Valley: Renal Functions Flashcards
1
Q
—— are 90% of total osmolality of the extracellular fluid
A
Sodium salts
2
Q
When we talk about regulating osmolality, we are talking about regulating — concentration
A
sodium
3
Q
Normal osmolality is about — mOsm/l
A
300 ; 270-310
4
Q
Conservation of non-ionic components of plasma: (5)
A
Glucose, amino acids, proteins, water, vitamins
5
Q
Excretion of non-volatile end-products of metabolism: (6)
A
HP042-, Urea, Uric Acid, S042-, Creatinine, Lactic Acid
6
Q
Maintenance of extracellular fluid volume is achieved by controlling — and — excretion
A
salt (NaCI) and water
7
Q
3 Endocrine functions:
A
Erythropoietin, renin-angiotensin system, vitamin D
8
Q
Renal hormone that acts on bone marrow and stimulates red blood cell production
A
Erythropoietin
9
Q
the patient with chronic renal disease is anemic because there is a deficiency of —.
A
erythropoietin
10
Q
Enzyme-hormone system that participates in blood pressure regulation, potassium excretion,
and sodium excretion
A
Renin-angiotensin system
11
Q
The kidney converts — to its physiologically active form (Vitamin D3)
A
vitamin D
12
Q
The patient with chronic renal disease becomes — because calcium absorption from the intestine is impaired when there is a deficiency of
vitamin D.
A
hypocalcemic
13
Q
About —% of the total quantity of blood pumped by the heart each minute, or —liters/min, passes
through the kidneys.
A
25 ; 1.25
14
Q
As it turns out, the kidneys re-work the extracellular fluid about once every two —, thereby maintaining its composition and volume.
A
hours
15
Q
dialysis machines are capable of re-working the extracellular space of anephric (kidney-free) patients once every 8-12 —.
A
hours
16
Q
Blood is delivered to the glomerulus via the — arteriole and exits the glomerulus via the — arteriole.
A
Afferent ; efferent
17
Q
What are the two types of nephrons?
A
Cortical nephrons and juxtamedullary nephrons
18
Q
Cortical nephrons have — loops of Henle and glomeruli located near the —.
A
Short ; surface of the kidney
19
Q
Juxtamedullary nephrons have — loops of Henle and glomeruli located deep in the cortex near the —.
A
Cortical medullary junction
20
Q
Blood passes through the —, the —, the —, and the — before it drains into the venous system.
A
Afferent arterioles ; glomerular capillaries ; efferent arterioles ; peritubular capillaries
21
Q
The — branches into a capillary network that entwines the renal tubule.
A
Efferent arteriole
22
Q
The — arise from the efferent arteriole and engulf the renal tubule.
A
Peritubular capillaries
23
Q
The — are the peritubular capillaries of the loops of Henle of the juxtamedullary nephrons.
A
Vasa recta
24
Q
The vasa recta constitute a — exchange system.
A
Countercurrent
25
A substance may be transported form the tubule to the capillary
Reabsorption
26
A substance may be transported from the capillary to the tubule
Secretion
27
Hairpin-shaped capillaries of the long loops of Henle of the juxtamedullary nephrons
Vasa recta
28
What 3 parts of the kidney are found in the cortex?
Glomeruli, proximal tubules, and distal tubules
29
What 2 parts of the kidney are found in the medulla?
Loops of Henle and collecting ducts
30
The — of the kidney is most vulnerable to ischemia (secondary to hypotension)
Inner stripe of the outer medulla
31
Name most of the kidney (pic)
32
Movement, under pressure, of plasma water and most of its dissolved constituents from the glomerular capillary into Bowman’s capsule.
Glomerular filtration
33
The beat of the heart creates the high glomerular capillary — pressure that is required for the filtration process
Hydrostatic
34
Transport of substances out of the lumen of the renal tubule
Tubular reabsorption
35
Transport of substances into the lumen of the renal tubule
Tubular secretion
36
Reabsorbs the bulk of the filtered fluid and its dissolved constituents
Proximal tubule
37
Provides the coarse control mechanisms for the renal regulation of extracellular fluid volume and composition.
Proximal tubule
38
Establishes and maintains an osmotic gradient in the medulla of the kidney.
Loop of Henle
39
The — plays a critically important role in the regulation of water balance.
Osmotic gradient
40
The fluid leaving the loop of henle is —
Hypo-osmotic
41
In the loop of Henle, the handling of — and — occur independently.
NaCl and water
42
The loop of Henle is a — multiplier.
Countercurrent
43
Make final adjustments on urine pH, osmolality, and ionic composition, depending on the needs at the moment.
Distal tubule and collecting duct
44
The reabsorption of water is under the control of — hormone.
Antidiuretic
45
The reabsorption of sodium and the secretion of potassium are under the control of —.
Aldosterone
46
The distal tubule and collecting duct provide the fine control mechanisms for the renal regulation of — fluid composition and volume.
Extracellular
47
The — deposit sodium chloride in the medullary interstitium, and, in doing so, produce a gradient in osmolality that increases progressively from the corticomedullary junction to the papilla.
Loops of Henle
48
In humans, the osmolality in the medulla increases from — mOsm (corticomedullary junction) to — - — mOsm deep in the medulla.
300 ; 1200-1500
49
The — is required for making the urine concentrated or making the urine dilute.
Osmotic gradient
50
The cycling of — from tubules to interstitium is crucial.
Urea
51
Osmolality in cortex?
300
52
Osmolality in outer medulla?
400-600
53
Osmolality in inner medulla?
800-1200
54
The kidneys regulation of the composition of the — fluid.
Extracellular
55
The kidneys — of toxic substances and non-volatile end-products of metabolism.
Excretion
56
The kidney produces a variety of enzymes (—) and hormones (— and —) that participate in many body functions.
Renin ; erythropoietin and vitamin D
57
What is the functional unit of the kidney?
Nephron
58
One of the three basic nephron processes, is the movement of cell-free and albumin-free fluid into Bowman’s capsule from the glomerular capillaries
Glomerular filtration
59
Approximately — liters of blood are pumped by the heart each minute.
5
60
Approximately — liters (—%) of the cardiac output are delivered to the kidneys each minute.
1.25 ; 25
61
Approximately — liters (— milliliters) of blood plasma and its dissolved constituents (excluding
large proteins) are filtered into the renal tubules each minute.
0.125 ; 125
62
The bulk of the — (67%) is reabsorbed as it passes through the proximal tubule.
glomerular filtrate
63
The loop of Henle establishes the — in the medulla of the kidney.
osmotic gradient
64
The valuable constituents of the filtrate (e.g., H20, HC03 -, glucose, amino acids, Na +, K+) are reabsorbed to a large extent from the — and returned to the general circulation via the —.
proximal tubule ; peritubular capillaries
65
End-products of metabolism (urea, uric acid, creatinine, P042-, SOl-) are reasonably poorly — by the renal tubules.
reabsorbed
66
Renal — of these metabolites prevents their accumulation in the extracellular space, and cell function is thereby maintained at an optimal level.
excretion
67
The distal tubule and collecting duct are the nephron locations where exquisite control of — fluid composition and volume is achieved.
extracellular
68
Excretion of substances such as Na +, K+, and H20 are finely controlled at these sites.
The distal tubule and collecting duct
69
The influence of antidiuretic hormone (ADH = vasopressin) is responsible for the exquisite control of — excretion.
water
70
influence of aldosterone is responsible for the exquisite control of — and — excretion.
sodium and potassium
71
The proximal tubule has a maximum capacity for reabsorbing glucose; this maximum reabsorptive capacity for glucose is referred to as the "—" or "—':
transfer maximum ; transport maximum
72
All of the filtered glucose is normally completely reabsorbed from the — by active transport mechanisms.
proximal tubule
73
In untreated —, the amount of glucose filtered exceeds the transfer (transport) maximum of the proximal tubule.
diabetes mellitus
74
All segments of the renal tubule beyond the — are impermeable to glucose.
proximal tubule
75
— is a disease in which in adequate amounts of insulin are produced by the pancreas.
Diabetes mellitus (sweet urine)
76
An increase in plasma — concentration is one of the consequences of the insulin deficiency.
glucose
77
When DM happens, glucose will appear in the urine because the —, —, and — are impermeable to glucose.
loop of Henle, distal tubule, and collecting duct
78
If glucose escapes reabsorption in the —, it is excreted.
proximal tubule
79
What happens to urine output in the untreated patient with diabetes mellitus? Why?
Urine flow increases because unreabsorbed glucose causes an osmotic diuresis.
80
The rate of — hormone release into the bloodstream is directly related to the osmolality of the extracellular fluid.
antidiuretic
81
An — in extracellular fluid osmolality is corrected by ingesting water and adding it to the extracellular fluid.
increase
82
A — in extracellular fluid osmolality is corrected by excreting water and removing it from the extracellular fluid.
decrease
83
Extracellular fluid osmolality (and hence sodium concentration) is regulated by — (—, —)
antidiuretic hormone (ADH, arginine vasopressin)
84
ADH is synthesized in the paraventricular and supraoptic nuclei of the —.
Hypothalamus
85
ADH is transported in the axoplasmic fluid of the hypothalamic-hypophyseal nerves to storage sites in nerve terminals of the —.
Posterior pituitary (neurohypophysis)
86
Nerve action potentials stimulate release of ADH from the —.
Posterior pituitary
87
The posterior pituitary is also known as the —.
Neurohypophysis
88
Which is the more potent vasoconstrictor, ADH or angiotensin II?
ADH is more potent.
89
In response to an increase in extracellular fluid osmolality, paraventricular and supraoptic nuclei shrink and nerve axons fire action potentials, which cause — release from the posterior pituitary
ADH
90
An — in extracellular fluid osmolality is the most powerful stimulus triggering the release of ADH.
increase
91
When ADH reaches the — and —, the reabsorption of water is increased (a small volume of concentrated urine is formed)
distal tubule and collecting duct
92
In response to a decrease in extracellular fluid osmolality, cells of the paraventricular and supraoptic nuclei swell and nerve action potentials are inhibited, so ADH release is —.
depressed
93
In the — of ADH, the distal tubule and collecting duct are impermeable to water. A large volume of dilute urine is formed.
absence
94
Stresses, including —, —, and — trigger the release of ADH.
hypovolemia, hypotension, and pain
95
Besides stressors, what other things cause an increase in ADH release?
CPAP, PEEP, volatile agents
96
Approximately —% of the filtered water is reabsorbed from the proximal tubule and —% from the descending limb of Henle's loop.
67 ; 13
97
The ascending limb of Henle's loop is impermeable to —.
water
98
Since NaCI is reabsorbed from the ascending limb, the urine becomes — (osmolality = — mOsm) when it reaches the distal tubule.
dilute ; 100
99
Antidiuretic hormone (ADH, arginine vasopressin) — the permeability of the distal tubule and collecting duct to H20.
increases
100
When circulating levels of ADH are high, a — volume (—ml/kg/hr) of concentrated urine is formed)
Small ; .5
101
When ADH is absent, H20 is trapped in the — and —, even though there is a large osmotic force for H20 movement.
distal tubule and collecting duct
102
When ADH is absent, the urine osmolality may decrease to — mOsm because salts are reabsorbed in the distal tubule and collecting duct and water is not.
50
103
When circulating levels of ADH are —, a large volume (up to —ml/min or — ml/kg/hr) of dilute urine (— - — mOsm) is formed.
Low ; 25 ; 25 ; 50-100
104
5 step responses following a decrease in body fluid osmolality:
1. The hypothalamic nuclei swell, and a decrease in nerve impulse frequency in the hypothalamic-
hypophyseal tract results.
2. There is a decrease in ADH release.
3. With reduced circulating levels of ADH, the distal tubules and collecting ducts become relatively
impermeable to H20.
4. The decrease in H20 reabsorption from the distal tubules and collecting ducts results in the production of large volumes of dilute urine.
5. The increased H20 excretion causes body fluid osmolality to return to normal.
105
6 step responses following an increase in body fluid osmolality:
1. The hypothalamic nuclei shrink, and an increase in nerve impulse frequency in the hypothalamic-hypophyseal tract occurs.
2. There is an increase in ADH release. A 2% increase in osmolality (from 300 to 306 milliosmoles per kg)
is sufficient to stimulate the release of large quantities of ADH.
3. ADH increases the permeability of the distal tubules and collecting ducts to H20.
4. The increased H20 reabsorption from the distal tubules and collecting ducts results in the excretion of small volumes of highly concentrated urine.
5. Steps 1-4 serve to conserve existing body H20 and to prevent further increases in osmolality.
6. The increased body fluid osmolality also triggers the sensation of thirst. H20 ingestion causes the
osmolality to return to normal.
106
the body corrects a hyperosmotic state by adding — to the extracellular fluid until the osmolality is restored to normal.
ingested water
107
the body corrects a hypo-osmotic state by increasing renal excretion of —, thereby removing — from the extracellular space until osmolarity is restored to normal.
water ; water
108
Sodium intake and excretion are — important in regulating extracellular fluid osmolality because significant changes in body sodium content take a long time to be achieved.
not
109
it would take — days to excrete enough sodium to correct a hyperosmotic state, but only — to — hours are required to dilute the extracellular fluid by ingesting water.
three ; one to three
110
+ADH: Urine osmolality and urine volume
1200-1500 mOsm and 0.5 mL/kg/hr (low)
111
-ADH: Urine osmolality and urine volume
50-100 mOsm and 2-25 mL/kg/hr (high)
112
What are the 2 causes of diabetes insipidus?
1. Failure of ADH synthesis or ADH release (most common cause)
2. Insensitivity of the distal tubules and collecting ducts to ADH (nephrogenic)
113
Inappropriate secretion of — can occur as a result of surgery or any of several diverse pathological
processes including intracranial tumors, hypothyroidism, porphyria, and small (Oat's) cell carcinoma of the lung
ADH
114
An inappropriately increased urine sodium concentration and urine osmolality in the presence of hyponatremia and decreased plasma osmolality are virtually diagnostic of —.
inappropriate ADH secretion
115
The amount of — in the body is the major determinant of extracellular fluid volume.
sodium
116
— follows sodium.
Water
117
When the amount of — in the body increases,
osmolality increases.
sodium
118
With an — in osmolality, thirst mechanisms are activated and water is ingested.
increase
119
The primary event in increasing extracellular volume is the increase in body — content.
sodium
120
When the amount of sodium in the body decreases, ADH output is — and water excretion —.
decreased ; increases
121
— is the most important hormone for regulating extracellular fluid volume.
Aldosterone
122
sodium content (sodium load) determines — fluid volume.
extracellular
123
— (also known as —) is released from the right atria and also acts on the kidney to increase sodium excretion.
Atrial natriuretic peptide (atrial natriuretic factor)
124
Sodium excretion — when glomerular filtration rate increases and — when glomerular filtration rate decreases.
increases ; decreases
125
What are the 3 determinants of sodium excretion?
1. GFR
2. Aldosterone
3. Atrial natriuretic factor
126
What are the 3 mechanisms to increasing Na excretion?
1. Increase GFR
2. Decrease aldosterone
3. Increase atrial natriuretic factor (peptide)
127
What are the 3 mechanisms to decreasing Na excretion?
1. Decrease GFR
2. Increase aldosterone
3. Decrease atrial natriuretic factor (peptide)
128
Aldosterone is a hormone produced in the zona glomerulosa of the —.
adrenal cortex
129
Aldosterone acts on the late — and — (primarily the —) to alter two renal tubular functions simultaneously.
distal tubule and collecting duct ; collecting duct
130
Aldosterone — the rate of Na reabsorption from the late distal tubule and collecting duct and thereby — the rate of Na excretion.
increases ; decreases
131
Aldosterone — the rate of K secretion into the late distal tubule and collecting duct and thereby — the rate of K excretion.
increases ; increases
132
Na reabsorption occurs from — segment of the renal tubule in the presence of aldosterone.
each
133
The bulk of the filtered Na is reabsorbed from the — (67%) and — (25%), but there also is significant reabsorption in the — and — (7.2%) if aldosterone is present.
proximal tubule ; ascending limb of Henle's loop ; late distal tubule and collecting duct
134
Na reabsorption in the ascending limb of Henle's loop occurs through a channel that simultaneously reabsorbs — and —.
K+ and CI-
135
Na secretion in the descending limb of Henle's loop is —.
passive
136
Na reabsorption is an — process (—) in the proximal tubule, distal tubule and collecting duct.
active (energy-requiring)
137
Without aldosterone, about 8% of the filtered Na may be excreted because the — and — are importable to Na.
Distal tubule and collecting duct
138
When sodium intake is high, body sodium content increases, and body fluids become concentrated.
ADH output — to conserve existing water, and thirst causes water ingestion, which restores osmolality but expands fluid volume.
increases
139
The major consequences of sodium retention (increased content/amount of sodium) are extracellular fluid volume — (—) and a tendency for arterial blood pressure to —-.
expansion (hypervolemia) ; increase
140
Hypervolemia is corrected by — the renal excretion of sodium.
increasing
141
Sodium excretion is increased because: (a) GFR —, (b) renin release —, and (c) output of atrial natriuretic peptide —. Water is excreted along with the sodium to keep body fluid osmolality at 300 mOsm. This process of correcting a hypervolemic state takes several days.
increases ; decreases ; increases
142
When sodium intake is low, body sodium content (amount) decreases, and body fluids become dilute.
ADH output —, and a dilute, high-volume urine is formed. Osmolarity is restored to normal, but fluid volume is contracted.
decreases
143
The major consequences of sodium loss (decreased content/amount of sodium) are fluid volume — (—) and a tendency for a — in arterial blood pressure.
contraction (hypovolemia) ; decrease
144
Hypovolemia is corrected by promoting sodium —.
retention
145
Sodium retention (increased content/amount of sodium) occurs because: (a) GFR is —, (b) renin release is —, and (c) output of atrial natriuretic factor is —. Water is retained along with the sodium to maintain body fluid osmolality at 300 mOsm.
decreased ; increased ; decreased
146
—% of the filtered K is reabsorbed from the proximal tubule and —% is reabsorbed from the ascending limb of Henle's loop.
67; 25
147
In the presence of aldosterone, substantial quantities of potassium are secreted into the late — and —.
distal tubule and collecting duct
148
Aldosterone acts on late distal tubules and collecting ducts. Aldosterone acts primarily on the principal cells of the —.
collecting ducts
149
With reduced levels of aldosterone, secretion of potassium into the late distal tubules and collecting ducts is —.
decreased
150
K+ normally is excreted as a result of —.
secretion
151
Glomerulus: K+ is — filtered.
freely
152
Proximal tubule: About —% of the filtered K+ is reabsorbed in this segment. The reabsorptive process for K+ in the proximal tubule is mainly —.
67 ; active
153
Descending limb of Henle's loop: The concentration of K+ — progressively during the descent, mostly because of H20 reabsorption but also partly because of passive K+ secretion.
increases
154
Ascending limb of Henle's loop: Approximately —% of the filtered K+ is reabsorbed in this segment. The K+ reabsorption occurs through a channel that simultaneously transports — and —. About 92%
of the filtered K+ is reabsorbed before the distal tubule is reached.
25 ; Cl- and Na+
155
Distal tubule and collecting duct: Under normal conditions circulating aldosterone is high and there is net K+ secretion, with about 75% of the excreted K+ derived from the secretion of potassium into the late distal tubule and collecting duct. Therefore, most
of the K+ appearing in the urine normally is a result of —.
secretion
156
If a high extracellular concentration of K+ is present, aldosterone levels — and — K+ secretion occurs in the late distal tubule collecting duct.
rise ; increased
157
During times of K+ deprivation and low circulating aldosterone, active K+ secretion is greatly — (— may occur) in the late distal tubule and collecting duct; thus, when aldosterone levels are —, negligible quantities of K+ are —.
diminished (reabsorption) ; low ; excreted
158
About 92% of the filtered K+ is — from the proximal tubule and the loop of Henle, regardless of prevailing conditions.
reabsorbed
159
The control of K+ — occurs in the late distal tubule and the collecting duct.
excretion
160
What are three factors that alter K+ transport in the late distal tubules and the collecting ducts?
1. Aldosterone
2. Distal tubular flow rate
3. Bicarbonate ion (HCO3-)
161
Aldosterone acts on the distal tubule and collecting duct to — the rate of K+ —.
increase ; secretion
162
— is the important physiological regulator of K+.
Aldosterone
163
K+ — is — when the flow through the distal tubule is increased
excretion ; increased
164
K+ — is — when flow through the distal tubule is decreased.
excretion ; decreased
165
Increased K+ excretion occurs with high ceiling diuretics like — (—) as well as osmotic diuretics like —.
furosemide (lasix) ; mannitol
166
When the HC03- concentration in the distal tubule is — (the urine is —), the K+ secretion rate is increased.
increased ; alkaline
167
One antidote for hyperkalemia is the administration of — (—)
sodium bicarbonate (NaHC03).
168
Sodium bicarbonate (NaHCO3) makes the urine — and induces an increase in K+ —.
Alkaline ; secretion
169
Bicarbonate also alkalinizes the blood, which triggers a H+-K+ exchange that drives K+ — body cells.
into
170
What are the 4 loop diuretics?
1. Furosemide (lasix)
2. Bumetanide (bumex)
3. Ethacrynic acid (edecrin)
4. Torsemide (demadex)
171
Mechanism of action for loop diuretics?
Bind to the Na+-K+-2CI- symporter and inhibit the reabsorption of these ions from the ascending limb of Henle's loop.
172
A protein channel in the ascending limb of Henle's loop simultaneously transports Na+, K+ and CI- in the — direction.
same
173
This channel is referred to as Na+-K+-2CI- symporter, since for each sodium reabsorbed, there is — K+ and — Cl- reabsorbed.
One ; two
174
After a loop diuretic is administered, urine osmolality approaches the osmolality of the "washed out" renal medulla, namely — mOsm.
300
175
With loop diuretics, because the osmotic gradient in the medulla is dissipated when a loop diuretic is administered, the amount of water reabsorbed from the collecting duct is — and water excretion —.
reduced ; increases
176
Furosemide also triggers the release of — from the kidneys; the circulating prostaglandins cause — so blood pressure begins falling (secondary to decreased preload) even before urine output increases.
prostaglandins ; venodilation
177
What are the 4 common side effects with loop diuretics?
1. Hypokalemia
2. Fluid volume deficit
3. Orthostatic hypotension
4. Reversible deafness
178
What three additional side effects are common with the loop diuretic ethacrynic acid?
1. Nausea
2. Vomiting
3. Diarrhea
179
What two diuretic groups act on the distal tubule and collecting duct to inhibit Na+ reabsorption?
Thiazides and potassium-sparing diuretics
180
What are the 4 common thiazide agents?
1. Chlorothiazide (diuril)
2. Hydrochlorothiazide (esidrix, hydrodiuril)
3. Chlorthalidone (hygroton)
4. Metolazone (zaroxolyn)
181
What 3 agents are potassium-sparing diuretics?
1. Spironolactone (aldactone)
2. Triamterene (dyrenium)
3. Amiloride (midamor)
182
Thiazides inhibit sodium reabsorption in early —.
distal tubule
183
Spironolactone (Aldactone) competitively inhibits —, and this action inhibits sodium reabsorption in the late — and — (it also decreases K+ —).
aldosterone ; distal tubule and collecting duct ; secretion
184
Triamterene and amiloride decrease sodium reabsorption from late — and —.
distal tubule and collecting duct
185
What is the side effect with thiazides?
Hypokalemia due to increased K+ secretion
186
What is the side effect with potassium-sparing diuretics?
Hyperkalemia
187
Spironolactone is a competitive — antagonist that works on the late distal tubule and collect duct (mostly the collecting duct).
Aldosterone
188
Spironolactone — sodium excretion and promotes potassium —.
Increases ; retention
189
Which agent is a carbonic anhydrase inhibitor?
Acetazolamide (diamox)
190
What is the mechanism for acetazolamide (diamox)?
Inhibits the enzyme, carbonic anhydrase
191
Inhibition of carbonic anhydrase in the proximal tubule of the kidney inhibits — reabsorption; — reabsorption also diminishes.
bicarbonate ; sodium
192
Inhibition of sodium and bicarbonate reabsorption causes diuresis; — also results.
hyperchloremic metabolic acidosis
193
Inhibition of carbonic anhydrase decreases the rate of formation of aqueous humor; hence, intraocular pressure —; one of the principle therapeutic uses of acetazolamide is to — intraocular pressure.
decreases ; decreases
194
An — is induced when an agent is administered that is freely filtered into Bowman’s capsule and remains trapped in the renal tubule (i.e., the substance very poorly permeates the tubule wall). The impermeable substance exerts an osmotic force and hinders the reabsorption of water.
osmotic diuresis
195
— is a substance that is capable of producing an osmotic diuresis.
Mannitol
196
What is a side effect of osmotic diuresis?
Hypokalemia develops because K+ secretion is increased secondary to increased flow through the
distal tubule and collecting duct. Remember: Anytime flow through the distal tubule increases, K+
secretion and hence K+ excretion increase.
197
Perioperative acute renal failure accounts for — of all patients requiring acute dialysis.
1/2
198
Acute renal failure in the surgical setting is associated with a mortality of —% to —%.
40% to 90%
199
What are the 3 prerenal etiology of perioperative oliguria?
1. Decreased renal blood flow
2. Hypovolemia
3. Decreased cardiac output
200
What are the 4 renal etiology of perioperative oliguria?
1. Renal tubular damage (acute tubular necrosis)
2. Renal ischemia due to prerenal causes
3. Nephrotoxic drugs
4. Release of hemoglobin or myoglobin
201
What are the 3 postrenal etiology of perioperative oliguria?
1. Obstruction of urine flow
2. Bilateral ureteral obstruction
3. Extravasation due to bladder rupture
202
Ischemic acute renal failure is a syndrome triggered by — of the kidneys resulting in the rapid deterioration of renal function and accumulation of — wastes (azotemia).
hypoperfusion ; nitrogenous
203
Renal — plays an important pathophysiologic role in the development of all nonnephrotoxic-mediated acute renal failures.
underperfusion
204
4 overview events underlying pathophysiology of ischemic acute renal failure.
1. Renal underperfusion (decreased GFR; prerenal oliguria)
2. Ischemia of renal medulla
3. Deterioration of tubular cells
4. Tubular obstruction
205
Perioperative ischemia (— failure) can lead to acute renal failure.
Prerenal
206
In acute renal failure, the renal tubule reabsorbs sodium —, so a — amount of sodium appears in the urine; the fractional excretion of filtered sodium (FENa) is —.
poorly ; large ; high
207
In prerenal failure, the filtered sodium is extensively — because flow through the tubule is slow (there is considerable time for sodium reabsorption), so the amount of sodium appearing in the urine is —; the fractional excretion of filtered sodium (FENa) is —.
reabsorbed ; diminished ; low
208
What is FENa mean?
Fractional excretion of filtered sodium
209
Best test for distinguishing prerenal failure from renal failure is?
Fractional excretion of filtered sodium (FENa) is 90% specific and sensitive in distinguishing prerenal oliguria from acute tubular necrosis (ATN).
210
The — are renal function tests used to distinguish prerenal failure from renal failure.
Fractional excretion of filtered sodium
211
Normal GFR?
125
212
Decreased renal reserve GFR?
50-80
213
Renal insufficiency GFR?
12-50
214
Uremia GFR?
<12
215
The best test of renal reserve is — clearance.
Creatinine
216
Creatinine clearance measures —.
GFR
217
Hemoglobin of 5-8 gldl is a well-recognized complication of —.
chronic renal failure
218
Decreased production of renal — is responsible for the anemia.
erythropoietin
219
Treatment for chronic anemia?
Recombinant erythropoietin
220
For chronic anemia, administer recombinant erythropoietin until hematocrit reaches —% to —%.
30% to 33%
221
A side-effect of erythropoietin is the development of — or the exacerbation of co-existing —.
Hypertension ; hypertension
222
— occurs in most patients with end-stage renal disease.
Pruritus
223
Administration of — lowers the plasma concentration of histamine and may decrease the intensity of pruritus.
erythropoietin
224
Bleeding tendency is exhibited by renal failure patients' despite normal —, —, and —.
prothrombin time, plasma thromboplastin time, and platelet count.
225
The screening test best correlated with a bleeding tendency is the — for chronic renal failure.
bleeding time
226
Among the recognized hemostatic abnormalities is the release of defective — factor for chronic renal failure.
von Willebrand's
227
4 manifestations of uremic bleeding with chronic renal failure?
1. GI tract (most frequent)
2. Epistaxis (nose bleed)
3. Hemorrhagic pericarditis
4. Subdural hematoma
228
4 treatment options for coagulopathies with chronic renal failure?
1. Adequate dialysis and elevation of hematocrit (main treatment)
2. Desmopressin or cryoprecipitate (especially if surgery is planed)
3. Estrogen therapy
4. Erythropoietin (shortens bleeding time)
229
What are the 4 common electrolyte disturbances in chronic renal failure?
1. Hyperkalemia
2. Hypocalcemia
3. Hypermagnesemia
4. Hyperphostemia
230
— is the most serious electrolyte abnormality in chronic renal failure
Hyperkalemia
231
5 ECG changes for hyperkalemia?
1. Peaked T waves
2. Prolonged P-R interval
3. Widened QRS complex
4. Heart block
5. PVCs and ventricular fibrillation
232
What fluids should be avoided with hyperkalemia?
LR (it contains 4 mEq/L K+)
233
With hyperkalemia, avoid elective surgery unless K+ is less than —mEq/L.
5.5
234
If surgery cannot be delayed for hyperkalemia, what 3 strategies may be included to help:
1. Hyperventilation, which lowers plasma potassium concentration (0.5 mEq/L for each 10mmHg decrease in PaC02)
2. IV administration of insulin-glucose
3. IV administration of calcium
235
Hypocalcemia 2 causes?
1. Hyperphosphatemia, resulting form decrease in GFR, leads to reciprocal decrease in plasma calcium concentration.
2. Diminished renal production of the active form of vitamin D results in diminished intestinal absorption of calcium, which aggravates the hypocalcemia.
236
Hypocalcemia causes secondary —.
Hyperparathyroidism
237
Hypocalcemia stimulates the release of — (negative feedback).
parathyroid hormone
238
Parathyroid hormone stimulates bone resorption of — (renal osteodystrophy), making patients
vulnerable to pathologic fractures (e.g., during positioning for anesthesia and surgery).
calcium
239
Why is hypermagnesemia common in chronic renal failure?
Due to magnesium retention and possibly also to ingestion of magnesium-containing antacids.
240
3 signs and symptoms for hypermagnesemia?
1. Coma
2. Hypoventilation
3. Hypotension
241
Hypermagnesemia interaction with neuromuscular relaxants:
-Nondepolarizing blockade is — by hypermagnesemia
-Depolarizing blockade (succinylcholine) is — by hypermagnesemia
potentiated ; potentiated
242
80% of patients with end-stage renal disease have —.
Hypertension
243
Hypertension is a significant risk face for what 3 things?
1. Stroke
2. Congestive heart failure
3. Myocardial infarction
244
Chronic renal failure most likely has which acid base problem?
Metabolic acidosis
245
— is the most common cause of death in patients with renal failure.
Sepsis
246
— effects excitability because it is the major determinant of the resting membrane potential.
K+
247
— controls the resting potential
potassium
248
— effects excitability because it is a determinant of the threshold potential.
Ca++
249
— controls threshold.
Calcium
250
A decrease in plasma — concentration (—) leads to an increase in nerve and muscle excitability because the threshold shifts toward the resting potential.
Ca++ ; hypocalcemia
251
With — there is an increased firing of sensory neurons (tingling sensations especially around lips and in hands) and motor neurons (twitches, tetany).
hypocalcemia
252
Control of Cell Excitability by — and —.
K+ and Ca++
253
For this excitable tissue (cardiac ventricular cell), the normal resting potential is —mV and the normal threshold is —mV.
-90 mV ; -60 mV
254
With acute hypokalemia, the resting membrane potential becomes more —.
negative
255
With acute hypokalemia, the cell —; the resting membrane potential moves — from threshold
hyperpolarizes ; away
256
With acute hypokalemia, cells become — excitable because it is more difficult to reach threshold.
less
257
Dysrhythmias are associated with acute hypokalemia, because there is increased automatic firing of — (phase — depolarization is faster).
Purkinje fibers ; 4
258
With acute hyperkalemia, the resting membrane potential becomes — negative
less
259
With acute hyperkalemia, the cell —; the resting membrane potential moves — threshold
hypopolarizes ; toward
260
With acute hyperkalemia, cells become —
excitable because it is easier to reach threshold.
more
261
With cardioplegic solution (K+ = 15-40 mEq/L) the resting membrane — to a level — threshold.
depolarizes ; above
262
With cardioplegic solution, as the resting membrane potential moves past threshold, the sodium gates snap —, and then snap — in the inactivated state.
open ; shut
263
With cardioplegic solution, action potentials cannot now be elicited, so the heart remains electrically — until normal K+ concentration is restored. The heart muscle is essentially in a permanent — state.
arrested ; absolute refractory
264
With acute hypercalcemia, the threshold potential shifts — from the resting potential (the threshold potential becomes — negative).
away ; less
265
With acute hypercalcemia, cells become — excitable because it is more difficult for the resting membrane to depolarize to threshold.
less
266
Giving — quickly protects the heart from acute hyperkalemia.
calcium
267
With acute hypocalcemia, the threshold potential becomes — negative (moves toward the resting potential). Excitability —.
more ; increases
268
Can signs and symptoms of hypocalcemia be elicited when the patient hyperventilates?
Yes. Hyperventilation causes a respiratory alkalosis. Ionized calcium decreases, thus eliciting signs and symptoms of hypocalcemia.
269
What are the 7 therapies and mechanisms for treating hyperkalemia?
1. Administer HCO3-
2. Hyperventilate
3. Give insulin-glucose
4. Give Ca++
5. Administer beta2 agonist (to stimulate Na-K pump)
6. Dialyze patient
7. Give Kayexalate
270
When HC03 - is administered, H+ concentration
in plasma — (—). H+ shifts out of cells to buffer the alkalosis, and, in exchange, K+ shifts into cells.
decreases (metabolic alkalosis)
271
With hyperventilation, H+ concentration in plasma — (—). H+ shifts out of cells to buffer the alkalosis, and, in exchange, K+ shifts into cells.
decreases (respiratory alkalosis)
272
With hyperventilation to treat hyperkalemia: for each 10 mmHg decrease in PaC02, serum [K+] decreases — mEq/L.
0.5
273
Insulin, by stimulating the sodium-potassium pump,
drives K+ — cells. Insulin also opens glucose channels. Glucose is administered along with the insulin to prevent hypoglycemia.
into
274
A resting membrane potential exists across the plasma membrane of excitable tissues (nerve, skeletal muscle, and cardiac muscle).
a. The inside of the cell is — charged with respect to the outside.
b. The resting potential of nerve varies, but usually is taken to be about — mV.
negatively ; -70
275
The resting membrane potential is established because
a. K+ is highly concentrated — the cell, and the diffusion of K+ — is relatively high.
b. K+ diffuses — of the cell down its electrochemical gradient through open channels; negatively charged substances, namely proteins, are trapped behind.
within ; out ; out
276
The resting potential is altered by shifts in — concentration.
extracellular K+
277
a. With hyperkalemia, — of the cell membrane occurs, i.e., the membrane potential shifts toward — mV (the membrane becomes less charged = hypopolacized (less polarized) = depolarized).
depolarization ; 0
278
b. With hypokalemia, — of the cell membrane occurs, ie., the membrane potential shifts farther — from 0 mV (the membrane becomes more charged).
hyperpolarization ; away
279
When the resting membrane depolarizes (e.g., with —), the resting potential shifts closer to threshold, and there is an increased likelihood of spontaneous action potentials. EXCITABILITY (IRRITABILITY) —. In the heart, there are — and, with severe hyperkalemia, —.
hyperkalemia ; INCREASES ; PVCs ; ventricular fibrillation
280
Cardioplegic solution used during CABG surgery has a high concentration of —, and the cardiac cells depolarize to a level between threshold and 0 mV. As the cardiac cells depolarize to and beyond threshold, an action potential is elicited and a corresponding contraction occurs. Thereafter, however, there is no electrical activity. The sodium gates are shut in the — state until normal — is restored.
K+ ; inactivated ; K+
281
When the resting membrane —, the membrane potential moves farther away from threshold. It becomes more difficult to — the cell to threshold and elicit an action potential. EXCITABILITY (IRRITABILITY) IS —.
hyperpolarizes ; depolarize ; DECREASED
282
— leads to a decrease in excitability of cardiac ventricular cells as well as of nerve, skeletal muscle, and smooth muscle cells. In the heart, the SA and AV nodes may become completely depressed. There are, however, ventricular Purkinje cells that more readily depolarize to threshold and PVCs occur.
Hypokalemia
283
The threshold potential is controlled by —.
calcium
284
Hypocalcemia alters the threshold: threshold potential moves toward the — potential, thereby increasing the likelihood that unwanted (spontaneous) action potentials will develop in nerve and muscle. Threshold potential — (value is farther from zero than normal).
resting ; increases
285
The symptoms of — are related to an increased firing of motor neurons (possibly leading to tetany) and an increased firing of sensory neurons (tingling of fingers and lips).
hypocalcemia
286
With —, threshold moves away from the resting potential, which decreases excitability. This explains why calcium protects the heart of the patient who is hyperkalemic.
hypercalcemia
287
Both — and — bind to plasma proteins (Prot)
H+ and Ca++
288
With —, the H+ concentration decreases; proteins release H+ (law of mass action), thus freeing up Prot- which can bind ionized calcium (Ca++) and correspondingly lower plasma concentration of ionized calcium (Ca ++).
hyperventilation
289
With acute respiratory alkalosis (hyperventilation), free ionized calcium concentration — in plasma signs and symptoms of — may be manifested.
Decreases ; hypocalcemia
290
Signs and symptoms of what two electrolyte abnormalities may be manifested in the hyperventilating patient?
hypokalemia and hypocalcemia; Remember, however, that with hyperventilation there may develop a true hypokalemia but a true hypocalcemia does not develop (total calcium, ionized plus nonionized, does not change). Signs and symptoms of hypocalcemia may develop during hyperventilation because of the decrease in free ionized calcium.
291
From value of —, determine whether patient is acidotic or alkalotic.
pH
292
From values for — and —, determine if primary disturbance is respiratory or metabolic in origin.
PaC02 and HC03-
293
The primary disturbance is respiratory if the change in — is compatible with the change in pH.
PaC02
294
The primary disturbance is metabolic if the change in — is compatible with the change in pH.
[HC03-]
295
Normal pH is —, normal HC03- is —mEq/l; normal PaC02 is —mmHg.
7.35-7.45 ; 22-27 ; 35-45
296
Respiratory acidosis and respiratory alkalosis — be completely compensated.
can
297
Complete compensation — be achieved if there is metabolic acidosis or metabolic alkalosis.
cannot
298
If an acid-base disturbance is completely compensated, it is a — disturbance.
Respiratory
299
— an increase in blood H+ concentration (a decrease in blood pH) caused by hypoventilation and CO2 retention.
Respiratory acidosis
300
— a decrease in blood H+ concentration (an increase in blood pH) caused by hyperventilation and a loss of CO2.
Respiratory alkalosis
301
— a decrease in blood H+ concentration (an increase in blood pH) caused by the loss of acids from, or the addition of bases to, body fluids. A metabolic alkalosis has a non-respiratory origin.
Metabolic alkalosis
302
— an increase in blood H+ concentration (a decrease in blood pH) caused by the addition of acids to, or the loss of bases from, body fluids. A metabolic acidosis has a non-respiratory origin.
Metabolic acidosis
303
The strategy for identifying a single acid-base disorder employs three steps:
1. First, look at the pH.
2. Second, determine if the pH change is caused by a change in PaC02 or by a change in [HC03 -].
3. Third, determine if there is a compensation for the acid-base disorder. For a respiratory acidosis,
renal compensation will be indicated by an increased [HC03-]. For a respiratory alkalosis, renal compensation will be indicated by a decreased [HC03-]. For a metabolic acidosis, respiratory compensation will be indicated by a decreased PaC02. For a metabolic alkalosis, respiratory compensation will be indicated by an increased PaC02. Compensation may be partial or complete. Compensation is complete if pH is returned to the normal range. Only respiratory acidosis and respiratory alkalosis can be completely compensated.
304
State whether there is no compensation, partial compensation, or complete compensation.
pH = 7.48, [HC03-] = 38 mM; PaC02 = 53 mmHg.
partial compensation of metabolic alkalosis
305
State whether there is no compensation, partial compensation, or complete compensation.
pH = 7.37, [HC03-] = 36 mM, PaC02 = 65 mmHg.
complete compensation of respiratory acidosis (only respiratory disturbances can be completely compensated, so this cannot be a completely compensated metabolic alkalosis)
306
State whether there is no compensation, partial compensation, or complete compensation.
pH = 7.32, [HC03-] = 32 mM; PaC02 = 65 mmHg.
partial compensation of respiratory acidosis.
307
pH=7.56, PaCO2=28mmHg, [HCO3-]=24mM
Uncompensated respiratory alkalosis
308
pH=7.30, PaCO2=25mmHg, [HCO3-]=12mM
Partially compensated metabolic acidosis
309
pH=7.58, PaCO2=20mmHg, [HCO3-]=18mM
Partially compensated respiratory alkalosis
310
pH=7.43, PaCO2=22mmHg, [HCO3-]=14mM
Completely compensated (chronic) respiratory alkalosis
311
pH=7.34, PaCO2=50mmHg, [HCO3-]=26mM
Uncompensated respiratory acidosis
312
pH=7.29, PaCO2=65mmHg, [HCO3-]=30mM
Partially compensated respiratory acidosis
313
pH=7.36, PaCO2=55mmHg, [HCO3-]=30mM
Completely compensated (chronic) respiratory acidosis
314
pH=7.56, PaCO2=38mmHg, [HCO3-]=33mM
Uncompensated metabolic alkalosis
315
pH=7.69, PaCO2=50mmHg, [HCO3-]=35mM
Partially compensated metabolic alkalosis
316
pH=7.24, PaCO2=43mmHg, [HCO3-]=18mM
Uncompensated metabolic acidosis
317
— exchange is the fundamental event in the kidney's regulation of acid-base balance.
Na+—H+
318
Specifically, Na+ -H+ exchange permits bicarbonate ions to be — and acids to be —.
reabsorbed ; excreted
319
Acetazolamide (Diamox) is a carbonic anhydrase —.
inhibitor
320
Acetazolamide (Diamox) acts on the kidney to inhibit reabsorption of — and — ions, and thus is a diuretic.
sodium and bicarbonate
321
Most of the filtered HC03 - (90%) is reabsorbed from the — tubule.
proximal
322
The small quantity of HC03- (10%) which escapes reabsorption in the proximal tubule is normally reabsorbed from later segments of the — tubule.
renal
323
HC03- is normally not —.
excreted
324
— is actively secreted into the lumen of the proximal tubule in exchange for Na+, which enters the cell passively.
H+
325
Carbonic anhydrase, an enzyme of the brush border, catalyzes the formation of — and — in the tubular lumen.
CO2 and H20
326
The CO2 that is produced in this reaction diffuses into the tubular cell where it is utilized to re-synthesize —.
HC03-
327
The HC03- that is generated diffuses into the peritubular capillaries from the tubular cells. — is
regenerated and becomes available for use in another HC03- reabsorption cycle.
H+
328
This elaborate mechanism for HC03- reabsorption is required because HC03- very slowly diffuses across the luminal membrane of the renal tubule. "Ions — cross membranes:' The low HC03- luminal membrane permeability to HC03- permits only a small percentage of the filtered load to be reabsorbed directly.
don't
329
The kidneys produce bicarbonate by excreting —.
acids
330
The — exchange mechanism is the key step in excretion of hydrogen ions.
H+-Na+
331
— and — are the acids excreted by the kidneys
Titratable acids and ammonia (NH3)
332
When NH3 enters the tubular lumen, it reacts with H+ to form ammonium ion (NH4+). NH4+ very poorly penetrates cell membranes. Hence, NH4+ remains trapped in the tubular lumen and is excreted.
This process is called —.
diffusion trapping
333
Ammonia production is stimulated by —.
acidosis
334
The anion gap is determined from measurements of plasma —, — and —.
[Na+], [CI-] and [HC03-].
335
Anion gap = [—] - [—] + [—]
Na+ ; CI- ; HC03-
336
The total concentration of the unmeasured anions is equivalent to — mM, the normal anion gap.
12 mM
337
When non-chloride acids (H+ Anion-) are added to the body fluids, there will be an — in the anion gap because the HC03- that reacts with the H+ is replaced by the unmeasured anion of the acid.
increase
338
When HC03- is lost from the body fluids, CI- replaces the lost HC03-. The anion gap does not — because the [CI-] increases (hyperchloremia).
decrease
339
Determination of the unmeasured anions (anion gap) is useful for the differential diagnosis of —.
metabolic acidosis
340
What region of the kidney is most vulnerable to ischemia?
a. Cortex
b. Outer stripe of outer medulla
c. Inner stripe of outer medulla
d. Inner medulla
c. Inner stripe of outer medulla
341
Normally, all of the glucose filtered into the renal tubule is reabsorbed from the
a. proximal tubule.
b. loop of Henle.
c. distal tubule.
d. collecting duct
a. proximal tubule.
342
Where is antidiuretic hormone synthesized and what stimulates its release?
a. Neurohypophysis ; Increased osmolality
b. Neurohypophysis ; Decreased osmolality
c. Hypothalamus ; Increased osmolality
d. Hypothalamus ; Decreased osmolality
c. Hypothalamus ; Increased osmolality
343
What is urine volume and osmolality when antidiuretic hormone release is inhibited?
Osmolality ; Volume
a. Low ; Small
b. Low ; Large
c. High ; Small
d. High ; Large
b. Low ; Large
344
How does aldosterone affect sodium and potassium excretion?
Sodium Excretion ; Potassium Excretion
a. Increased ; Increased
b. Increased ; Decreased
c. Decreased ; Decreased
d. Decreased ; Increased
d. Decreased ; Increased
345
What hormone controls extracellular fluid volume, and what hormone controls extracellular sodium
concentration?
Sodium Volume ; Concentration
a. Aldosterone ; Aldosterone
b. Aldosterone ; Antidiuretic hormone
c. Antidiuretic hormone ; Antidiuretic hormone
d. Antidiuretic hormone ; Aldosterone
b. Aldosterone ; Antidiuretic hormone
346
What diuretic works by inhibiting the Na+-K+-Cl- symporter?
a. Chlorothiazide
b. Spironolactone
c. Furosemide
d. Mannitol
c. Furosemide
347
Spironolactone acts primarily on what segment of the renal tubule?
a. Proximal tubule
b. Ascending limb of Henle's loop
c. Distal tubule
d. Collecting duct
d. Collecting duct
348
What test helps distinguish prerenal from renal failure?
a. Fractional excretion of filtered sodium
b. Creatinine clearance
c. Blood urea nitrogen
d. Plasma creatinine concentration
a. Fractional excretion of filtered sodium
349
The chronic renal failure patient has a tendency for increased bleeding, in part because of the production of defective
a. antithrombin III.
b. thrombin.
c. fibrinogen.
d. von Willebrand's factor.
d. von Willebrand's factor.
350
What electrolyte disturbance is NOT seen in the chronic renal failure patient?
a. Hyperkalemia
b. Hypercalcemia
c. Hypermagnesemia
d. Hyperphosphatemia
b. Hypercalcemia
351
What is the most common cause of death in the patient with chronic renal failure?
a. Sepsis
b. Myocardial infarction
c. Stroke
d. Respiratory arrest
a. Sepsis
352
Which combination of acute electrolyte abnormalities will most stabilize nerve, skeletal muscle, and cardiac ventricular muscle cells?
a. Hypokalemia and hypocalcemia
b. Hypokalemia and hypercalcemia
c. Hyperkalemia and hypocalcemia
d. Hyperkalemia and hypercalcemia
b. Hypokalemia and hypercalcemia
353
A clinically appropriate K+ concentration for cardioplegia solution is
a. 5 mEq/liter
b. 10 mEq/liter
c. 30 mEq/liter
d. 50 mEq/liter
c. 30 mEq/liter
354
Each of the following interventions drives K+ into cells EXCEPT:
a. Administering sodium bicarbonate
b. Administering calcium gluconate
c. Hyperventilating the lungs
d. Administering insulin-glucose
b. Administering calcium gluconate
355
Hyperventilation can produce signs and symptoms of which of the following electrolyte disturbances?
a. Hyperkalemia
b. Hypermagnesemia
c. Hyponatremia
d. Hypocalcemia
d. Hypocalcemia
356
The patient with a pH of 7.30, PaC02 of 25 mmHg, and HC03- of 12 has what single acid-base disturbance?
a. Completely compensated metabolic acidosis.
b. Partially compensated metabolic acidosis.
c. Uncompensated metabolic acidosis.
d. Overcompensated respiratory alkalosis.
b. Partially compensated metabolic acidosis.
357
The kidney's role in maintaining acid-base balance includes:
a. reabsorption of bicarbonate ions and reabsorption of hydrogen ions.
b. excretion of bicarbonate ions and reabsorption of hydrogen ions.
c. reabsorption of bicarbonate ions and excretion of hydrogen ions.
d. excretion of bicarbonate ions and excretion of hydrogen ions.
c. reabsorption of bicarbonate ions and excretion of hydrogen ions.
358
The threshold of cell membrane excitability is most directly controlled by
a. potassium
b. chloride
c. calcium
d. sodium
c. calcium
359
Approximately two-thirds of electrolyte reabsoption occurs in this renal tubuluar segment.
a. Bowman's capsule
b. proximal tubule
c. loop of Henle
d. distal tubule
b. proximal tubule
