renal final index cards exam I Flashcards

Question

What is the main determinant of plasma osmolality

Answer 1

Syndrome of Inappropriate ADH secretion (SIADH), result from overproduction of ADH. Production does not respond to normal osmotic stimuli and therefore cannot be suppressed by reduced plasma osmolality.

Answer 2

ECF: Na and associated anions ICF: K and associated anions

Answer 3

tumors inadequate suppression of ADH secretion from the neurophypophysis complication of surgery (excess use of IV fluids) gain of function mutations in ADH receptor

Answer 4

True. They're negatively charged and can attract counterions.

Answer 5

low plasma Na because ADH increases water uptake

Answer 6

Donnan Effect. Plasma proteins attract small cations, therefore the concentration of the small cations is 5% higher in the aqueous phase than in the interstitial fluid, and the concentration of small Anions is 5% lower.

Answer 7

asymptomatic since the conditions develop slowly, and therefore brain cells adapt by lowering the intracellular concentration of organic osmolytes

Answer 8

occurs in conditions where ECFV is normal or increased, but the blood volume available for tissue perfusion is inadequate, and thus the body responds as if it was volume depleted (triggering ADH release). Occurs in states of heart failure, liver cirrhosis, sepsis, use of vasodilator drugs

Answer 9

2[Na] + [Glucose]/18 + [BUN]/2.8

Answer 10

Na. Kidneys regulate the size of ECFV by regulating the Na content of the body. A high blood volume --> kidneys eliminate salt (fluid follows) --> ECFV is returned to normal

Answer 11

Osmolar gap = measured osmolality - calculated osmolality. An increased osmolar gap indicates the presence of a toxin that contributes to the osmolality

Answer 12

adjusting plasma volume via changes in ECFV and RBC volume via EPO

Answer 13

of osmotically active particles present

Answer 14

Increase BV --> Increase Pcap --> Increase filtration | Decrease BV -> decrease Pcap -> increase reabsorption

Answer 15

1) Since Na is restricted to the ECF, this draws fluid out of the cells until ECF=ICF osmolality (but the total number of osmoles is higher in the ECF) 2) ECFV is increased, and this extra fluid is redistributed between the ISFV and plasma in a 3:1 ratio since the endothelium is freely permeable to Na. 3) Hct decreases because a) plasma volume is increased and 2) increased osmolality of the plasma (due to ingestion of Na) results in cell shrinkage

Answer 16

Blood volume, which determines CO and ultimately BP

Answer 17

mechanisms that regulate the renal handling of NaCl

Answer 18

hydrostatic pressure (promotes fluid exit) and oncotic pressure (draws fluid in)

Answer 19

since NaCl is so scarce, it is a behavioral response that is analgous to the thirst mechanism; signals come from the kidney

Answer 20

reflection coefficient of the capillary membrane for protein.

Answer 21

high pressure receptors in carotid sinus/aortic arch = important for short-term control of BP and serve to protect the brain from ischemia. baroreceptors in large arteries = adapt to changes in BP (ie hypertenison) by undergoing anatomical restructuring, and thus a transient increase in wall tension is transient. High pressure receptors in the afferent arterioles do NOT undergo restructring because they are a single layer of cells.

Answer 22

Sum of all hydrostatic and effective oncotic pressures

Answer 23

High pressure receptors in the afferent arteriole contain renin-producing ganular cells, which are TRUE renal baroreceptors because 1) they lack contractile fibers 2) they are composed of a single layer of muscle ells 3) always experience a stretch that is proportional to the actual BP

Answer 24

fluid moves out of the capillary (ultrafiltration)

Answer 25

Low pressure receptors are important for intermediate regulation of BP. They reside in the cardiac atria, vena cava, and large pulmonary vessels (all of which are much more distensible). They are similar because tey undergo restructuring to accommodate chronic changes in BP (ie hypertension)

Answer 26

fluid moves into the capillary (absorption)

Answer 27

low pressure receptors, because they reside in structures that are much more distensible (ie vena cava, atria, pulmonary vessels)

Answer 28

measure of water permeability

Answer 29

Total blood volume - unmeasurable amount of pooled blood that circulates slugglishly

Answer 30

measure of protein permeability

Answer 31

1) regulating ECFV | 2) regulating RBC volume via EPO

Answer 32

vasoactive hormones and cytokines

Answer 33

in water immersion, the hydrostatic pressure compresses the tissues, thereby increasing venous return to the atria. The low-pressure receptors in the promote natriuesis (get rid of Na, water follows) to restore blood volume back to "normal"

Answer 34

It goes from + --> - such that most of the ultrafiltrate produced in the initial portion of the capillary gets reabsorbed at the venous end.

Answer 35

even though there is an increase in venous pressure, the renal arterial pressure decreases, which sends signals to increase blood volume (by increasing Na reabsorption)

Answer 36

hydrostatic pressure (promotes fluid exit) and oncotic pressure (draws fluid in): increases/decreases in capillary hydrostatic pressures will cause fluid to be drawn in or seep out from the capillaries

Answer 37

RAAS system and renal sympathetic nerves

Answer 38

increase in venous pressure reduced oncotic pressure (fluids seeps out of capillary) changes in capillary wall permeability (endothelial injury/inflammation) obstruction of lymphatics (tumors/parasites)

Answer 39

Edema, since there is reduced oncotic pressure, fluid will seep out of the capillary and into the interstitum

Answer 40

granular cells of afferent arterioles

Answer 41

``` Increase Kf (increase water permeability) decrease s (capillary becomes more permeable to proteins) ```

Answer 42

1) stimulates Na reabsorption in the PCT via Na/H exchanger 2) lowers the set point and heightens sensitivity to TGF (an increase in NaCl load --> MD will trigger a more robust decrease in GFR) 3) constricts efferent arteriole, thus tilting the peritubular starling forces in favor of reabsorption by PCT (due to decreased hydrostatic/increased oncotic pressure) 4) reduces medullary blood flow, which enhances urine conc. ability and increases Na reabsorption in thin ascending limb (not to be confused with TALH -> thick ascending limb)

Answer 43

Na and glucose

Answer 44

stimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetitestimulate aldosterone secretion, thirst, and to a lesser degree Na appetite

Answer 45

expand ECFV, reduce ICFV

Answer 46

It helps to maintain GFR, NOT increase it. Counterintuitive because one would think that it would increase it, but AII is only produced when the blood pressure declines, and thus AII helps to preserve GFR

Answer 47

expand ECFV and ICFV

Answer 48

aldosterone 1) stimulates salt appetite 2) heightens sensitivity of taste buds to salt by reducing the salivary Na concentration

Answer 49

nothing, ECF stays the same

Answer 50

angiotensin II

Answer 51

Increases Na reabsorption by: 1) upregulates ENaC and Na/K-ATPase in CD 2) upregulating NaCl cotransporter in the DT also enhances Na reabsorption in the colon and sweat glands main driver of Na intake (salt appetite, sensitivity)

Answer 52

1) TGF (increased Na delivery to MD --> afferent arteriole constriction --> reduce GFR) 2) AII --> afferent arteriole constriction in TGF/Na reabsorption in PCT via Na/H exchanger 3) catecholamines (Epi) - Na/reabsorption in PCT/ via Na/H exchanger 4) aldosterone - Na reabsorption in DCT

Answer 53

plasma expanders (ie albumin, gelatins, dextrans, starches)

Answer 54

Low BP/NaCl or high sympathetic activity --> Renin Release. Renin --> AII AII --> provides NEGATIVE FEEDBACK control for renin production (increased level of pressor hormones inhibit renin release) but STIMULATES aldosterone secretion

Answer 55

oral rehydration therapy: Na w. glucose in a slightly hypotonic solution (net: expand ECFV and ICFV)

Answer 56

AII and high plasma K (in the CCD, Na reabsorption is coupled to K secretion)

Answer 57

active reabsorption of the ultrafiltrate, specifically Na (via Na/K ATPase)

Answer 58

AII, catecholamines (sympathetic innervation)

Answer 59

False. In the kindey, blood flow drives O2 consumption (because more blood flow = more active reabsorption = more O2 consumption)

Answer 60

ANP is made in the heart and released in distension of the atria. Promotes natriuresis

Answer 61

Unlike other organs, renal tissue pO2 is independent of blood flow and is thus proportional to arterial pO2 content. Therefore, RBC production is regulated by the kidneys

Answer 62

1) increase GFR, and medullary blood flow 2) inhibit Na reabsorption in medullary CD 3) block renin/aldosterone production 4) antagonize ADH in CD, thus inhibiting Na reabsorption and promoting water excretion

Answer 63

afferent arteriole --> glomeruli --> efferent arteriole --> peritubular capillaries

Answer 64

a back-up system for regulating ECFV. Kidneys have an intrinsic capacity to increase Na excretion in response to an increase in BP. With an increase in perfusion pressure, Na reabsorption is inhibited, which results in an exponential increase in Na excretion in spite of a constant GFR

Answer 65

Blood flow is highest in the superficial cortex. The medulla has no direct arterial blood supply, but it does receive blood from juxtamedullary glomeruli thrrough the peritubular network in the outer medulla and vasa recta in the inner medulla. Blood flow in outer medulla is 6-10% of cortical flow, and only 1/10 of that is transmitted to the vasa recta. The low blood flow in medulla and the coutnercurrent arrangement of flow in the vasa recta is critical for conserving the medullary hyperosmolality required for concentration of urine.

Answer 66

ECFV Expansion: - O2 carrying capacity decreases (due to hemodilution) - PCT O2 consumption decreases (less being absorbed to return ECFV to normal). NET: PO2 is constant, and therefore no change in EPO. ECFV Contraction - O2 carrying capacity increases (due to hemocontraction) - PCT O2 consumption increases (more being absorbed to increase ECFV to normal). NET: PO2 is constant, and therefore no change in EPO.

Answer 67

ultrafiltration is drive by hydrostatic pressure in glomerular capillary (PGC), opposed by hydrostatic pressure in bowman's space (PBS), and the oncotic pressure in the glomerular capillary (pGC)

Answer 68

Polycythemia (increase in RBC volume, which increases O2 carrying capacity) - PCT Na reabsorption (and O2 consumption) is normal or low - tissue PO2 is elevated, and therefore EPO is suppressed

Answer 69

hydrostatic pressure in glomerular capillary (PGC) hydrostatic pressure in bowman's space (PBS) oncotic pressure in the glomerular capillary (pGC) permeability of the membrane for small molecules (filtration coefficient Kf)

Answer 70

Tissue PO2 is reduced and therefore more EPO is released

Answer 71

GFR = Kf [(PGC-PBS)-pGC] pBS is not included because the reflection coefficient for glomerular filtration barrier for protein is ~1 and thus fluid in BS under physiological conditions is practically protein free

Answer 72

It has a high Kf (filtration coefficient)

Answer 73

Uptake of K -> swelling | Loss of K -> shrinking

Answer 74

Because glomerular capillaries have large fenestrations that allow the passage of small molecules (and therefore a much larger fraction of the total surface area is available for the passage of H2O/small molecules)

Answer 75

RMP and excitability

Answer 76

FF = GFR/RPF (renal plasma flow)

Answer 77

vasoconstriction

Answer 78

Since PGC is the main determinant of GFR: RBF, GFR, and FF changes in parallel with changes in afferent tone (ie afferent constriction --> decrease RBF, GFR, and FF)

Answer 79

vasodilation

Answer 80

Since PGC is the main determinant of GFR, GFR and FF changes in opposite directions with changes in efferent tone (ie efferent constriction --> increase GFR and FF), but RBF will change in parallel (efferent constriction --> decrease RBF)

Answer 81

the BBB/glial cells/CSF shelter the brain from changes in plasma K (since minor changes in extracellular K can cause major disruptions in neuronal function

Answer 82

Increase GFR, decrease RBF, increase fluid reabsorption from the tubules by decreasing hydrostatic pressure and increasing oncotic pressure in the peritubular capillaries

Answer 83

Na/K ATPase

Answer 84

Filtration barrier rejects Igs based on their large size. Albumin is rejected based on charge (the filtration barrier carries a significant negative surface charge, which restricts the passage of negatively charged proteins)

Answer 85

high affinity for substrate; therefore the receptor is usually saturated and increasing the substrate concentration doesn't change the activity very much.

Answer 86

damage to the filtration barrier

Answer 87

low affinity for substrate; therefore the receptor is usually NOT saturated and increasing the substrate concentration changes the enzyme activity substantially

Answer 88

kidney disease --> proteinuria

Answer 89

Km for K = 1, which means that changes in plasma K within the physiological rage (3-5mM) has marginal effect on the activity of the transporter. Km for Na = 4, which means that changes in plasma Na within the physiological rage (3-5mM) has a large effect on the activity of the transporter. Thus changes in the activity of Na-coupled transporters (ie Na/H exchanger) that alter intracellular Na have a large influence on Na/K ATPase activity, and consequently, K distribution

Answer 90

virtual volume of plasma completely cleared from a substance (s) per unit time

Answer 91

Insulin Exercise and catecholamines Acid/Base balance Plasma osmolality

Answer 92

``` Clearance = (Us x V)/(PaS) Us = conc. of urine in substance V = urine flow rate PaS = concentration of substance in arterial plasma ```

Answer 93

NET: increases K uptake via 1) stimulating Na/K ATPase 2) increase glucose uptake, which requires phosphate intake with Na (turnover) 3) activates Na/H exchanger #2/3 increases intracellular Na, which increases the Na/K ATPase activity to dump Na out, which results in K uptake

Answer 94

GFR = (Uinulin x V)/PaInulin ``` U = conc. of inulin in urine V = urine flow rate Pa = concentration of inulin in arterial plasma ```

Answer 95

plasma K decreases because insulin stimulates K uptake

Answer 96

PAH is used to measure RPF. It is actively secreted into tubular fluid from the peritubular capillaries and is almost completely cleared from the blood after a single passage (renal concentration ~0)

Answer 97

During an action potential, the depolarization (Na influx) is shorter than the repolarization/hyperpolarization (K efflux), resulting in a net K efflux from the cell. This K accumulates and causes local vasodilation.

Answer 98

Inulin is used to measure GFR. It is freely filtered by the glomerulus and is neither reabsorbed nor secreted by the tubules.

Answer 99

Norepineprhine inhibits Na/K ATPase, thus promoting K loss from the cells. Epinephrine stimulates Na/K ATPase, thus promoting K uptake from the cells. EPI = INSULIN on K balance

Answer 100

creatinine, because it is produced in the body at a relatively constant rate and is eliminated primarily by glomerular filtration

Answer 101

exercise results in a large increase of K from muscle cells (lots of APs --> hyperkalemia). Body anticipates this by secreting epinephrine at the onset of exercise (which stimulates Na/K ATPase, thus lowering plasma K levels)

Answer 102

low GFR (they're inversely related)

Answer 103

After the cessation of exercise, the mechanisms that stimulate K uptake (epinephrine) cannot be turned off immediately. However, the increased norepinephrine levels released from sympathetic nerve endings buffer this effect by promotes K efflux by (inhibiting Na/K ATPase)

Answer 104

Epinephrine stimulates their insulin-like effects on K uptake via beta-receptors. b-blocker would result in hypERkalemia b-agonist can be used to treat hyperkalemia (b-agonist will stimuate K uptake) to lower K levels

Answer 105

RBF remains relatively constant over a wide range of mean arterial pressure (~80-180)

Answer 106

Due to the H/K exchanger, cellular K depletion results in intracellular acidosis, while K depletion results in intracellular alkalkination. (H/K exchanger = antiport. K in = H out and vice versa).

Answer 107

afferent arteriole, which stabilizes glomerular capillary pressure (the main determinant of GFR)

Answer 108

In hyperosmolality, cell shrinks --> intracellular K concentrates --> K leaks out --> increased plasma K

Answer 109

1) myogenic response | 2) tubuloglomerular feedback (TGF)

Answer 110

In hypo-osmolality, cell enlarges --> intracellular K becomes diluted --> K enters -> decreased plasma K note: this occurs to a lesser degree

Answer 111

when the afferent arteriole contracts in response to an increase in blood pressure (stretching of the vessel)

Answer 112

Insulin promotes K and glucose uptake. In DM patients, they lack insulin, which result in a reduction of K intake --> hyperkalemia. Also, since there is no insulin, glucose is an effective osmole, which its accumulation in the ECF increases osmolality. This results in cell shrinkage, and thus K concentrates and leaks out --> hyperkalemia

Answer 113

tubuloglomerular feedback (TGF) - an increase in arterial pressure temporarily increases GFR, and thus more salt and water is delivered to the tubules. In response to an increased NaCl load, the macula densa sends a humoral signal to the neighboring afferent arteriole to contract and thus decrease GFR.

Answer 114

regulating renal K excretion

Answer 115

increased NaCl load detected by the macula densa

Answer 116

Na transport along the nephron is unidirectional (i.e. reabsorption), renal K transport involves both reabsorption and secretion by different nephron segments.

Answer 117

macula densa sends a humoral signal to the neighboring afferent arteriole to CONTRACT, thereby decreasing GFR

Answer 118

it is reabsorbed: passive, paracellular and is mediated by solvent drag and by the lumen-positive voltage in the second half of the PT

Answer 119

reabsorption

Answer 120

In the thin ascending limb, K is secreted into the tubular fluid passively and is driven by the high [K] in the medullary interstitium. Some of the K in the tubular fluid is reabsorbed in the TALH, which establishes a cortico-papillary gradient for K, with the highest in the medullary interstitium, which is important to minimize K back-leak from the medullary collecting duct

Answer 121

inhibit reabsorption

Answer 122

1) In the thin ascending limb, K is secreted into the tubular fluid passively (due to high medullary concentration) 2) some (~20%) K is reabsorbed in the TALH 3) active K reabsorption of K via luminal H/K ATPase in the medullary CD All 3 help to establish the cortico-papillary gradient for K, with the highest in the medullary interstitium, which is important to minimize K back-leak from the medullary collecting duct

Answer 123

1) decreased stretch of granular cells in afferent arteriole 2) decreased Na load to macula densa 3) increased sympathetic tone in response to reduced systemic BP 4) increased AII

Answer 124

On normal intake, K transport in the DT and cortical CD is bidirectional, but in the medullary CD, it reabsorbs K

Answer 125

Angiotensin II

Answer 126

It reabsorbs Na via ENaC and secretes K. This is energized by the Na/K ATPase

Answer 127

preserve GFR by counteracting the direct effects of reduced perfusion

Answer 128

It reabsorbs K and secretes H. This is energized by the K/H ATPase

Answer 129

sympathetic nervous system, adenosine

Answer 130

cortical collecting duct

Answer 131

decrease RBF, GFR, and FF

Answer 132

medullary collecting duct - this helps to establish the corticopapillary gradient for K, which prevents back-leak from the medullary collecting duct

Answer 133

angiotensin II, endothelin, ADH

Answer 134

principle cells (Principle K Kicks Kids Out)

Answer 135

decrease RBF, but increase GFR and FF

Answer 136

a-ICC (think "ICK for taking K in"

Answer 137

dopamine, ANP

Answer 138

Increase in plasma K stimulates aldosterone secreton (potent stimulus).

Answer 139

Increase RBF, GFR, FF

Answer 140

1) increase in plasma K 2) aldosterone (which is stimulated by the increase in plasma K) 3) K is coupled to Na transport; aldosterone increases plasma reabsorption, which promotes K secretion

Answer 141

prostaglandins, NOs, kinins

Answer 142

Diuretics prevent less from being reabsorbed, and therefore more Na is delivered to the late DCT and CCD. This results in an increase in Na reabsorption, but more K secretion

Answer 143

they are degraded by the same enzyme (ACE) that generates Angiotensin II. Thus, AII and kinins have opposing effects

Answer 144

Cl- in the CCD is reabsorbed primarily through the paracellular pathway, creating a less (-) (or more +) lumen voltage, thereby creating a LESS favorable driving force for K secretion. Therefore more Cl --> more reasorbed --> more + lumen charge --> less K secretion

Answer 145

NSAIDs block prostglandins production (which is a normal vasodilator). NSAIDs normally have no significant effects on GFR in healthy patients, but in a person with congestive heart failure (which is already hypertensive), this can cause renal insufficiency.

Answer 146

1) high flow rate washes away K, and prevents tubular K from equilibrating with intracellular K. Thus K to be secreted continually. 2) high flow rate bends the cilia on principle cells, which stimulates K secretion (Principal K kicks Kids out)

Answer 147

Renal failure - condition in which the kidneys fail to adequately filter waste products from the blood

Answer 148

stimulates K secretion

Answer 149

It is a hypertensive drug (ACE normally breaks down Kinins, which are vasodilators. If ACE is blocked, then you get unapposed effects of AII, which is an efferent constrictor)

Answer 150

closes them

Answer 151

endothelin and NO. Endothelin is potent vasoconstrictor on the efferent arteriole. NO is a vasodilator think "TEN"

Answer 152

used to diagnose the causes of hyperkalemia or hypokalemia

Answer 153

ANP is a vasodilator and acts on the afferent arteriole. Therefore RBF and GFR will increase

Answer 154

hypokalemia (either non-renal or cause of K depletion)

Answer 155

SNS is a vasoconstrictor of the afferent arteriole. Therefore RBF and GFR will decrease

Answer 156

hyperkalemia

Answer 157

Angiotensin II is a vasoconstrictor of the efferent arteriole. Therefore RBF will decrease, but GFR will increase

Answer 158

Adenosine is a vasodilator of the afferent arteriole. Therefore RBF and GFR will increase

Answer 159

CO2-bicarbonate buffer system

Answer 160

Endothelin is a vasoconstrictor of the efferent arteriole. Therefore RBF will decrease, but GFR will increase

Answer 161

dissociate into H2O + CO2

Answer 162

Adenosine is a vasoconstrictor of the afferent arteriole. Therefore RBF and GFR will decrease

Answer 163

"Open" means that CO2 can be eliminated or retained via the lungs whenever an acid or alkali load is added to the system. During an acid load, CO2 is leaves the system. During an alkali load, additional CO2 can be retained to generate more HCO3-

Answer 164

Increase in AII/NE (vasoconstrictors) promote the release of prostaglandins (vasodilators)

Answer 165

Respiratory Buffering = CO2 can be eliminated or retained via the lungs whenever an acid or alkali load is added to the system. Respiratory Compensation = hyper-/hypo-ventilation that ensues to adjust PCO2 in attempt to normalize blood pH after a fixed acid/base challenge

Answer 166

ADH is a vasoconstrictor of the efferent arteriole. But because it selectively targets a tiny population of nephrons, it has no significant effects on total RBF and GFR

Answer 167

CO2 can cross cell membranes, and thus changes in extracelluar pH typically parallel those in the ECF (ECF=ICF), but not always

Answer 168

they both increase

Answer 169

phosphate, creatine phopshate

Answer 170

they both increase, but due to certain a.a. that serve as substrates for NO production. Increased NO --> vasodilation --> increased glomerular hypertension and acceleration of renal disease

Answer 171

Acute setting: bone acts as an ion exchange resin: H+ are exchanged for Na, K ions. The bone contains a readily exchangable pool of of HCO3- and CO3(2-) ions. Surface of bone contains crystalline alkaline salts (hydroxyapatite, carbonate)

Answer 172

1) Eliminate metabolic end products (urea, creatinine) via ultrafiltration 2) keep volume/electrolyte composition of ECF/ICF constant

Answer 173

leads to breakdown of bone matrix and mobilization of alkali supply (hycroxyapatite, carbonate)

Answer 174

reabsorption of Na by the tubules (Na/K ATPase, ENaC)

Answer 175

practically all of it is reabsorbed in the tubules

Answer 176

the DCT has limited reabsorption capacity, and therefore the MD is located at the beginning of the DCT to ensure a constant Na load via the tubuloglomerular feedback mechanism

Answer 177

phosphate (via HPO4-), urate, creatinine, citrate, ketoacids, NH3/NH4

Answer 178

the PCT/LOH function more along the lines of Na reabsoprtion (energetically favorable) whereas the DCT has limited reabsorption capacity and functions to establish the steep concentration gradients (energetically demanding)

Answer 179

excretion of NH4

Answer 180

1) reabsorption of 2/3 of the filtered water and Na, 80% of bicarbonate and phopshate, and all nutrients. 2) Secretion of xenobiotics

Answer 181

any disruptions of CO2 removal can lead to profound ACIDOSIS

Answer 182

HCO3 is primarily reabsorbed in the PT, and this process is indirect. 1) PT secretes H+, which combines with filtered HCO3- to form carbonic acid (catalyzed by carbonic anhydrase), which dissociates into CO2 and H2O and is reabsorbed into the PCT cells 2) In the cell, CO2 and H2O are converted back to carbonic acid by an intracellular carbonic anhydrase and H2CO3 spontaenously dissociates into H+ and HCO3-. 3) HCO3- is exported to the blood by an Na/HCO3 on the basolateral side, while the H+ is secreted into the tubular fluid by the Na/H exchanger for another round

Answer 183

pH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSISpH. (NOT PO2)Any disruptions of CO2 removal can lead to profound ACIDOSIS

Answer 184

It is a carbonic anhydrase inhibitor, and therefore it increases Na excretion (and is therefore, a potent diuretic)

Answer 185

it's eliminated via lungs

Answer 186

1) reabsorption of Na, glucose, lactate, and inorganic phosphates increases the osmolality of the interstitial fluid (while reducing the osmolality of the tubular fluid). 2) Due to preferential reabsorption of Na with HCO3-, phosphates, and other ions, the concentration of Cl- in the tubular fluid gradually increases towards the later segments of Cl-, and this differene allows Cl- to diffuse through the paracellular pathway, which creates a luminal (+) voltage

Answer 187

a fixed acid load is generated - lactic acid from carbohydrates - ketoacids from fats accumulates during vigorous exercise or starvation

Answer 188

passive movement of lipid soluble weak acid and bases in their undissociated forms through the cell membrane.

Answer 189

Transport of Cl- is mediated by the Cl-/A- and Na/H exchangers. 1) Uphill movement of Cl- into the cell is driven by the higher concentrations of organic anions (formate) inside the cell than in the tubular fluid. 2) Secretion of H+ neutralizes the secreted organic anions, the neutralized organic acid becomes lipophilic and diffuses into the cell 3) resulting cellular alkalination (due to the H+ secretion) aids the dissociation of organic acid into an anion and H+ inside the cell. 4) Na is then transported into the blood via basolateral Na/K ATPase, while Cl- exits via basolateral K/Cl cotransporter.

Answer 190

Add Na-acetate (CH3COONa) to the dialysis fluid, which catabolism of the carboxyl moiety will generate OH to correct renal failure

Answer 191

to keep the intracellular concentrations of Na low so that Na can be reabsorbed (energetically favorable movement of ions down its concentration gradient)

Answer 192

Citrus juice contains citric acid and citrate. Metabolism of citric acid results in an equal amount of base that fully neutralizes the added H+, while metabolism of citrate anions generates additional base. Thus, the net effect of ingesting citrus juice is alkalinzation of body fluids.

Answer 193

Pro: the PCT is relatively leaky and therefore large amounts of Na/H2O are reabsorbed with relatively little energy expenditure Cons: since the PCT is so permeable, it is prone to back-leak Net: since the PCT is so leaky, its rate of transport is so high that the rate of uptake into the peritubular capillary can become limiting

Answer 194

1) glomerulotubular balance | 2) Hormonal and neural regulation (AII, dopamine, ANP)

Answer 195

balance between reabsorption of solutes in the proximal renal tubules and glomerular filtration, which must be as constant as possible. The PT always reabsorbs a constant fraction of the filtered load. The purpose is to stabilize the rate at which Na and water is delivered to the LOH and ultimately to the distal nephron, which has limited transport capacity. Balance is maintained by neural, hormonal, and other mechanisms

Answer 196

It is converted to urea and H+ in the liver

Answer 197

AII/endothelin is present during low ECFV, and they act to constrict the efferent arteriole. This results in 1) increased hydrostatic pressure in the glomerulus bed, which enhances filtration of a protein-free filtrate and thus leads to increased oncotic pressure entering the peritubular capillaries. 2) increased oncotic pressure + decreased hydrostatic pressure in the peritubular bed results in an enhanced reabsorption of fluid from the tubular fluid/interstitium, thereby reducing the likelihood of backflow in the PCT

Answer 198

neutral = equal amounts of acid + base generated dibasic = H+ generated dicarboxylic = OH generated Sulfur-containing a.a. = sulfuric acid generated

Answer 199

AII/endothelin constricts the efferent arteriole under low ECFV. This results in 1) increased hydrostatic pressure in the glomerulus bed, which enhances filtration of a protein-free filtrate and thus leads to increased oncotic pressure entering the peritubular capillaries. 2) increased oncotic pressure + decreased hydrostatic pressure in the peritubular bed (due to constriction of efferent arteriole) results in an enhanced reabsorption of fluid from the tubular fluid/interstitium, thereby reducing the likelihood of backflow in the PCT

Answer 200

phosphoric acid is generated, which contributes to the daily acid load

Answer 201

Angiotensin II (but also catecholamines/sympathetic) via the Na/H exchanger

Answer 202

for every H secreted, an HCO3- exits on the basolateral side and enters the blood

Answer 203

low-pressure receptors in the atria/large veins

Answer 204

During food ingestion, gastric acid is produced, and H+ ions derived from intracellular H2CO3 are secreted into the stomach lumen while HCO3- enters the blood

Answer 205

increased renal sympathetic activity -> increased secretion of catecholamines -> increased Na/H activity to stimulate water and salt reabsorption

Answer 206

increase in plasma HCO3- after a meal. During food ingestion, gastric acid is produced, and H+ ions derived from intracellular H2CO3 are secreted into the stomach lumen while HCO3- enters the blood

Answer 207

dopamine and ANP

Answer 208

HCO3- secretions neutralize the acid in the duodenum (H+ ions are delivered to the blood) which results in a lowering of blood pH

Answer 209

they are actively taken up through the PCT basolateral membrane via high affinity transporters and then secreted into the tubular fluid. Thus, they are cleared at a rate comparable to RBF.

Answer 210

urinary pH cannot be lowered below 4.5 or increased above 8.0

Answer 211

they are actively taken up through the PCT basolateral membrane via high affinity transporters and then secreted into the tubular fluid. Thus, they are cleared at a rate comparable to RBF. This is the basis of PAH clearance and is used to measure RBF

Answer 212

~30% of H+ ions are excreted in buffered form (buffer = phosphate), which is called titratable acid excretion. The rest are eliminated indirectly via NH4

Answer 213

1) oligopeptides are degraded by ectopeptidases in the brush border 2) larger proteins are taken up by the cell via receptor mediated endocytosis and degraded intracellularly. --> amino acids are returned to blood through the basolateral membrane

Answer 214

indirect transepithelial pathway; linked to H+ ion secretion because HCO3- does not actually traverse the apical membrane.

Answer 215

descending limb

Answer 216

Na/H exchanger and luminal H-ATPase in PCT - together, they reabsorb 80% of the filtered HCO3 (via carbonic anhydrase in the lumen) Na/H exchanger in the TALH (no carbonic anhydrase in lumen) H-ATPase and H/K-ATPase in the CD (no carbonic anhydrase in lumen) All of these dump H+ into the tubular lumen, which combines together with the filtered HCO3- to form H2CO3, which will spontaneously dissociate into H2O and CO2, which diffuses into the cell. Once in the cell, intracellular carbonic acid catalyzes the formation of HCO3 and H+. HCO3 reenters the blood stream via the basal side, while the H+ is transprted back into the lumen for another round of HCO3 reabsorption

Answer 217

thick ascending limb (TALH)

Answer 218

increases because water is reabsorbed (H2O + CO2 --> HCO3- + H)

Answer 219

False. It is water impermeable

Answer 220

1) reduced fractional reabsorption of HCO3- in proximal tubule. HCO3- reabsorption in the proximal tubule has a transport maximum (Tm), thus when filtered HCO3- load exceeds this Tm, more HCO3- is delivered downstream and ultimately excreted 2) active HCO3- secretion in CD (via b-intercalated cells)

Answer 221

The descending limb is where most water is absorbed, but the TALH is where it is water impermeable, and therefore water cannot follow the reabsorbed salt in the TALH. Thus: - > tubular fluid becomes hypo-osmotic - > the medullary interstitium becomes hyperosmotic due to accumulation of reabsorbed salt)

Answer 222

drives the reabsorption of water from the thin ascending limb and from the collecting ducts if ADH is present

Answer 223

at physiological pH, NH3 is fully protonated (reaction is shifted towards the left)

Answer 224

Na/K/2Cl cotransporter

Answer 225

HCO3 is reabsorbed, thus "replenishing" body stores

Answer 226

Na/K/2Cl cotransporter is an electroneutral transporter, but it facilitates reabsorption of Na. K is returned to the tubular lumen, which generates a lumen (+) voltage. This drives the reabsorption of cations through the paracellular pathway.

Answer 227

excreted NH4+ is no longer available to generate H+ in the urea cycle

Answer 228

Na/K/2Cl cotransporter; prevents the reabsorption of Na, resulting in an ablation of the countercurrent multiplier gradient, and can result in isoosmotic urine production (because there is no concentration capability of the kidneys)

Answer 229

The problem is solved through a cooperative effort between the liver and kidneys. The liver converts NH4+ into glutamine (non-toxic intermediate), which is transported to the kidney. The kidney converts it to NH4+ and a-ketoglutarate. a-ketoglutarate is converted to 2 molecules of HCO3 "new bicarbonate", which is ultimately returned to the blood circulation

Answer 230

Chronic use prevents the reabsorption of Na, resulting 1) increases Na load arriving to the DT, which results in an upregulation of the NaCl cotransporters in the DT. 2) an ablation of the countercurrent multiplier gradient, and can result in isoosmotic urine production (because there is no concentration capability of the kidneys)

Answer 231

The kidney converts glutamine (from the liver) to NH4+ and a-ketoglutarate. a-ketoglutarate is converted to 2 molecules of HCO3 "new bicarbonate", which is ultimately returned to the blood circulation

Answer 232

TAL increases the rate of Na reabsorption with an increase in salt delivery, and its purpose is to buffer changes in salt load arriving to the distal tubule (which has limited transport capacity)

Answer 233

Glutamine from the blood and the tubular fluid and converted to NH4+ ions, which is secreted into the tubular fluid through two separate pathways: 1) Na+/NH4+ exchanger (NH4+ substitutes for H+ ions on the Na+/H+ exchanger) on the apical membrane 2) a fraction of NH4+ ions dissociate into NH3 and H+ inside the cell. NH3 is a gas and diffuses through the apical membrane AND basolateral membrane is considerable. In the tubular fluid NH3 is converted back into NH4+ by secreted H+ ions.

Answer 234

The TAL reabsorbs significant amounts of Ca and Mg without water into the medullary interstitium. These cations have limited solubility and are prone to precipitate at high concentrations. When activated, this sensor inhibits the apical K channels in the TAL, which eliminates the (+) luminal voltage that drives the paracellular reabsorption of Ca.

Answer 235

As water is reabsorbed in the descending limb of the Henle’s loop, the concentration of HCO3-, and with it, the pH of the tubular fluid increases. This alkalinization favors the dissociation of NH4+ into NH3 and H+, and some NH3 may diffuse out into the medullary interstitium

Answer 236

K channels (allows K to leave the cell into the lumen)

Answer 237

NH4+ reabsorption is mediated primarily by the Na/K/2Cl cotransporter, where NH4+ masquerades as a K+ ion. Additional NH4+ is reabsorbed paracellularly and through apical K channels in both cases driven by a favorable electrical gradient. The result is the accumulation of NH4+ in the medullary interstitium and the development of a corticopapillary gradient. Practically all of the NH4+ secreted by the proximal tubule is reabsorbed in the loop.

Answer 238

Tubuloglomerular feedback. The MD senses the increased NaCl load arriving to the distal tubule, and inihits the TGF to ensure that the downstream segments are not overwhelmed by a Na load

Answer 239

An unusual property of the ascending limb is that it is impermeable to NH3, but it actively reabsorbs NH4+.

Answer 240

TGF and Renin secretion

Answer 241

Occurs in the CD, where the final step in the excretion of NH4+ is its transfer from the medullary interstitium --> urine. Ongoing HCO3- reabsorption in the ascending limb and collecting duct alkalinizes the medullary interstitium, which promotes conversion of NH4+ --> NH3 (recall that practically all of the NH4+ secreted by the proximal tubule is reabsorbed in the loop.) Unlike the ascending limb, the collecting duct is highly permeable to NH3, but is impermeable to NH4+. As NH3 diffuses into the tubular fluid, it is converted to NH4+ by secreted H+ and thus is “trapped” and excreted. In the deep medulla, levels of interstitial NH4+ are high enough to allow active NH4+ uptake into the cell, conversion to NH3, diffusion of NH3 into the tubular fluid and its subsequent trapping as NH4+.

Answer 242

TALH and DCT

Answer 243

intracellular pH. Acidification of tubule cells → increases H+ secretion (want to get rid of H+) Alkalinization of tubule cells → inhibits H+ secretion

Answer 244

through a NaCl cotransporter

Answer 245

Short-term: - allosteric regulation/postsynthetic modifications to increase the activity of transporters existing in the membrane - insertion of new transporters from an intracellular pool of vesicles. Long-term: - synthesis of transporters - cellular remodeling in the collecting duct that affects the ratio of α- vs β-intercalated cells.

Answer 246

They block the NaCl cotransporter in the DCT, which results in decreased Na reabsorption; chronic use leads to salt wasting.

Answer 247

Evolutionarily the two main acid challenges are: - lactic acidosis (vigorous exercise) “acid cough” - happens quickly and is resolved spontaneously when the accumulated lactate anions are metabolized into HCO3-. Excretion of acid is not desirable, as it would result in alkalosis following recovery from anaerobic metabolism. - ketoacidosis during starvation - develops slowly during starvation and thus there is ample time for the kidneys to adjust.

Answer 248

ENaC - highly selective for Na

Answer 249

ongoing H+ secretion

Answer 250

low intracellular Na concentration (due to basolateral Na/K/ATPase) and negative potential inside of cell

Answer 251

Na reabsorption (via ENaC) and K secretion (via K channels)

Answer 252

blocks ENaC or blocks the effects of aldosterone, therefore K excretion is reduced due to the coupling of Na reabsorption to K secretion in the CD

Answer 253

proximal tubule + ascending limb via the Na/H exchanger

Answer 254

Increases Na reabsorption by: 1) upregulates ENaC in CD 2) upregulating NaCl cotransporter in the DT

Answer 255

AII increases the activity of Na/H exchanger in the PCT, which increases H+ secretion (coupled to Na reabsorption)

Answer 256

It caues the insertion of AQP2 water channels in the apical side of the priniciple cells, which allows water to be reabsorbed.

Answer 257

Mxn #1: Na+ reabsorption in principal cells occur through ENaC, which renders the lumen negative as Na+ exit. This voltage creates a favorable electrical gradient for the operation of the H-ATPase in the neighboring α-ICC cells As the rate of Na+ reabsorption increases, the lumen becomes more negative, which enhances H+ secretion from the α-cells. Mxn #2: In principal cells, an increase in Na reabsorption via ENaC is typically accompanied by an increase in K+ secretion. Some of this K is reabsorbed via the H/K-ATPase cotransporter by α-ICC cells, thereby leading to further stimulation of H+ secretion. Mxn #3: Aldosterone, stimulates Na and K transport, and also acts on α-ICC cells to increase the # of apical H-ATPase.

Answer 258

ANP, prostaglandins, divalent cations (Ca/Mg)

Answer 259

volume depletion triggers the RAAS system, which increases the # of apical H-ATPase (thus promoting H+ secretion) Primary hyperaldosteronism makes patients more susceptible to the development of alkalosis In both cases, aldosterone causes more H-ATPase to be inserted into the luminal side of the a-ICC cells

Answer 260

K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K) K depletion leads to cellular acidification and extracellular alkalemia (because H can't be removed from the cell if there isn't K)

Answer 261

K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K) K depletion leads to cellular alkalemia and extracellular acidificaiton (because H is removed from the cell in exchange for K)

Answer 262

ADH increases urea permeability of the inner medullary CD (which is normally impermeable to urea), which allows urea to be reabsorbed. This is to maximize water conservation during dehydration (since water follows urea reabsorption): if the CD is impermeable to urea but permeable to water, urea excretion would require the excretion of additional water.

Answer 263

hypokalemia increases H+ excretion throughout the nephron and also stimulates NH4+ transport and excretion in the proximal tubule, so that K can be reabsorbed in order to maintain a normal plasma K concentration. This can lead to extracellular alkalosis. This process occurs via Na/K/2Cl in the TALH and the H/K ATPase in the CD. **Remember that K can be substituted for NH4

Answer 264

50% is reabosrbed in the PCT by paracellular diffusion and solvent drag, and about 20% is reabsorbed in the thin limb of LOH. The rest of the nephron has low urea permeability.

Answer 265

hyperkalemia results in diminished acid and NH4+ excretion (so that K can be excreted in order to maintain a normal plasma K concentration), leading to extracellular acidosis.

Answer 266

Extrusion or uptake of electrolytes in every tissue would dramatically change the electrolyte composition of the ECF

Answer 267

brain and intestines

Answer 268

respiratory compensation

Answer 269

It's limited by changes in excitability that result from transmembrane ion fluxes. The brain cells eventually adapt to an abnormal osmolality by regulating the conc. of small organic molecules that do not disturb cell function (ie taurine, sorbitol, etc)

Answer 270

Bone dissolution because remember that in the acute setting: bone acts as an ion exchange resin: H+ are exchanged for Na, K ions. (bone contains a readily exchangable pool of of HCO3- and CO3(2-) ions.)

Answer 271

Na, by regulating the Na concentration (via adjusting the amount of water)

Answer 272

False. Can be remedied through breathing

Answer 273

by adjusting the amount of water (because it changes much more readily than the amount of Na)

Answer 274

True. It may also lead to tetany

Answer 275

water excess/overhydration (NOT a Na problem)

Answer 276

measure arterial bood gas, which should give you pH and pCO2. Use Hendersen-Hasselbalch eqn to figure out HCO3-

Answer 277

water deficit/dehydration (NOT a Na problem)

Answer 278

because the kidneys ability to excrete H2O is compromised. Therefore oligouria is the cause, not consequence, of hyponatremia

Answer 279

PCO2, HCO3-

Answer 280

low urine volume

Answer 281

respiratory acidosis respiratory alkalosis metabolic acidosis metabolic alkalosis

Answer 282

high urine volume

Answer 283

Although CO2 and HCO3- are linked in the acid-base disturbances, they are regulated independently by the lungs and the kidneys, respectively. An excess of CO2 cannot be converted to a fixed acid and excreted by the kidneys. Similarly, a decline in [HCO3-] resulting from the addition of a fixed acid cannot be corrected by the lung because there is no mechanism to convert a fixed acid into CO2.

Answer 284

water loss that you can't measure (water lost via evaporation from the lungs and skin)

Answer 285

adjustments in PCO2

Answer 286

osmoreceptors - located in the CNS in an area where it is "leaky. This allows neurons to sense a change in plasma Na concentration (since these neurons are sensitive to changes in cell volume)

Answer 287

adjustments in HCO3-

Answer 288

ADH secretion and consequently water secretion

Answer 289

pH. determined by the ratio of [HCO3-] and PCO2

Answer 290

The kidneys ability to conserve water becomes exhausted (it can only conserve up to 1L/day via ADH) and therefore water balance depends almost exclusively on the thirst mechanism

Answer 291

because the compensatory response is initiated by the change in pH, and thus full restoration of pH would eliminate the signal that drives the compensation.

Answer 292

lower. Thus, under normal conditions, water balance is maintained by regulating ADH secretion and consequently water secretion

Answer 293

Respiratory compensation begins almost instantly through changes in the activity of peripheral chemoreceptors. However, the full response, which includes central chemoreceptors, takes a few hours to develop because HCO3- penetrates only slowly through the blood-brain barrier.

Answer 294

behavioral response of thirst determines water intake | ADH regulates renal water excretion by altering permeability of the collecting duct

Answer 295

Renal compensation of respiratory disturbances takes several days. Consequently, acute and chronic respiratory disorders can be distinguished based on the degree of renal compensation (i.e. change in [HCO3-]).

Answer 296

they temporarily inhibit the sensation of thirst to prevent overhydration. This is because the osmoreceptors regulation of water intake is insufficient.

Answer 297

respiratory disturbances can develop much more quickly but the metabolic/renal compensation can take several days

Answer 298

prevent changes in plasma osmolality, and therefore cell volume

Answer 299

degree of renal compensation (change in [HCO3-])

Answer 300

under normal conditions, regulation of cell volume takes precedence over regulation of ECFV. But with extreme disturbances of ECFV (ie hypovolemic/hemorrhagic shock, the body tolerates changes in plasma osmolality to prevent circulatory collapse.

Answer 301

physicochemical buffering

Answer 302

CO2-bicarbonate system

Answer 303

reabsorbing solute without H2O generates dilute urine, but generates a hyperosmotic medulla. This occurs in the TALH, and this is called the "single effect" of urinary concentration

Answer 304

generates CO2 | H + HCO3 => H2O + CO2

Answer 305

ascending limb of LOH, DT, and in the absence of ADH, the CD (since all of these areas are water-impermeable)

Answer 306

requires input/consumption of CO2, but generates HCO3 | NaOH + CO2 => Na + HCO3-

Answer 307

removal of CO2

Answer 308

deposition of Na into the interstitium (without water)

Answer 309

retention of CO2

Answer 310

at any one level in the medulla, there is only a modest difference in the salt concentration of the tubular fluid in the ascending limb of LH and the interstitium, but the counterflow arrangement generates a large axial (corticopapillary) salt gradient

Answer 311

non-bicarbonate buffers, including intracellular proteins

Answer 312

blood flow through the vasa recta in the medulla at a sluggish rate and in opposite directions.

Answer 313

buffering with intracellular proteins, or non-bicarbonate buffers the CO2-bicarbonate system cannot be used because in this case the source of H+ ions is H2CO3. Remember that in respiratory acidosis, CO2 accumulates (due to hypoventilation) and causes the reaction (H + HCO3 => H2O + CO2) to go in the opposite direction, thus generating H+. These H+ are taken up by proteins, which ultimately affects protein structure and function.

Answer 314

an increased medullary blood flow results in an incomplete equilibration between the ascending and descending blood, and thus the vasa recta carries away more salt from the medulla than what the TAL can produce

Answer 315

Respiratory disturbances can only be buffered by non-bicarbonate buffers, including intracellular proteins. This problem is intensified by the ease with which CO2 (diffusion) can enter cells relative to HCO3- (requires transporter)

Answer 316

1) increased medullary blood flow 2) increased luminal flow 3) loop diuretics (block salt reabsorption in TALH, thereby abolishing the corticopapillary salt gradient) all three reduces the time available for equilibration with the interstitium, which increase tubular flow, and consequently diminishes renal concentrating ability

Answer 317

loss of bicarbonate or gain of fixed acid

Answer 318

to maintain the medullary osmotic gradient

Answer 319

decrease, decrease, decrease

Answer 320

1) increase H2O permeability along the entire length of the CD. 2) increase urea permeability in the terminal portion of the CD. NET: corticopapillary urea gradient established

Answer 321

primary event: HCO3 loss | compensation event: PCO2 (hyperventilation)

Answer 322

rapid: increase AQP2 transcription chronic: increase AQP2 transcription

Answer 323

prevent large decreases in PH

Answer 324

cortical collecting duct

Answer 325

PAG = [Na+] - [Cl-] - [HCO3-] PAG is the difference between the concentrations of anions and cations that were not measured or are not included in the formula

Answer 326

ADH increases urea permeability of the inner medullary CD (which is normally impermeable to urea), which allows urea to be reabsorbed. Urea deposited into the medullary interstitium is taken up by the thin limbs of LH, which has constitutively high urea permeability. During anti-diuresis, tubular fluid exiting the LH contains more urea than what was filtered. The subsequent segments up to the point of the terminally medullary CD are impermeable to urea, and due to water reabsorption under the influence of ADH, urea concentration increases in the cortical and outer medullary.

Answer 327

8-10 mEq/L. largely attributed to the presence of albumin

Answer 328

Na and urea

Answer 329

diagnosis of metabolic acidosis

Answer 330

rate of urea excretion is reduced, and therefore urea concentration in the blood increases. Since urea is not an effective osmole, the increased blood urea does not change ICFV, and the accumulated urea can be excreted upon rehydration?

Answer 331

Its value increases during metabolic acidosis, or whenever an acid other than HCl is added to plasma: - ketoacids in diabetes mellitus - lactate during exercise - unusual anions resulting from the ingestion of certain toxins (ex: formic acid from methanol)

Answer 332

ineffective osmole - increased blood urea does not change ICFV

Answer 333

renal defect in H+ ion secretion --> acidosis. Increases PAG

Answer 334

In renal failure plasma creatinine and BUN increase in parallel (because the problem lies within the ability of the urine to filter/reabsorb stuff)

Answer 335

[HCO3-] declines by dilution, thus fooling the body to think that there is less buffering capacity (blood becomes more acidic). Ventilation increases to get rid of CO2 to make the body “less acidic” but in reality, you’re decreasing the HCO3, or buffering capacity even more due to ventilation H + HCO3 => H2O + CO2 (expelled)

Answer 336

During dehydration (as long as GFR is maintained) creatinine excretion and thus plasma creatinine remain constant whereas BUN increases. (because ADH causes increased urea permeability, whereas creatinine is not affected by ADH)

Answer 337

too much bicarbonate retention

Answer 338

ANP inhibits Na reabsorption in the CD and antagonizes the effect of ADH. This results in rapid reduction of the ECFV.

Answer 339

increase, increase, increase

Answer 340

it antagonizes the effect of ADH.

Answer 341

primary event: HCO3 | compensation event: PCO2 (hypoventilation)

Answer 342

ADH-like effects (because they inhibit prostaglandins, which normally antagonize ADH). As a result, ADH can act on the CDs, resulting in increased urine osmolality

Answer 343

bicarbonaturia (excretion of HCO3)

Answer 344

The CD monitors urinary [Ca] via luminal Ca++ receptors. If the urine Ca concentration is too high (which increases risk of precipitation, these receptors are activated to inhibit the effect of ADH on the CD, thus generating more dilute urine.

Answer 345

to decrease pH and HCO3 levels

Answer 346

TALH and cortical CD

Answer 347

1) transport maximum for bicarbonate reabsorption in the proximal tubule is only slightly above the normal filtered load, and thus an increase in plasma [HCO3-] results in increased bicarbonate delivery out of the proximal tubule 2) alkalosis suppresses HCO3- reabsorption in other segments, and also stimulates HCO3- secretion by β-intercalated cells

Answer 348

decreased (more water is retained)

Answer 349

repeated vomiting, which also leads loss of Na/K in the urine (resulting in a negative Na and K balance). It is the secondary effects of Na and K depletion that are responsible for perpetuating the alkalosis.

Answer 350

repeated vomiting, which also leads loss of Na/K in the urine (resulting in a negative Na and K balance). It is the secondary effects of Na and K depletion that are responsible for perpetuating the alkalosis.

Answer 351

Increased HCO3 + Negative Na and K balances The kidney responds to the initial loss of HCl (vomiting) and the resulting alkalosis by bicarbonaturia (HCO3 secreted in urine). Due to the coupling of Na and HCO3- reabsorption in the nephron, HCO3 secretion results in the loss of Na. Less HCO3 and Na reabsorption means that there is greater tubular flow, which enhances K secretion in the CD. Reduced intake of Na and K due to the upset stomach also contributes to the negative Na and K balance.

Answer 352

In a bulemic person (repeated vomiting), Na and K loss occurs, resulting in activation of the sympathetic nervous system and RAAS.

Answer 353

1) increase HCO3 --> loss of Na (due to coupling of transport) 2) less HCO3 and Na reabsorption --> greater tubular flow, which enhances K secretion in the CD. 3) Reduced intake of Na and K due to the upset stomach --> negative Na and K balance 4) activation of the sympathetic nervous system and the RAAS. Catecholamines and AII stimulate the apical Na/H exchanger (HCO3- reabsorption) in the proximal tubule. Aldosterone acts on Na/H exchanger in the CD to stimulate Na reabsorption, H secretion, and K secretion, thereby aggravating the K depletion.

Answer 354

hypokalemia leads to intracellular acidosis due to enhanced H/K exchange, to which tubule cells respond accordingly: - increased NH4+ production and excretion - increase in HCO3- reabsorption

Answer 355

administer K and NaCl levels

Answer 356

dehydration (loss of water) or treatment with diuretics can result in contraction alkalosis.

Answer 357

increased arterial PCO2; usually due to depressed alveolar ventilation or, rarely, because of excessive CO2 production.

Answer 358

the H+ ions derived from H2CO3 are buffered by non-bicarbonate buffers (Hb, proteins, etc)

Answer 359

large increase in [HCO3-] and pH is returned to near normal values

Answer 360

alveolar hyperventilation. As with respiratory acidosis, the change in [HCO3-] is relatively small acutely, but is substantial if hyperventilation persists for several days.

Answer 361

False. Mixed acid/base disturbances can either amplify or neutralize each other.

Answer 362

1) arterial pH - acidemia or alkalemia is present? 2) HCO3/PCO2: low HCO3 = metabolic acidosis; low PCO2 = respiratory alkalosis, and vice versa. 3) if the compensation response is excessive or inadequate, then a second disorder is present. For instance, in a patient with metabolic acidosis and [HCO3-] of 14mEq/L, you expect PCO2 of ~30 mmHg. A higher PCO2 indicates coexistent respiratory acidosis, while a lower value suggests concurrent respiratory alkalosis. 4) Calculate PAG = [Na+] - [Cl-] - [HCO3-]. A elevated PAG indicates a coexistent metabolic acidosis even if pH is normal or alkalemic. 5) If the PAG is wide, compare the ΔPAG to ΔHCO3-. A 1:1 ratio is expected with a “pure” organic metabolic acidosis. If the ΔPAG > ΔHCO3, a concurrent metabolic alkalosis may be present. If the Δ PAG < Δ [HCO3-], a concurrent metabolic acidosis may be present

Answer 363

UAG = UAG = [Na+] + [K+] - [Cl-] used to indirectly measure urinary NH4+ excretion. The logic behind UAG is that the difference between unmeasured anions and cations is attributable mainly to [NH4+]

Answer 364

near zero or is positive

Answer 365

PAG increases, UAG becomes negative (P+, U-)

Answer 366

Extracellular Ca2+ and Pi are near to levels where they tend to precipitate

Answer 367

Ca is an important 2nd messenger and this function requires that intracellular [Ca2+] be kept very low.

Answer 368

bone. It is in an insoluble form that exchanges with the ECF very slowly (months); acts as a buffer against changes in plasma [Ca2+].

Answer 369

~50% is complexed with small anions (~10%) and to albumin (40%) and cannot be filtered by the glomeruli

Answer 370

50% (free, not complexed)

Answer 371

Ca2+/Na+ exchanger | plasma membrane Ca-ATPase.

Answer 372

demineralization of bones, and may result in fractures or the development of rickets.

Answer 373

increased blood pressure, muscle weakness, and constipation. During hypercalcemia Ca salts may precipitate in soft tissues, leading to their calcification and the development of kidney stones.

Answer 374

Ca2+ negatively affects voltage-gated Na channels (prevents them from opening). Hypocalcemia results in less inhibition of the VG Na channels, thus resulting in spontaneous firing of motor neurons that may result in tetany and bronchospasm.

Answer 375

the distribution of Ca between ECF and bone.

Answer 376

majority is reabsorbed in the PCT and ascending loop (via passive, paracellular transport). In the DCT, Ca is reabsorbed via an active transcellular route, and is the prime site of regulation

Answer 377

Ca ions enter DCT cells via a luminal Ca-channel and are pumped out at the basolateral side by a Ca-ATPase and a Na/Ca exchanger. The intracellular free [Ca2+] needs to be kept very low in order for Ca entry into the cell, otherwise an increased intracellular Ca would limit transport. Therefore, distal tubule cells (as well as epithelial cells of the small intestine) have calbindin, which binds to Ca to maintain a high total intracellular [Ca] thereby allowing a high rate of intracellular diffusion, while maintaining normal ionized [Ca2+] Ca ions enter DCT cells via a luminal Ca-channel and are pumped out at the basolateral side by a Ca-ATPase and a Na/Ca exchanger. The intracellular free [Ca2+] needs to be kept very low in order for Ca entry into the cell, otherwise an increased intracellular Ca would limit transport. Therefore, distal tubule cells (as well as epithelial cells of the small intestine) have calbindin, which binds to Ca to maintain a high total intracellular [Ca] thereby allowing a high rate of intracellular diffusion, while maintaining normal ionized [Ca2+] Ca ions enter DCT cells via a luminal Ca-channel and are pumped out at the basolateral side by a Ca-ATPase and a Na/Ca exchanger. The intracellular free [Ca2+] needs to be kept very low in order for Ca entry into the cell, otherwise an increased intracellular Ca would limit transport. Therefore, distal tubule cells (as well as epithelial cells of the small intestine) have calbindin, which binds to Ca to maintain a high total intracellular [Ca] thereby allowing a high rate of intracellular diffusion, while maintaining normal ionized [Ca2+]

Answer 378

Paracellular Ca reabsorption in the proximal tubule and the loop of Henle is driven by Na reabsorption. Consequently, factors that alter Na reabsorption in these segments, like changes in ECFV or diuretics that act here, result in corresponding changes in Ca reabsorption.

Answer 379

DCT, blocks NaCl cotransporter (and thereby Na reabsorption), which stimulates Ca reabsorption. AKA Ca sparing

Answer 380

Stimulate Na reabsorption in the collecting duct

Answer 381

Decreases, because Ca2+ binds to albumin at alkaline pH. In a chronic setting, this has no effect on plasma ionized Ca because regulation via parathyroid hormone (PTH) maintains Ca concentrations constant.Decreases, because Ca2+ binds to albumin at alkaline pH. In a chronic setting, this has no effect on plasma ionized Ca because regulation via parathyroid hormone (PTH) maintains Ca concentrations constant.

Answer 382

close, therefore Ca excretion increases

Answer 383

opens, therefore Ca excretion decreases

Answer 384

Alkalosis results in a shift of Pi from extracellular fluid into cells (reduction of plasma Pi)

Answer 385

PCT (85% of phosphate (Pi) is reabsorbed here)

Answer 386

PTH and calcitriol (active form of Vitamin D)

Answer 387

low plasma Ca

Answer 388

Chief cells express a Ca-sensing receptor (CaSR; a typical G-protein-coupled receptor). CaSR is a negative regulator of PTH release. PTH secretion is under tonic inhibition by the Ca-bound CaSR, and hypocalcemia relieves the chief cells from this inhibition.

Answer 389

1) induces Ca and Pi release from bone 2) stimulates Ca reabsorption in the distal tubule 3) inhibits Pi reabsorption in the PCT by retrieving Na/Pi transporters from the luminal (thus lowering the TM) 4) activates the enzyme to convert Vit-D3 to its active form, calcitriol (1,25‐(OH)2‐vitamin D3).

Answer 390

active form of vitamin D3

Answer 391

stimulates Ca absorption in the gut

Answer 392

hormone produced by bone, which is a potent inhibitor of Pi reabsorption

Answer 393

hyperphosphatemia lowers (more reabsorbed) and hypophosphatemia increases (more reabsorbed) the Tm for Pi

Answer 394

closes them

Answer 395

Mg channels normally induce K channels to close. Mg depletion thus increases the open probability of the apical K channels in the cortical collecting that mediate K secretion

Answer 396

opens them

Answer 397

Mg decreases the open probability of several Ca channels, and thus, Mg deficiency results in elevated intracellular [Ca2+] (less is transported out of the cell)

Answer 398

LOH, via a paracellular pathway

Answer 399

DCT because Mg reabsorption in this segment occurs by a transcellular mechanism

Answer 400

Mg plasma conc.

Answer 401

1) regulation of reabsorption for the three ions: PCT = Pi, early DCT = Mg, late DCT = Ca 2) CaSRs in the basolateral side of the TALH and in the luminal side of collecting duct cells (principle and a-ICC)

Answer 402

An increase in local [Ca] activates CaSR, and initiates a signaling cascade that results in decreased Ca and Mg transport, thereby protecting against nephrocalcinosis.

Answer 403

In the TALH, Ca and Mg are reabsorbed without water. An increase in local interstitial [Ca] activates CaSR, which inhibits further Ca and Mg reabsorption. In principal cells, CaSRs inhibit ADH-dependent water reabsorption, thereby preventing concentration of the tubular fluid. In a-ICC cells, CaSRs stimulate H+ secretion, thereby inhibiting the formation of salts (CaPO4, Mg/NH4PO4) that tend to precipitate at alkaline pH.

Answer 404

Citrate is a natural Ca-and Mg-chelator, and thereby increases the solubility of these ions in the urine

Answer 405

Ca and Pi are the main components of the bone matrix. Extracellular [Ca2+] and [Pi] need to be kept near their solubility limits for normal bone function. If the solubility limits for Ca and Pi are exceeded, calcification of soft tissues may take place.

renal final index cards exam I Flashcards

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