Section5. Renal physiology Flashcards

1
Q

the active process by which substances are transported out of blood from peritubular capillaries into the tubular filtrate is termed:

A

secretion

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2
Q

define filtration

A

process by which fluid is forced through a membrane or other barrier d/t hydrostatic and/or osmotic pressure differences

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3
Q

Which portion of the functional nephron normally reabsorbed the most solute and water?

A

proximal convoluted tubule

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4
Q

What percentage of plasma is filtered by glomeruli as it passes through the kidney?

A

20%

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5
Q

The composition of the normal glomerular filtrate is most similar to:

A

interstitial fluid

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6
Q

What percentage of Na, Cl and H20 filtered by the primate kidney is normally reabsorbed back into blood?

A

99%

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7
Q

The renal function with which the oxygen consumption of the kidney correlates with

A

the rate of active Na transport

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8
Q

Which forces normally oppose ultrafiltration at the glomerulus?

A

plasma colloid osmotic pressure

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9
Q

What factor can best explain an increase in the glomerular filtration rate?

A

increases glomerular capillary hydrostatic pressure

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10
Q

What substance normally has low renal clearance?

A

Glucose– freely filtered by glomeruli, but not secreted by renal tubules, however it is extensively reabsorbed in proximal tubules

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11
Q

Major resistance to blood flow in the kidney occurs in the:

A

afferent and efferent arterioles

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12
Q

Renal blood flow normally accounts for what percentage of the cardiac output?

A

23%

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13
Q

Which organs receive 65% of the cardiac output?

A

liver, brain and kidneys

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14
Q

What is the intrinsic mechanism for keeping renal blood flow (RBF) and glomerular filtration rate (GFR) relatively constant in the face of varying systemic arterial pressures is termed:

A

Autoregulation

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15
Q

Which extrinsic regulator of renal blood flow causes vasoconstriction of both afferent and efferent arterioles?

A

prostaglandins (E2 and I2)

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16
Q

Besides prostaglandins, what is the another stimulus for to renal vasoconstriction

A

hyoxia
(arterial oxygen content false to less than 50% of nromal)

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17
Q

What is the effect of catecholamines on renal blood flow?

A

constrict renal vessels, with greatest effect of norepinephrine being exerted on interlobular arteries and afferent arterioles

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18
Q

What is the effect of angiotensin II on renal blood blow?

A

exerts a selective vasoconstrictor effect on efferent arterioles

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19
Q

What is the effect of dopamine on renal blood flow?

A

concentration-dependent relaxation of both afferent and efferent arterioles, the receptors mediating this vascular relaxation at the D2 subtype

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20
Q

What is the effect of atrial natriutretic peptide effect on renal blood flow?

A

vasodilates afferent and constricts efferent arterioles

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21
Q

Reabsorption of which molecules are extensive, normally yield a tubular filtrate to plasma concentration ratio (TF/P)?

A

glucose
amino acid
bicarbonate

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22
Q

although peptides and proteins are filtered to a minor extent at the kidney, these molecules are almost completely reabsorbed by:

A

pinocytosis at the proximal renal tubular cells

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23
Q

The entry of Na into proximal renal tubular cells is passive and inolves diffusion down a concentration gradient, while the movement of what ion is in the reverse direction (active and demands a secretory pump?

A

H

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24
Q

List some compounds that are actively reabsorbed by the proximal tubules of the kidney?

A

uric acid
ketone bodies
ascorbic acid
lactate

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25
Q

Does metabolic alkalosis or acidosis enhance urinary excretion of calcium?

A

metabolic acidosis

–>tends to INC Ca filtered load

metabolic alkalosis would cause the opposite effect

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26
Q

Ca reabsorption at the kidney are stimulates by:

A

both parathyroid hormone (PTH) and active form of vitamin D (1,25 DHC)

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27
Q

Phosphate reabsorption in proximal tubules of the kidney is coupled to:

A

the reabsorption of Na

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28
Q

Magnesium reabsorption in the kidney is increased in the present of

A

PTH

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29
Q

What is the difference between the ascending limb, distal tubule and descending limb of LOH?

A

the thin, descending loop of henle is freely permeable to water

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30
Q

The thick, ascending limb of the LOH actively transports

A

Na, K and Cl from the tubular lumen into renal tubular cells

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31
Q

The thin, ascending limb of the LOH, is usually permeable to:

A

both urea and NaCl, but impermeable to water

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32
Q

The thick, ascending limb of the LOH, has a high content of what enzyme than any other part of the renal tubule?

A

Na-K ATPase

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33
Q

Loop diuretics, tend to inhibit Ca and Mg reabsorption at what part of the renal tubule?

A

Ca and Mg reabsorption in the thick ascending limb of the LOH
**promoting their wasting into urine

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34
Q

Which portions of the functional nephron are in general most permeable to water?

A

proximal tubule and thin, descending limb of the LOH

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35
Q

Aldosterone regulates Na reabsorption at which location of the renal tubule?

A

variable in the distal tubule joins the collecting duct

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36
Q

What is the primary effect of aldosterone on active electrolyte transport in the distal convoluted tubules is to:

A

increase active transport of Na from the tubular lumen into the interstitium, then to the bloodstream

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37
Q

Urinary K concentrations largely reflect the quantity of K that is secreted during the passage of tubular fluid through the

A

distal tubule and cortical collecting duct

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38
Q

Aldosterone excess would be expected to lead to the development of:

A

mild systemic metabolic alkalosis, which can be aggravated by the depletion of K

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39
Q

What factors may cause increase K secretion in the distal nephron?

A

a high dietary intake of K
A high dietary intake of Na
Thiazide diuretics
systemic metabolic alkalosis

***hypokalemia

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40
Q

What is the cellular mechanism of action of aldosterone?

A

it binds to amineralocorticoid receptor inside target cells, and like other steroids, the steroid-receptor compelx acts in teh nucleus to increase transcription of DNA, and the induced mRNA stimulates protein synthesis at the ribosomal level

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41
Q

production of concentrated urine is largely due to the presence of which hormone?

A

antidiuretic hormone

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42
Q

how does antidiuretic hormone cause water conservation?

A

-secreted from posterior pituitary
-increases permeability of the collecting ducts to water by causing rapid insertion of water channels into the luminal membrane of responsive cells

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43
Q

What are the 3 distinct cell types in teh cortical collecting ducts?

A
  1. aldosterone sensitive primary cells that reabsorb Na and secrete K (primarily Na-K Atpase)
  2. alpha-intercalated cells that actively pump H into the tubular lumen and reabsorb both K and HCO3
  3. beta-intercalated cells that secrete HCO3 in exchange for Cl and reabsorb H via H-ATPase located in the basolateral membrane
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44
Q

Sodium is actively transported out of all portions of the renal tubules, except

A

the thin portions of the loop of Henle

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45
Q

What are molecules that inhibit the action of aldosterone at the collecting ducts?

A

atrial natriuretic peptide (ANP)
prostaglandins
diuretics (amiloride)

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46
Q

Sodium reabsorptin the in collecting ducts is

A

load dependent, increased amount of Na is reabsorbed if an increased load of Na is delivered to this region

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47
Q

When vasopressin is absent, the collecting duct epithelium is:

A

relatively impermeable to water

48
Q

Patients with diabetes insipidus have

A

-low production of ADH from hypothalamic nuclei
-low secretion of ADH from the posterior pituitary
-insufficient renal response to normal endogenous levels of ADH

49
Q

Antidiuretic hormone secretion is regulated by:

A

the osmolarity of plasma

also changes in blood volume/pressure

50
Q

Where is ADH synthesized and stored?

A

synthesized: nuclei of the hypothalamus (supraoptic and paraventricular nuclei)

-stored and released from axon terminals located in the neurohypophysis (posterior pituitary)

51
Q

What is the ADH receptor in collecting ducts of th ekidney

A

V2, it is a G protein-coupled and works through CAMP

52
Q

Urea undergoes reabsorption from where?

A

50% net reabsorption
from proximal renal tubules into blood

53
Q

What is the effect of ADH on urea reabsorption?

A

INC ADH= INC urea absorbed into medullary interstitial fluid from the collecting ducts

54
Q

The excretion of urea by the kidney is dependent upon what two primary factors?

A
  1. the plasma urea concentration
  2. glomerular filtration rate
55
Q

Urea is important osmolite for what purpose?

A

it accounts for approximately 25% of the osmolites needed to establish the medullary interstitial fluid concentration gradient

56
Q

Uric acid is formed from

A

purine oxidation– that occurs in the liver and gut from dietary and endogenous sources

57
Q

Which nitrogenous compound is secreted by nonionic diffusion?

A

Ammonia–> NH3 is secreted into the proximal tubular filtrate and then changed to NH4 (tends to stay in the tubular filtrate), thus maintaining a concentration gradient for further NH3 secretion

58
Q

Why are plasma proteins not normally filtered by the kidney?

A

because the negative charge of the glycoproteins on the surface of the filtration barrier of the glomerulus prevents them from being filtered

59
Q

Glutamine is taken up form both filtrate and peritubular capillaries by proximal renal tubular epithelial cells, where it is broken down into:

A
  1. two nitrogen groups enzymatically removaed as ammonium ions: one NH4 comes from the amino group of Gln (deamination, the other from its amide side group (deamidation)
  2. alphaketoglutarate– can be metabolized in proximal renal tubualr cells either to glucose or to CO2 and Water
60
Q

What are characteristics of medullary blood flow through the vasa recta of the kidney?

A

-blood flow is normally slow, approximately 50 to 60 seconds for a single red cell to travel through
-represents 1 to 2% of the total renal blood flow
– slow and sluggish blood flow– removal of medullary solutes is minimized thus helping to maintain and not wash out the medullary concentration gradient

61
Q

Blood vessels of the vasa recta have what absorptive capabilities?

A

they are freely permeable to electrolytes and water– transport fluid/solutes entirely by passive diffusion (no active transport mechanisms)

62
Q

Increased blood flow through the vasa recta can be stimulated by:

A

certain prostaglandins

63
Q

What are the functions of the vasa recta in the kidney?

A

-helps to maintain medullary interstitial fluid osmotic gradient
- helps bring needed nutrients and oxygen to thei thick ascending limb of the LOH

64
Q

Ingesting ammonium chloride (NH4Cl) is equivalent to adding what to circulation?

A

HCl

65
Q

Loop diuretics reduce NaCl couple reabsorption in the

A

ascending thick limb of the loop of henle

66
Q

Loop diuretics would be expected over time to increase urinary excretion of:

A

Ca and Mg
Na
K
H

67
Q

Thiazide diuretics inhibit the excretion of:

A

Na reabsorption in the proximal portion of the distal tubule

68
Q

How do potassium paring natriuretics function?

A

act by inhibiting Na-K exchange in the distal portion of the distal tubule and early collecting duct, by inhibiting the action of aldosterone

69
Q

ADH antagonists would be expected to increase urinary excretion of:

A

urea

70
Q

Carbonic anhydrase inhibitors are moderately effective as diuretic agents because they

A

reduce renal Na reabsorption– inhibit acid secretion by decreasing the supply of carbonic acid,; Na excretion is increased because H secretion is decreased

71
Q

The anion gap may not change in what conditions?

A

hyperchloremic acidosis d/t ingestion of ammonium chloride
OR
hypochloremic alkalosis

**b/c plasma bicarb changes equally with Cl

72
Q

The anion gap is a weak tool for determining the total number of unidentified anions present in a patient with:

A

hypoproteinemia b/c protein ions are taken taken into account when making the calculation

73
Q

What is the urinary anion gap calculation?

A

Na + K - CL

74
Q

Which one of the following conditions is best associated with the development of metabolic acidosis?
a. renal insufficiency
b. vomiting (gastric contents only)
c. hperadrenal corticoidism
d. administration of K wasting diuretics
e. respiratory insufficiency

A

a. renal insufficiency– there is failure to secret protons into the renal filtrate & metabolic acidosis ensues

75
Q

Administration of K wasting diuretics, like loop and thiazide diuretics, would cause a metabolic acidosis/alkalosis?

A

metabolic alkalosis: b/c excessive K and H secretion

76
Q

In metabolic acidosis, approximately how much (%) of the additional H generated is buffered cellularly, and how much is buffered extracellularly?

A

57% and 43%

77
Q

What are associated with untreated, diabetic ketoacidemia?

A

hypochloremia
hypotension
osmotic diuresis
tissue dehdyration

78
Q

Administration of carbonic anhydrase inhibitors would lead to what acid/base abnormality?

A

metabolic acidosis–proximal renal H secretion and HCO reabsorption would be suppressed

79
Q

Explain why distal renal tubular K secretion increases in metabolic alkalosis?

A

because excess HC03 functions as an impermeant anion, thereby stimulating K secretion by increasing the transepithelial potential different and the elevated pH enhances permeability of luminal membranes in the distal tubules to K

80
Q

Regarding renal compensation in respiratory acidosis, what occurs with chloride?

A

Renal CL excretion is increased in respiratory acidosis as plasma bicarb is increased

81
Q

What is the difference between metabolic and respiratory disturbances in the CSF and blood?

A

metabolic acid/base disturbances evoke opposite changes in the pH of CSF and blood, while respiratory disturbances bring about parallel changes

82
Q

In acid/base disturbances, the K and H ECF concentrations tend to

A

parallel each other

83
Q

What are two pathways along the acinus in the liver for ammonium ion (NH4) removal?

A

hepatic urea and glutamine synthesis

84
Q

What does the strong ion difference method quantify?

A

-the effect of concentration alkalosis or dilution acidosis
-reveal Cl abnormalities that otherwise would be obscured by free water abnormalities
-the effects of protein abnormalities
-the total concentration fo unidentified anions

85
Q

Rapidly-acting neural control mechanisms that help return blood volume and arterial pressure to levels compatible with normal circulatory hemodynamics following hemorrhage are:

A

baroreceptor feedback mechanism
CNS ischemic response
chemoreceptor

86
Q

What are examples of intermediate and long-term renal control mechanisms for return of blood volume and arterial pressure following hemorrhage?

A

intermediate: vascular control and renin-angiotensin vasoconstrictor mechanisms

long term: aldosterone (renin-angiotensin-aldosterone system) and vasopressin (ADH) systems

87
Q

Where are mechanoreceptors (stretch receptors or baroreceptors) located within the body?

A

-walls of heart (atria- superior/inferior vena cava)
-carotid sinus and aortic arch
-afferent arterioles of the kidneys

88
Q

Which baroreceptors are classified as low pressure receptors, that respond primarily to distension or fullness of the vascular tree?

A

atrial and pulmonary vascular baroreceptors

89
Q

The cardiovascular control center located in the brain stem (medulla) and is inhibited by baroreceptors via:

A

IX: glossopharyngeal: innervates the carotid sinuses
X: vagus: innervates the aortic arch and low pressure volume receptors in the atria and pulmonary circulation

90
Q

The highest blood perfusion rate (ml/ mg tissue/min) of any cell mass in teh body is found in the:

A

carotid and aortic chemoreceptors

91
Q

Although carotid chemoreceptor stimulation affects heart rate minimally, the cardiac response to peripheral chemoreceptor stimulation is nonetheless the resultant of primary and secondary reflex mechanisms, what are true of these?

A

The primary reflex effect on the SA node is inhibitory

92
Q

The reverse stretch relaxation mechanism refers to:

A

The ability of blood vessels in storage areas of the body to tighten around the amount of blood that is left following hemorrhage, thus attempting to re-establish circulatory tension

93
Q

What is the stress relaxation mechanism?

A

The ability of vascular smooth muscle to accommodate stretch in this areas during period when blood volume and pressure are elevated

94
Q

What is the mechanism for capillary fluid shift following acute blood loss is a direct application of:

A

the principle of Starlings Forces in systemic capillary beds

95
Q

The capillary fluid shift that occurs following acute blood loss is though to return arterial pressure to what percent back toward its normal value?

A

75%
**usually takes longer than the nervous reflex mechanisms to take effect

96
Q

An increase in which of the following would release renin into circulation?

A

sympathetic nervous system activity

97
Q

The release of what hormones will decrease renin release?

A

angiotensin II, vasopressin and atrial natriuretic peptide

98
Q

When blood flow through the kidneys is decreases, which cells sense this?

A

juxtaglomerular cells
– located in the walls of the afferent arterioles immediately proximal to glomeruli to then secrete renin into blood

99
Q

What are factors that increase renin release?

A

sympathetic nervous system activity
circulating catecholamines
decreased stretch of JG cells
local prostaglandins

100
Q

What is the major effect of angiotensin II?

A

Potent vasoconstrictors– affecting both arterioles and to a lesser extent, veins

101
Q

Renin is an enzyme that results in the stimulation/formation of angiotensin 1, that then is split to form

A

angiotensin II, which occurs in small vessels of the lungs catalyzed by the enzyme angiotensin converting enzyme

102
Q

aldosterone is produced by what cells?

A

zona glomerulosa or subcapular layer of the adrenal cortex
**salt retaining steroid

103
Q

Aldosterone release is inhibited by which hormone?

A

atrial natriuretic peptide

104
Q

What are factors that stimulate aldosterone release?

A

angiotensin II & III
decreased plasma Na
Increased K concentration

105
Q

What is the effect of atrial natriuretic peptide on aldosterone release?

A

ANP inhibits aldosterone release

106
Q

What are the system effects of angiotensin II?

A

-promotes norepinephrine release from sympathetic nerve endings & epi/NE from the adrenal medulla
-vasoconstricts peripheral arterioles, efferent arterioles of kidney and veins
-aldosterone release from adrenal cortex and ADH release from the neurohypophysis
-direct positive effects on proximal tubular NaCl reabsorption
-stimulates thirst

107
Q

Why is it better to have sensors for the Na and Cl concentration located in cells of the macula densa rather than in juxtaglomerular cells of the afferent arteriole?

A

because a reduction in blood volume would not necessarily change the concentration of Na and Cl in plasma, but would change their renal filtrate concentrations at the macula densa

108
Q

Synthesis and release of renin substrate (angiotensinogen) from the liver is stimulated by:

A

estrogen
cortisol

109
Q

A catecholamine secreting tumor of the adrenal medulla (a pheochromocytoma), would be associated with what systemic changes?

A

-high renin hypertension and an increase in the basal metabolic rate
-increases in red blood cell mass
-increases in urinary metanephrine and vanillymandelic acid excretion
-glucosuria and ketonuria

110
Q

Which one of the following would be most beneficial in the treatment of low-renin hypertension?
a. cyclooxygenase inhibitors (eg aspirin)
b. Beta-blockers (eg, pronanolol)
c. Angiotensin converting enzyme inhibitors (eg captopril)
d. Aldosterone antagonists (eg, spirolactone)
e. competitive inhibitors of the angiotensins (eg, saralasin)

A

D. aldosterone antagonists

111
Q

Congestive hart failure, a defect in the pumping action of the heart is associated with:

A

hypotension
abnormal salt and water retention by the kidneys
accumulation of fluid in interstitial fluid spaces of the body (edema)

112
Q

The renin-angiotensin system is activated in congestive heart failure in an attempt to:

A

restore blood volume, thus increasing the aldosterone concentration, which promotes renal salt and water retention

113
Q

The net loss of hypotonic fluid from the body (ie: excessive loss of hypotonic urine) results in:

A

hydropenia/ hypertonic dehydration

114
Q

Isotonic dehydration (eg hemorrhage) causes:

A

increases sympathetic nervous system activity, arteriolar vasoconstriction, reduced capillary hydrostatic pressure and an enhanced reabsorption pressure

115
Q

What is key in the development of of hypotonic dehydration?

A

a net negative balance of Na salts

116
Q

Overhydration may result in

A

hemolysis, with consequent in appearance of hemoglobin in urine