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Form and Function > Renal > Flashcards

Renal Flashcards

1
Q

What is the name for the anatomical structure in the kidney where the blood vessels/ureter exit?

A

Hilus

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2
Q

List the 5 main anatomical structures of the kidney from the outside in.

A

Renal cortex
Renal medulla
Renal pyramid
Renal calyx
Renal pelvis

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3
Q

In which anatomical structures are the nephrons primarily found?

A

Renal pyramid

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4
Q

List the components of the renal tubule starting from the glomerulus

A

Bowman’s capsule
Proximal tubule
Loop of Henle (descending then ascending limbs)
Distal tubule
Connecting tubule
Collecting duct

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5
Q

Approximately what % of left cardiac output goes to the renal artery?

A

22

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6
Q

What are the two capillary networks associated with a single nephron?

A

Glomerulus and peritubular capillaries

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7
Q

What is the primary role of the glomerulus?

A

Filtration

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8
Q

What is the primary role of the peritubular capillaries?

A

Reabsorption

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9
Q

Name the two different types of nephrons.

A

Cortical nephron
Juxtamedullary nephron

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10
Q

Which nephron type is the most common?

A

Cortical nephrons

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11
Q

What are the distinguishing characteristics of a cortical nephron?

A

Relatively short loop of Henle which does not descend far into the medulla, and an extensive network of peritubular capillaries

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12
Q

What are the distinguishing characteristics of a juxtaglomerular nephron?

A

Long loops of Henle which descend deep into the medulla, and peritubular capillaries which run parallel to the loop of Henle

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13
Q

What is the vasa recta and with what structure in the kidney is it associated?

A

Peritubular capillary network running parallel to the loop of Henle in juxtaglomerular nephrons

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14
Q

What are the three main processes involved in production of urine?

A

Filtration, reabsorption, and secretion

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15
Q

How is the urinary excretion rate calculated? Which factors contribute the most to this rate?

A

Excretion = filtration - reabsorption + secretion

Filtration and reabsorption contribute the most

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16
Q

What types of substances will only be filtered by the kidney (not secreted or reabsorbed)?

A

Waste products

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17
Q

What types of substances will be filtered and partially reabsorbed by the kidney?

A

Electrolytes

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18
Q

What types of substances will be filtered and completely reabsorbed by the kidney?

A

Nutritional substances (e.g. glucose and amino acids)

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19
Q

What types of substances will be filtered AND secreted by the kidney?

A

Substances which require rapid clearance (e.g. organic acids)

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20
Q

What is the name for the fluid found in Bowman’s capsule?

A

Glomerular filtrate

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21
Q

What is the approximate % of plasma which is filtered by the glomerulus and what is the term for this fraction?

A

20% - filtration fraction

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22
Q

What are the two main factors which determine the filtration fraction/GFR?

A

Glomerular capillary filtration coefficient (Kf), and filtration forces

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23
Q

What are the three layers which act as a barrier between the blood and glomerular filtrate?

A

Endothelium of glomerular capillaries, basement membrane of capillaries, epithelial cells of Bowman’s capsule

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24
Q

What is the name given to epithelial cells of Bowman’s capsule?

A

Podocytes

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25
Q

What characteristic of glomerular capillary endothelium allows for filtration?

A

Fenestrae

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26
Q

What characteristic of glomerular capillary basement membrane allows for filtration?

A

Permeability due to proteoglycans

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27
Q

What characteristic of Bowman’s capsule epithelium allows for filtration?

A

Slit pores between projections of podocytes

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28
Q

What characteristic, other than particle size, restricts filtration of molecules?

A

Charge - filter components are slightly negatively charged, so neutral/positive particles filter more effectively

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29
Q

Why do plasma proteins (e.g. albumin) typically not enter the glomerular filtrate?

A

Size (too large to pass easily) and charge (generally negatively charged)

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30
Q

What are the four forces which contribute to filtration force in the glomerulus?

A

Glomerular hydrostatic pressure (PG)
Bowman’s capsule hydrostatic pressure (PB)
Glomerular osmotic pressure (PiG)
Bowman’s capsule osmotic pressure (PiB)

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31
Q

Which of the four factors contributing to filtration force in the glomerulus is typically considered to be zero?

A

Bowman’s capsule hydrostatic pressure

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32
Q

What does “high osmotic pressure” refer to?

A

High solute concentration

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33
Q

How is the filtration coefficient (Kf) determined?

A

Estimated - Filtration force is assumed to be approx. 10, so Kf = GFR/10

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34
Q

When Kf/GFR is calculated, does it represent one kidney or both?

A

Both

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35
Q

Under what circumstances is Kf modified?

A

Pathological conditions only (hypertension, diabetes can reduce Kf)

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36
Q

Under what circumstances is Bowman’s capsule hydrostatic pressure modified?

A

Pathological conditions only (e.g. ureter blockage)

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37
Q

Under what circumstances is glomerular osmotic pressure modified?

A

Changes in plasma protein levels, or changes in filter fraction (higher FF = higher osmotic pressure)

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38
Q

What is the primary factor which the body utilizes to modify GFR?

A

Hydrostatic pressure in glomerular capillaries

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39
Q

What changes in the body contribute to changes in glomerular hydrostatic pressure?

A

Arterial pressure (MAP), afferent arteriolar resistance, efferent arteriolar resistance

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40
Q

What is the main reason kidneys have such a high rate of oxygen consumption (double that of the brain)?

A

Active reabsorption of sodium

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41
Q

How is the renal pressure gradient estimated and which of the three factors is modified to regulate filtration?

A

(P(RA) - P(RV)) / (Renal vascular resistance)

Renal vascular resistance is modified

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42
Q

What are the three components which contribute to renal vascular resistance?

A

Interlobular arteries
Afferent arterioles
Efferent arterioles

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43
Q

What is the estimated pressure of the renal artery and renal vein?

A

RA = 100mmHg
RV = 3-4mmHg

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44
Q

What are the two broad categories of factors which affect renal vascular resistance?

A

Sympathetic nervous system activity, and hormones/autacoids

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45
Q

Under what conditions will sympathetic NS activation significantly impact renal vascular resistance?

A

Major activation of SNS where blood volume must be restored (e.g. hemorrhage, brain ischemia, etc.)

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46
Q

How do epinephrine/norepinephrine alter GFR?

A

Constriction of afferent AND efferent arterioles, thereby reducing blood flow/GFR

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47
Q

What hormone is produced by damaged endothelial cells?

A

Endothelin

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48
Q

How does endothelin modify the GFR?

A

Reduces blood flow (and thereby blood loss) when the endothelium is damaged. Reduces GFR in cases of toxemia, acute renal failure, chronic uremia

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49
Q

Under what circumstance is angiotensin II released and what is its primary function?

A

Blood volume depletion; acts to facilitate filtration of waste products while still retaining fluid

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50
Q

What is the effect of angiotensin II on the nephron/GFR?

A

Constricts efferent arteriole - increases GFR while maximizing reabsorption by peritubular capillaries due to lower pressure

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51
Q

How does nitric oxide alter GFR?

A

Vasodilator - increases GFR. Should be constitutively expressed

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52
Q

What are the important autacoids in the nephron?

A

Prostaglandins, PGI2, PGE2, bradykinin

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53
Q

How do autacoids alter GFR?

A

Reduce vasoconstriction effect of angiotensin II on the afferent arterioles, allowing for local constriction of efferent arterioles only

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54
Q

What are the two main effector cell types involved in the juxtaglomerular feedback mechanism?

A

Macula densa cells on the distal tubule, and granular (juxtaglomerular) cells on the afferent arteriole

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55
Q

How does a reduction in GFR change the NaCl concentration of filtrate in the distal tubule?

A

Decreased concentration - lower flow rate means greater time for absorption

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56
Q

How do macula densa cells respond to decreased NaCl concentration in the distal tubule?

A

Reduce afferent arteriole resistance to increase GFR

Increase renin release by juxtaglomerular cells (to cause angiotensin-mediated efferent arteriole constriction)

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57
Q

Explain the myogenic mechanism for autoregulation of GFR.

A

Stretch due to increased BP causes release of calcium into smooth muscle cells, causing contraction and reducing blood flow

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58
Q

What is the simplest formula to calculate urine excretion of a substance?

A

Glomerular filtration - tubular reabsorption + tubular secretion

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59
Q

What is the primary active transporter in the tubular epithelium?

A

Sodium-potassium ATPase

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60
Q

Where are sodium-potassium ATPase pumps typically located?

A

Basolateral membrane of the tubular epithelial cells

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61
Q

By what mechanism is sodium typically reabsorbed?

A

Active transport - ATPase at the basolateral membrane creates a concentration/charge difference which pulls sodium into the epithelial cell, and pushes sodium into the capillary

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62
Q

How are molecules like glucose and amino acids typically reabsorbed?

A

Via cotransport with sodium (secondary active transport; e.g. SGLT2) at the apical membrane, then passively via transporters (e.g. GLUT2/1) at the basolateral membrane

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63
Q

By what mechanism are hydrogen ions typically secreted?

A

Sodium-hydrogen exchanger (NHE) - secondary active secretion

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64
Q

By what mechanism are proteins typically reabsorbed?

A

Pinocytosis; digestion into AA then diffusion into the blood

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65
Q

What is meant by the “transport maximum” of a substance?

A

The absolute maximum rate at which a substance can be reabsorbed; associated with saturation of all transport proteins

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66
Q

What is meant by the “threshold level” of a substance?

A

The value below the transport maximum at which some nephrons have reached maximum reabsorption, but not all. It is the level at which a substance appears in the urine

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67
Q

How is water reabsorption typically accomplished?

A

Passively; either transcellular or paracellular

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68
Q

What is “solvent drag”?

A

Reabsorption of solutes along with water transfer

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69
Q

What are the two main mechanisms for chloride reabsorption?

A

Charge gradient between the lumen and extracellular space created by sodium

Water reabsorption (following sodium) creates a concentration gradient

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70
Q

Is urea reabsorbed?

A

Yes, some of it is (about 50%) as cells have a low level of permeability

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71
Q

What is renal clearance?

A

The volume of plasma per unit time (ml/min) that is completely cleared of a substance

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72
Q

How is excretion rate calculated?

A

urine concentration x urine flow rate

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73
Q

How is clearance rate calculated?

A

(urine concentration x urine flow rate) / (plasma concentration)

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74
Q

What makes a substance have a clearance rate equal to GFR?

A

Freely filtered, not reabsorbed or secreted

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75
Q

What are substances that can be used to determine GFR via calculating clearance rate?

A

Inulin and creatinine

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76
Q

What are characteristics of a substance with a clearance rate of 0?

A

Freely filtered and completely reabsorbed (or not filtered at all) - e.g. glucose

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77
Q

What are characteristics of a substance with a clearance rate greater than GFR? Example?

A

Freely filtered AND secreted (and not reabsorbed) - e.g. PAH

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78
Q

What is pressure natriuresis?

A

Increase in sodium excretion due to increased arterial pressure

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79
Q

What is pressure diuresis?

A

Increase in water excretion due to increased arterial pressure

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80
Q

What are three consequences of impaired GFR autoregulation due to kidney disease?

A

Increase in GFR/UOP

Reduced reabsorption of sodium/water due to increased interstitial pressure

Reduced angiotensin II formation

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81
Q

Where in the nephron are a majority of ions (65%) reabsorbed?

A

Proximal tubule

82
Q

What are three adaptations in proximal tubule cells that allow for high reabsorption of ions?

A

Mitochondria, enhanced surface area (brush border), and large numbers of transporters

83
Q

Where is the primary site of glucose/AA reabsorption in the nephron?

A

First half of the proximal tubule

84
Q

What types of substances are secreted in the proximal tubule?

A

Organic acids, and many drugs/toxins

85
Q

What is the concentration of filtrate in the proximal tubule relative to plasma concentration?

A

Isosmotic (water is absorbed at the same rate as solutes)

86
Q

Why do creatinine and urea become more concentrated along the proximal tubule?

A

Reabsorption of water causes concentration

87
Q

Describe reabsorption of substances in the thin descending arm of the Loop of Henle

A

Highly permeable to water (20% of total reabsorption), moderate permeability to solutes (not calcium/bicarb/magnesium)

88
Q

Describe reabsorption of substances in the thin ascending arm of the Loop of Henle

A

Largely impermeable

89
Q

How does urine concentration change in the thick ascending Loop of Henle?

A

Becomes diluted - impermeable to water but high levels of ion reabsorption

90
Q

What is the role of the thick ascending Loop of Henle in pH regulation?

A

Active secretion of protons via anion exchange

91
Q

How do “loop diuretics” (e.g. furosemide) act?

A

Inhibits ion Na-Cl-K cotransporter in the thick ascending Loop of Henle

92
Q

What are the reabsorptive characteristics of the early distal tubule?

A

Similar to thick ascending Loop. Na-Cl cotransport is especially important (5% of filtered load)

93
Q

What are the two important cell types in the late distal and collecting tubules?

A

Principal cells and intercalated cells

94
Q

What is the role of the principal cells of the late distal/collecting tubules?

A

Reabsorb sodium and secrete potassium

95
Q

How does aldosterone act on the late distal/collecting tubule?

A

Acts on principal cells to increase sodium reabsorption/potassium secretion

96
Q

What is the role of the intercalated cells in the late distal/collecting tubule?

A

Reabsorb potassium and bicarbonate

Secrete protons

(acid-base balance)

97
Q

Which segment(s) of the nephron are sensitive to ADH?

A

Late distal and collecting tubules, and collecting duct

98
Q

Describe the reabsorptive characteristics of the collecting duct?

A

Some sodium/water reabsorption (<10%)
Water permeability modulated by ADH
Secretes protons/reabsorbs bicarbonate
Permeable to urea

99
Q

Why does the formula for calculating reabsorption rely on hydrostatic/osmotic pressures for the interstitial fluid and not the lumen?

A

Most reabsorption from the interstitium to the blood is passive, while reabsorption from the lumen to the interstitium is often active anyways

100
Q

How does resistance in afferent/efferent arterioles affect hydrostatic pressure of peritubular capillaries?

A

Increased resistance reduces hydrostatic pressure (facilitates reabsorption)

101
Q

What two factors will modify the peritubular colloid osmotic pressure?

A

Systemic plasma colloid osmotic pressure and filtration fraction

102
Q

How is renal interstitial pressure (hydrostatic/osmotic) in the proximal tubule modified?

A

Primarily via peritubular capillaries

103
Q

What is the glomerotubular balance mechanism?

A

In cases of increased flow rate in the renal tubules, brush border cells sense the flow rate and trigger responses to increase transporters at the apical membrane

104
Q

What stimulates increased aldosterone secretion?

A

Increased extracellular potassium (or increased angiotensin II in cases of low sodium)

105
Q

How does aldosterone modify reabsorption?

A

Increases sodium reabsorption and increases potassium secretion by increasing the activity of basolateral sodium-potassium pumps (and by enhancing sodium permeability at the luminal membrane)

106
Q

What primarily stimulates the production of angiotensin II?

A

Low BP, low ECF volume

107
Q

How does angiotensin II modify reabsorption?

A

Stimulates aldosterone secretion (more sodium, less potassium)
Constricts efferent arterioles to increase the filtration fraction and decrease peritubular hydrostatic pressure
Stimulates sodium-potassium pumps, sodium-hydrogen exchangers, and sodium-bicarbonate cotransporters

108
Q

What is the molecular mode of action of ADH?

A

Binds V2 receptor
Activates cAMP
Activates protein kinase A
Aquaporin-2 moved to the apical membrane

109
Q

What stimulates the secretion of atrial natriuretic peptide?

A

Increased blood/plasma volume in the atria

110
Q

What is the main function of atrial natriuretic peptide in relation to renal reabsorption?

A

Reduces sodium/water reabsorption in collecting ducts, and inhibits renin/angiotensin formation

111
Q

What is the role of parathyroid hormone in the kidney?

A

Increases calcium reabsorption

112
Q

How do low/high levels of sympathetic NS activity affect renal reabsorption?

A

LOW: Increases reabsorption in the proximal tubules and thick ascending loop via a-adrenergic receptors
HIGH: reduces renal blood flow and GFR
Generally will stimulate renin/angiotensin

113
Q

Where in the body is 98% of calcium located?

A

intracellularly

114
Q

Approximately what percentage of dietary potassium is excreted in urine?

A

92%

115
Q

What is the body’s first response to changes in extracellular potassium concentration?

A

Movement of potassium into/out of cells

116
Q

What are four factors that can stimulate movement of potassium into cells?

A

Insulin, aldosterone, beta-adrenergic stimulation, alkalosis

117
Q

What are some factors that stimulate potassium movement out of cells?

A

Acidosis, cell lysis, strenuous exercise, increased extracellular osmolarity

118
Q

How does a decreased GFR modify blood potassium levels?

A

Causes hyperkalemia (because there is high reabsorption)

119
Q

What is the main target for day-to-day adjustments of potassium levels in the kidney?

A

Potassium secretion in late distal and collecting tubules

120
Q

What cells secrete potassium?

A

Principal cells in the late distal and collecting tubules

121
Q

What is the mechanism by which the body can ensure adequate potassium excretion even when more sodium is being excreted?

A

Increased tubular flow rate causes rapid flushing of secreted potassium, allowing for increased net secretion

122
Q

How does acidosis affect potassium excretion?

A

SHORT TERM: Inhibits Na/K pumps
CHRONIC: Increases secretion due to increased tubular flow

123
Q

What are the three forms of calcium in the plasma?

A

Ions, protein-bound, and non-ionized

124
Q

How does parathyroid hormone affect calcium levels?

A

Stimulates bone reabsorption, activates vitamin D associated intestinal reabsorption, and increases renal reabsorption

125
Q

Where does most reabsorption of calcium occur in the kidney?

A

Proximal tubule (independent of PTH)

126
Q

Where in the kidney does PTH (and vitamin D) modify calcium reabsorption?

A

Increases reabsorption at the distal tubule and in the thick ascending loop of Henle

127
Q

How is calcium reabsorbed?

A

Diffusion at the apical membrane, Ca-Na exchangers at the basolateral membrane

128
Q

Where does most reabsorption of magnesium occur?

A

Loop of Henle

129
Q

Where does most reabsorption of phosphate occur?

A

Proximal tubule (NOTE: transport maximum is low)

130
Q

By what mechanism is urine diluted?

A

Ascending Loop of Henle dilutes urine by reabsorbing solutes. In the absence of ADH, distal/collecting tubules are impermeable to water, so urine remains diluted even as it passes through the medulla

131
Q

By what mechanism is urine concentrated?

A

In the presence of ADH, distal/collecting tubules are permeable to water, so reabsorb large volumes as it passes through the renal medulla

132
Q

What is the maximum osmolarity that urine can reach?

A

Equal to the osmolarity of the renal interstitium (up to 10,000mOsm in some desert species)

133
Q

How is the osmolarity of the renal medullary interstitium maintained?

A

Ions are actively pumped out of the thick ascending Loop of Henle and collecting duct. Urea also diffuses into the interstitium with low water transfer

134
Q

How is the hyperosmotic medullary interstitium created?

A

Feedback loop between arms of the Loop of Henle (descending loses water > becomes concentrated > more ions to pump from ascending > more water drawn from descending > …)

135
Q

How does urea contribute to concentrating urine?

A

Urea is concentrated following water reabsorption in the descending Loop, then diffuses following its concentration gradient out of the collecting duct into the medullary interstitium via UT-1 and UT-3

136
Q

What is the obligatory urine volume?

A

Least volume of urine required to excrete excess solutes/waste

137
Q

What is the difference between urine specific gravity (USG) and urine osmolarity?

A

USG considers the number AND molecular weight of solutes. Osmolarity only considers the number of molecules.

138
Q

What is the main disadvantage to utilizing USG to measure urine concentration?

A

Large molecules (e.g. antibiotics) may skew the concentration (osmolarity) to appear greater than it actually is

139
Q

Other than renal medullary interstitial osmolarity, how else might a species be able to create more concentrated urine?

A

Increased relative medullary area

140
Q

What is the vasa recta?

A

U-shaped peritubular capillary that runs parallel to juxtamedullary nephrons

141
Q

Which portion of the brain detects osmolarity?

A

Hypothalamus

142
Q

What important renal hormone does the hypothalamus secrete?

A

ADH in response to increased osmolarity

143
Q

What stimuli other than increased osmolarity can trigger ADH release by the hypothalamus?

A

Decreased arterial pressure
Decreased blood volume
Nausea
Drugs (nicotine, morphine)

144
Q

Where is the thirst centre of the brain?

A

Near the hypothalamus (anterior-ventral wall of the third ventricle)

145
Q

What are stimuli (other than increased ECF osmolarity) that can stimulate the thirst centre?

A

Decreased MAP
Angiotensin II
Dryness of mouth/esophagus

146
Q

What are stimuli that depress the thirst centre?

A

Gastrointestinal distension
Wetting of mouth/esophagus

147
Q

Where is the salt appetite centre?

A

Anterior-ventral wall of the third ventricle (near hypothalamus)

148
Q

What stimulates the salt appetite centre?

A

Extreme sodium deficiencies (especially in Addison’s disease due to low aldosterone)
Decreased MAP/BV

149
Q

How does the body overcome intrarenal compensatory mechanisms for increased BP?

A

Pressure diuresis/natriuresis

150
Q

How does the sympathetic nervous system affect the kidneys with reduced blood volume?

A

Constricts renal arterioles to reduce GFR, stimulates renin-angiotensin II to increase sodium reabsorption

151
Q

What is the approximate range of pH at which the body can function?

A

6.8 - 8.0

152
Q

What is the range of urine pH?

A

4.5 to 8.0

153
Q

What are the ways the body can compensate for changes in the acid-base balance in order of speed of onset?

A

Buffer systems
Respiratory compensation
Renal compensation

154
Q

What are the main components of the body’s acid-base buffer system?

A

A weak acid and a salt

155
Q

How does the bicarbonate buffer system (NaHCO3 + H2CO3) compensate for a decreased pH?

A

Protons bind to ionized bicarbonate (from the salt), and are sequestered
H2CO3 remains protonated

156
Q

How does the bicarbonate buffer system (NaHCO3 + H2CO3) compensate for an increased pH?

A

Protons are released from carbonic acid to neutralize the base (e.g. NaOH + H+ = Na+ + H2O)

157
Q

What are the components of the phosphate buffer system?

A

H2PO4- = acid
NaHPO4- = base

158
Q

Where is the phosphate buffer system most important?

A

Intracellularly

159
Q

How do proteins act as pH buffers?

A

Overall negative charge, so act as a weak base to sequester protons

160
Q

Why are kidneys needed for acid-base balance instead of just the lungs?

A

Excretion of non-volatile acids from protein digestion

161
Q

What is the main principle of renal acid-base balance?

A

Reabsorption of bicarbonate and excretion of protons, which occur largely in tandem with one another

162
Q

Where does bicarbonate reabsorption NOT occur in the tubule?

A

Thin segments of Loop of Henle

163
Q

Explain the mechanism behind renal bicarbonate/proton exchange in the proximal tubule?

A

CA converts CO2 to bicarbonate + H+ inside the cell
Bicarbonate is reabsorbed
H+ exchanged for Na+ in the tubule
H+ reacts with bicarbonate in the tubule to form CO2
CO2 diffuses into the cell

164
Q

What is the lowest pH that urine can reach in the proximal tubule from bicarbonate/H+ exchange? Why?

A

6.7, because protons that are excreted are used to synthesize CO2 + H2O in the tubule

165
Q

Explain the mechanism behind bicarbonate/proton exchange in the late distal and collecting tubules.

A

CO2 diffuses in from the blood
CA converts CO2+H2O to bicarbonate and protons
Bicarbonate reabsorbed via exchange with chloride
Protons secreted via active transport

166
Q

What is the lowest urine pH that can be reached in the late distal/collecting tubules? Why?

A

4.5 - because most bicarbonate has already been reabsorbed in the proximal tubule, and this is mostly just proton secretion

167
Q

What are the main molecules in the tubule that sequester protons?

A

Phosphate (NaHPO4-) and ammonia (NH3)

168
Q

What is the role of glutamine in acid-base balance?

A

Reacts in the tubule cells to form bicarbonate (reabsorbed into blood) and ammonium (secreted)

169
Q

How does metabolic acidosis affect proton secretion in the proximal tubule?

A

Reduced bicarbonate in the blood = less bicarbonate in the filter = H+ doesn’t bind anything in the tubular fluid = more H+ will be excreted rather than reacting and having products (CO2/H2O) reabsorbed

170
Q

How does respiratory acidosis affect proton excretion?

A

More CO2 in the blood = more activity of CA = more H+ produced to be secreted

171
Q

How does metabolic alkalosis affect bicarbonate reabsorption in the proximal tubule?

A

Too much bicarbonate in the tubule = not enough protons to react and form CO2 = less bicarbonate reabsorption

172
Q

How does respiratory alkalosis affect bicarbonate reabsorption in the proximal tubule?

A

Less CO2 available for carbonic anhydrase

173
Q

How does aldosterone affect acid-base balance?

A

Increases proton secretion in the collecting duct

174
Q

How does angiotensin II affect acid-base balance?

A

Increases activity of anion exchangers

175
Q

NOTE: No flashcards for micturition since it was covered extensively in Neuroscience

A

No answer

176
Q

What is the main mechanism of action of osmotic diuretics?

A

Increasing osmotic pressure in the tubule to reduce water reabsorption

177
Q

What are examples of osmotic diuretics?

A

Urea, mannitol, sucrose

178
Q

What is the main mechanism of action of loop diuretics?

A

Reduce Na+/Cl-/K+ reabsorption by blocking transporters in the thick ascending Loop of Henle - increases osmotic pressure AND disrupts medullary interstitial osmolarity

179
Q

What is the most potent class of diuretic?

A

Loop diuretics - can increase urine volume up to 30% of total GFR

180
Q

What is the main mechanism of action of thiazide diuretics?

A

Reduces Na/Cl reabsorption in the distal tubule

181
Q

What is the main mechanism of action of carbonic anhydrase inhibitor diuretics?

A

Reduce bicarbonate reabsorption (reduces production)
Reduce sodium reabsorption (no protons to exchange)

182
Q

What is the main mechanism of action of aldosterone inhibitor diuretics?

A

Reduce sodium reabsorption
Reduce potassium secretion (potassium sparing)

183
Q

What is the main mechanism of action of sodium channel blocker diuretics?

A

Reduce sodium reabsorption in the cortical collecting tubule

184
Q

Why are sodium channel blockers considered potassium-sparing diuretics?

A

Potassium excretion in the collecting tubule requires exchange with sodium, so reduced sodium reabsorption thereby reduces potassium secretion

185
Q

What are the three types of acute renal failure?

A

Prerenal, intrarenal, postrenal

186
Q

What is the key defining feature of ACUTE renal failure?

A

Reversible

187
Q

What are the main consequences of acute renal failure?

A

Hyperkalemia due to reduced excretion
Metabolic acidosis due to impaired excretion of protons

188
Q

What would be some potential causes of prerenal acute renal failure?

A

Heart failure, reduced blood pressure, hemorrhage (basically just reduced renal blood flow)

189
Q

What is oliguria?

A

Reduced urine output below intake of water/solutes

190
Q

What are the three potential sites of intrarenal acute renal failure?

A

Glomerular capillaries, tubules, and renal interstitium

191
Q

What is acute glomerulonephritis?

A

Entrapment of antibody-antigen complexes (from an infection elsewhere in the body) in the glomerular capillaries, causing intrarenal acute renal failure

192
Q

What is tubular necrosis?

A

A form of intrarenal acute renal failure. Damage to tubular epithelial cells due to ischemia, toxins, drugs, etc.
Cell function is impaired, and dead cells may slough off to block the tubule

193
Q

What are some molecules that could cause tubular necrosis?

A

Heavy metals, antifreeze (ethylene glycol), insecticides, tetracyclines, chemotherapy

194
Q

What is interstitial nephritis?

A

Damage to renal interstitial tissue. Common with kidney infections, but can also be caused by drugs/toxins

195
Q

What causes postrenal acute renal failure?

A

Obstruction of the urinary collecting system (ureter, bladder, urethra)

196
Q

How is chronic renal failure defined?

A

Irreversible decrease in the number of nephrons/kidney function

197
Q

What percent decrease in number of nephrons can an animal potentially tolerate?

A

70%

198
Q

How can chronic renal failure be progressive?

A

Hypertrophy of remaining nephrons and reduced vascular resistance can predispose kidneys to further damage (e.g. from stretched vessels causing sclerosis)

199
Q

How are surviving nephrons altered following kidney damage?

A

Hypertrophy, increased filtration, reduced reabsorption

200
Q

What are three common causes of end-stage renal disease?

A

Diabetes mellitus, hypertension, glomerulonephritis

201
Q
A

Form and Function (2 decks)

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