 was renal artery stenosis

Answer 71

A

1-damage to nephrone= direct, rather than through pre-renal or post renal causes
common causes= many diff types of intrinsic renal disease or renal manifestation of systemic disease, like systemic lupus erythematosus
-drug induced toxicity= analgesic, aminoglycoside antibiotics, tetracycline & chemotherapy= tubular damage
-heavy metals
-infections= pyelonephritis-inflamm reaction in renal interstitium

Answer 72

A

1-factors that directly or indirectly result in urinary tract outflow obstruction—prolonged obstruction of urinary flow= volume & pressure damage to kidney (hydronephrosis), & more acute symptoms of pain & bacterial infection
Common causes= renal stones= blocking renal pelvis or ureter, bladder stones may obstruct urethra
-prostatic enlargement= in men=compression of urethra
ureter/bladder obstructive= obstruction by cancer if anatomic
if function= smooth muscle spasm, poor bladder emptying, incompetent valve at vesiculoreteral origice, urine to back up from bladder into ureters

Answer 73

A

1-retention of nitrogenou smetabolic end products in plasma, measured as elevations in plasma urea & creatinine…elevations in BUN & creatinine are due to insufficient GFR

renal dysfunction= most common reason why develops
laboratory finding…most likely suspect= reduction in GFR
can occur & resolve acutely

2-describe complex constellation of clinical manifestations & biochemical abnormalities w/ end-stage renal failure—patients who develop uremia require renal replacement therapy to continue life

develops when GFR is 15-10 mL/min, stage 5 or failure
signs & symptoms of uremia are reversible w/ renal transplantation
dialysis can relieve some clinical manifestations while others progress into severity
dialysis= removing excess fluid, K, & uremic toxins w/ aim of reducing edema, hyperkalemia & uremic symptoms

3-reduced excretion of electrolytes & H20

reduced excretion of organic solutes (uremic toxins)
reduced renal hormone synthesis (active vit D & erythropoietin)
activation of compensatory mechnaisms that can be maladaptive over time

Answer 74

A

1-Na & H20 retention lead to expansion of ECF and if excessive, peripheral & pulm edema formation

difficulty in excreting K= hyperkalemia
difficulty in excreting acute H20 load= hyponatremia
difficulty in excreting acid= metabolic acidosis
disorders of Ca & P metabolism= transient hypocalcemia & persistent hyperphosphatemia

2-retention of organic solutes= signs & symptoms of uremia (like creatining & urea)

neither urea nor creatining= among organic solutes to be responsible for signs & symptoms of uremia
different solutes may contribute to diff signs/symptoms
urea is a marker solute for adequacy of dialysis

3-anemia= erythropoietin synthesis by kidney = low bc of loss of renal mass
-altered C & P metabolism= bc dec synthesis of active vit D & retention of P= renal osteodystrophy

4-alterations in bone mineralization (altered C & P) that leads to bone loss, structural abnormalities in bone, bone & joint & fractures= too late

Answer 75

A

1-maintain plasma Ca. PTH will mobilize Ca from bone, reduce renal excretion of Ca, inc renal P excretion(no remineralization) & stimulate Vit D synthesis

2-raise plasma Ca & P (promote new bone)

enhanving Ca & PO4 absorption from gut & decreasing renal excretion of Ca & Po4
neg feedback on PTH, avoid excessive elevation in plasma Ca

3-renal retention of P = binding of PO4 to Ca & hypocalcemia

hyperphosphatemia inhibits Vit D
low Vit D= dec Ca absorption, promoting hypcalcemia, low Vit D3= neg feedback inhibition on PTH
low Ca stimulates PTH synth & release
2ndary hyperparathyroidism= enhanced bone resorption= low bone mass & weakened structure, specific bone disease= excessive PTH= osteitis fibrosa
excessive Ca & PO4= deposition of CaPO4 in tissues…happens when plasma Ca x PO4 is >60
chronic metabolic acidosis= bone loss via bone buffering of H for bone Ca

Answer 76

A

1-compensation for reduced calcitriol synthesis = excessive PTH secretion= bone disease

2-compensation of substantial nephron loss= glomerular hyperfiltration in remaining nephron

reduction in afferent arteriola resistance= inc glomerular capillary pressure
persistent glomerular hypertension= proteinuria, glomerulosclerosis & loss of functioning renal mass…concurrent hypertension exacerbates glomerular hypertension

3-huge numbers of renal disease states share small common core: syndromes
-reduces function of podocyte/slit diaphragm= loss of plasma protein in urine= nephrotic syndrome

Answer 77

A

1-site= subtle glomerular abnormalities
description= hematuria, proteinuria, no symptoms
common in= exercise or orthostatic proteinuria, early stages of disease

2-site= glomerular, podocyte injury, isolate problem or other glomerula disease
description= proteinuria>3.5 g, hypoalbuminemia, edema, lipiduria
common in= minimal change disease, focal segmental glomerulosclerosis

3-site= glomerular= abrupt onset & resolution, proliferative & inflamm reaction
description= azotemia, oliguria, gross hematuria, dysmorphic RBC, proteinuria, edema
common in= immune mediated, class presentation of post streptococcal, IgA nephropathy

Answer 78

A

1-site= glomerular= rapid progressive loss of renal function
description= hematuria, dysmorphic RBC or cast, proteinuria, severe oliguria & azotemia more than acure state
common in= immune mediated glomerula path, crescent in glomeruli, goodpasture

2-description= oliguria/anuria, decline in GFR, recent zotemia
common in= ichemia, ATN, urinary tract obstruction

3-site= GFR<15 mL
description= persistent azotemia, uremia, renal osteodystrophy
common in= renal diseases, diabetes mellitus, hypertension

4-site= crystal formation in renal tubule, Ca oxalate
description= previous stone passage, imaging evidence= flank pain
common in= genetic predisposition, dehydration, high protein diet

Answer 79

A

1-rapid reduction in renal function GFR = azotemia, oliguria (volume <400 mL) may be observed
AKI= reversible or result in chronic renal disease or death

2-anything that reduces O2 supply to kidney, prolonged systemic hypotension, sepsis, hypovolemia, & renal artery obstruction

3-acute glomerulonephritis GN, rapidly progressing GN

acute tubular necrosis= toxic effects of aminoglycoside antibiotics, tetracycline, radiocontrast material
acture tubular necrosis due to ischemia
sepsis= immune system activation= inflammation, sclerosis & obstruction

4-anything that causes urinary tract obstruction

5-dysfunction/death of renal tubular epithelial cells…prominent in proximal tubule & thick ascending limp of loop of henle
-occlusion of tubular lumen by cell debris & cell casts can = low GFR bc of intratubular obstruction & leakage of fluid back into interstitium

Answer 80

A

1-ATN recover needs regeneration of tubular cells

treatment is supportive & has dialysis
initial insule has been correct the return of GFR to normal= 3-21 days…depending on severity of insult
some cases recover doesnt occur or is incomplete= chronic kidney disease

2-presence of kidney damage or dec kidney function for 3 or more months no matter the cause,

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