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Pathophysiology II Exam 2 Renal > Renal Module II > Flashcards

Renal Module II Flashcards

1
Q

The glomerulus filters everything into Bowman’s space except what?

A

RBC/WBC, most proteins & fats

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2
Q

What happens if albumin and other proteins manage to get through glomerular filtration?

A

PCT will reabsorb proteins/albumin back into blood so they will not be excreted in urine

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3
Q

How much plasma is filtered into the nephrons each day? What is the body’s total plasma volume? How may times do the kidneys filter body’s total plasma volume each day?

A

filtered each day: 180 L
total body: 3 L
Kidneys filter total plasma volume 60 times a day

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4
Q

What is the urine output each day?

A

1-2L/day (kidneys reabsorb 178-179 L/day)
*kidneys must decide what is necessary to keep (reabsorb) in order for the body to be healthy vs. excreting

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5
Q

How much reabsorption happens in the PCT?

A

60-90% of everything that was filtered

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6
Q

What is reabsorbed by the PCT?

A

Glucose (100% reabsorbed)
Sodium, potassium, calcium, etc.
Bicarbonate
Urea
Amino acids/proteins that made it through filtration

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7
Q

What is secreted by the PCT?

A

Creatinine
Urea, ammonia
H+
Meds/drugs
Uric acid

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8
Q

Are there any significant dilute/concentration changes in the PCT?

A

No

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9
Q

What does the descending limb of the loop of Henle reabsorb?

A

Water

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10
Q

What does the descending limb of the loop of Henle secrete?

A

Urea (plays role in urine concentration gradients)

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11
Q

Are there any significant dilute/concentration changes in the descending limb of the loop of Henle?

A

Yes, concentrates tubular fluid

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12
Q

What does the thick ascending limb of the loop of Henle reabsorb?

A

Sodium, potassium, chloride

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13
Q

What does the thick ascending limb of the loop of Henle secrete?

A

Nothing

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14
Q

Are there any significant dilute/concentration changes in the thick ascending limb of the loop of Henle?

A

Yes, dilutes tubular fluid

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15
Q

What does the early DCT segment reabsorb?

A

Sodium, calcium

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16
Q

What does the early DCT segment secrete?

A

Nothing

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17
Q

Are there any significant dilute/concentration changes in the early DCT segment?

A

Yes, dilutes tubular fluid

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18
Q

What does the late DCT segment reabsorb?

A

Water, sodium, bicarbonate, urea

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19
Q

What does the late DCT segment secrete?

A

H+, potassium, ammonia

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20
Q

Are there any significant dilute/concentration changes in the late DCT segment?

A

Yes, concentrates tubular fluid

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21
Q

What is the central force in driving PCT reabsorption?

A

Sodium/potassium pump: actively pumps sodium from PCT cell into plasma

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22
Q

What follows sodium in the sodium potassium pump of the PCT? Why does this happen?

A

Water, glucose, amino acids, calcium, chloride, bicarbonate, phorphate, etc. into plasma
Because of osmotic gradient and/or cotransporters

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23
Q

PCT reabsorbs how much glucose & amino acids?

A

100%

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24
Q

PCT reabsorbs how much bicarbonate?

A

80-90%

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25
Q

PCT reabsorbs how much water, sodium, potassium, and chloride?

A

65%

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26
Q

PCT reabsorbs how much urea?

A

50%

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27
Q

Pathway for PCT to reabsorb water?

A

Na+ concentration gradients formed by active sodium/potassium pump promote water diffusion (osmosis) into bloodstream

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28
Q

What structures of the PCT cell allow for osmosis of H2O into the PCT cell/plasma?

A

Aquaporins

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29
Q

What further promotes ion reabsorption in the PCT?

A

Increased concentration of tubular fluid

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30
Q

How does the PCT create Na+ concentration gradients?

A

At the basolateral membrane, Na+ is pumped into interstitial space by sodium/potassium ATPase (potassium pumped into cell)
*active transport of Na+ creates concentration gradients

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31
Q

How do lipid-soluble substances diffuse across the PCT membrane?

A

transcellular route

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32
Q

How do various ions (Cl-, Ca2+, and K+) and urea diffuse across PCT membrane?

A

paracellular route

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33
Q

What is the major regulator of extracellular fluid volume (ECF)?

A

NaCl balance

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34
Q

Early PCT pathway for sodium reabsorption?

A

Sodium reabsorption is coupled with many filtrates (glucose, amino acids, etc.), and H+ secretion

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35
Q

Late PCT pathway for sodium reabsorption?

A

Sodium is reabsorbed w/ chloride as NaCl, also reabsorbed coupled w/ H+ scretion

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36
Q

What influences Na+ reabsorption in the PCT?

A

Hormones

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37
Q

What are the stimuli which increase NaCl reabsorption in the PCT?

A

Angio II, endothelin, smpathetics

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38
Q

What are the stimuli which decrease NaCl reabsorption in the PCT?

A

Natriuretic peptides (ANP, BNP, etc.)

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39
Q

What is necessary for reabsorption of bicarb in the PCT?

A

Na+/H+ exchange

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40
Q

Pathway for Bicarb reabsorption in the PCT?

A

-H+ secreted into lumen of cell, and Na+ goes into PCT cell
-H+ combines w/ filtered HCO3- to form carbonic acid (H2CO3)
-Carbonic acid dissociates into H2O and CO2 by carbonic anhydrase
-CO2 diffuses into the PCT cell where it will reform to carbonic acid –> dissociates into HCO3- and H+

*HCO3- reabsorbed back into blood stream
*H+ secreted back into lumen by Na+/H+ exchange

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41
Q

What inhibits bicarbonate reabsorption in the PCT?

A

Diuretics (carbonic anhydrase inhibitors)

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42
Q

What happens in the PCT if diuretics present?

A

-Filtered bicarb, sodium, and sodium chloride remain in lumen and tubular concentration increases
-Water stays in lumen due to less Na+ reabsorption/increased tubular fluid conc.

Net result: diuresis (H2O excretion) and natriuresis (Na+ excretion), along w/ bicarb excretion

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43
Q

Diuretics effect on acid-base balance?

A

Potential disruption due to plasma bicarb decreasing/becoming more acidic and urine bicarb increasing/becoming more alkaline

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44
Q

How is glucose reabsorbed in the PCT?

A

-Sodium-glucose cotransporters (SGLT 1/2): mediate Na+ and glucose cotransport into PCT cell
-Glucose transport carrier (GLUT 2): allows glucose to flow from PCT cell to bloodstream

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45
Q

Glucose transport in the PCT is limited by what?

A

of available cotransport carriers

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46
Q

What happens to the PCT if there is too much glucose in the plasma/hyperglycemia?

A

PCT cannot keep up with reabsorption and “glucose dumping” begins to occur

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47
Q

What are SGLT2 inhibitors?

A

Hypoglycemic medications that inhibit reabsorption of glucose to treat diabetes

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48
Q

What is the secondary benefit of SGLT2 inhibitors?

A

Antihypertensive benefit: inhibit sodium reabsorption/promote natriuresis and diuresis

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49
Q

What is the glucose transport maximum in the PCT?

A

Maximum rate a substance can be transported across PCT cell wall

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50
Q

What plasma glucose levels correspond with transport maximum of glucose in the PCT?

A

350 mg/dL

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51
Q

What is the glucose renal threshold (diabetes/hyperglycemia)?

A

Plasma values when glucose first appears in the urine (glucose dumping)

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52
Q

At what plasma glucose levels does glucose dumping begin to occur in urine?

A

180-200 mg/dL

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53
Q

What does the PCT secrete?

A

H+, small amount of creatinine, urea, ammonia/ammonium, meds/drugs, uric acid

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54
Q

How much H+ is secreted by the PCT?

A

Large amounts of H+ ions secreted when reabsorbing bicarbonate

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55
Q

How is there no net loss of H+ ions from the PCT?

A

The H+ ions get recycled

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56
Q

When does H+ secretion/excretion occur?

A

“Later” in the cells of the late DCT segment/collecting duct

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57
Q

How is creatinine formed?

A

Metabolic breakdown of creatinine phosphate in muscle, produced by body at a predictable rate

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58
Q

How is creatinine filtered through the glomerulus?

A

Freely

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59
Q

Is creatinine reabsorbed in the nephron?

A

No

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60
Q

How much creatinine is secreted in the PCT?

A

A small amount

61
Q

How is ammonia/ammonium secreted by the PCT?

A

Using a process called ammoniagenesis:
-Glutamine enters PCT cell from plasma and from filtered glutamine in lumen
-PCT cell converts glutamine into ammonium (NH4+) and bicarb (HCO3-)
-Ammonium is secreted into lumen and newly formed bicarb is absorbed into plasma

62
Q

Ammonium is eventually excreted from the nephron as part of what?

A

Acid-base regulation

63
Q

What is acute tubular necrosis (ATN)?

A

Nephron obstruction due to cell damage of PCT and other regions of nephron (may lead to necrosis if severe)

64
Q

What is acute tubular necrosis (ATN) caused by?

A

-Ischemia (hypotension/hypovolemic states)
-Toxins (drugs such as aminoglycosides, sulfa drugs, acyclovir, etc.)
-Endotoxins (myoglobin and hemoglobin
-Sepsis

65
Q

What do ischemia/toxins cause in ATN?

A

Acute kidney injury (cell damage to PCT and other regions)
Breakdown of epithelial cells–>form casts/possible nephron obstruction

66
Q

Urinalysis for ATN?

A

Muddy brown appearing urine from casts of epithelial cells

67
Q

Treatment for ATN?

A

Focused on underlying cause, prognosis dependent on underlying condition

68
Q

Loop of Henle has a critical role in what?

A

Regulating urine concentration

69
Q

How does the descending loop of Henle concentrate the filtrate?

A

Reabsorbs water & leaves behind electrolytes in descending loop lumen
*osmolarity of tubular fluid increases as it descends in loop

70
Q

How does the thick ascending loop (TAL) of Henle dilute the filtrate?

A

Reabsorbs sodium & other electrolytes
*osmolarity of tubular fluid decreases in the TAL

71
Q

Urine concentration in the PCT?

A

300 mOsm

72
Q

Urine concentration in the start of the loop of Henle?

A

300 mOsm

73
Q

Urine concentration in the descending portion of the loop of Henle?

A

Gradual increase to 1,200 mOsm at the bottom

74
Q

Urine concentration in the thick ascending portion (TAL) of the loop of Henle?

A

Gradual decrease to 100-200 mOsm

75
Q

Urine concentration in the early DCT segment?

A

Continues to dilute: 100 mOsm

76
Q

Urine concentration in the late DCT segment?

A

Begins to concentrate: 150 mOsm

77
Q

Urine concentration in the start of the collecting duct?

A

150 mOsm

78
Q

Finished urine concentration in the collecting duct?

A

Concentrated: 1,200 mOsm
or
Diluted: 100-200 mOsm

*dependent on the body’s needs

79
Q

Is the descending limb permeable to water?

A

Yes - allows water to be reabsorbed, but not sodium/other electrolytes

80
Q

What reabsorption does the narrow portion of the ascending limb of the Loop of Henle?

A

Passive sodium/chloride reabsorption

81
Q

What does the thick ascending limb (TAL) of the loop of Henle reabsorb?

A

Na+, Cl-, K+ and other electrolytes (HCO3-, Ca2+, Mg+)

82
Q

What is Na+ co-transported with in the thick ascending limb (TAL) of the loop of Henle?

A

Chloride (Cl-) and K+

83
Q

What does co-transport of Na+/Cl-/K+ create in the TAL of the loop of Henle?

A

Electrical potential gradient that promotes passive diffusion of Na+, K+, Ca2+, Mg2+

84
Q

The TAL reabsorbs how much of filtered sodium/filtered bicarb?

A

25% of sodium
20% of bicarb

85
Q

Is the TAL of the loop of Henle permeable to water?

A

No - water remains in the TAL lumen and osmolarity decreases/dilutes as fluid ascends

86
Q

What do loop diuretics inhibit?

A

Na+/K+/Cl- co-transport in the TAL
Also inhibit calcium reabsorption

87
Q

Reduced sodium reabsorption in the TAL due to loop diuretics promotes what?

A

Diuresis, Natriuresis, Potassium excretion (potential for hypokalemia)

88
Q

What can be used to offset potassium loss in the TAL?

A

Potassium sparing diuretics or potassium supplementation

89
Q

What is a potential risk of loop diuretics inhibiting Ca2+ reabsorption?

A

Hypocalcemia

90
Q

What can be used as a potential treatment for hypercalcemia ?

A

Loop diuretics and IV saline fluids
(Loop diuretics inhibit Ca2+ absorption)

91
Q

Is the early segment of the DCT permeable to water/sodium?

A

Not permeable to water, but permeable to sodium (continues to dilute tubular fluid by allowing Na+ to be reabsorbed/leaving water in lumen before it enters late DCT)

92
Q

How much filtered sodium is absorbed in the early segment of the DCT?

A

~5%

93
Q

How is sodium transported in the early DCT?

A

From lumen to DCT cell by NaCl co-transport mechanism

94
Q

How much filtered calcium is absorbed in the early DCT?

A

~10%

95
Q

What stimulates calcium reabsorption in the early DCT?

A

PTH and estrogen

96
Q

What do thiazide diuretics inhibit?

A

Na/Cl co-transport in the early DCT,
promote diuresis and natriuresis

97
Q

What can thiazide diuretics potentially cause?

A

Hypercalcemia (disrupt calcium reabsorption), Hypokalemia, metabolic alkalosis

98
Q

How can thiazide diuretics potentially cause hypokalemia and metabolic alkalosis?

A

Due to blocking of the NaCl co-transpoter in the early DCT, the Na+/K+/H+ exchange which occurs further down in late DCT/CD is disrupted (sodium increase in late DCT promotes sodium reabsorption)
*causes potassium secretion and hydrogen secretion

99
Q

What may be used w/ thiazide diuretics to offset potassium loss?

A

K+ sparing diuretics

100
Q

How do K+ sparing diuretics work?

A

Inhibit K+/Na+ exhange in late DCT/CD –> less K+ secretion and less sodium reabsorption

101
Q

Functions of the late DCT/CD?

A

-Regulate final urine conc. (urea resorption, Na+/water resorption)
-Regulate acid-base homeostasis
-Regulate potassium homeostasis

102
Q

Two types of cells in late DCT/CD?

A

Principal cells and intercalated cells

103
Q

Role of principal cells in late DCT/CD?

A

Reabsorb sodium and water, secrete potassium

104
Q

Role of Type A intercalated cells (A-IC) in late DCT/CD?

A

During acidosis: secrete H+ ions and reabsorb HCO3- and K+
*maintenance of acid-base homeostasis

105
Q

Role of Type B intercalated cells (B-IC) in late DCT/CD?

A

During alkalosis: reabsorb H+ ions and secrete HCO3- and K+
*maintenance of acid-base homeostasis

106
Q

What stimulates principal cells of late DCT/CD to reabsorb sodium and secrete potassium? How?

A

Aldosterone
Stimulates Na+/K+ pump to:
-transport sodium from DCT/CD cells into bloodstream
-transport potassium from bloodstream into DCT/CD cells

107
Q

What can inhibit aldosterone and therefore inhibit K+ secretion/Na+ reabsorption from principle cells in the DCT/CD?

A

K+ sparing diuretics

108
Q

What stimulates principal cells of late DCT/CD to reabsorb water?

A

ADH

109
Q

What are aquaporins? What is the effect of ADH on aquaporins?

A

Openings located on cell membrane of late DCT/CD that allow water to diffuse into DCT/CD cells and plasma

ADH stimulates expression of aquaporins in principle/intercalated cells

110
Q

Water reabsorption in late DCT/CD is regulated by what?

A

Sodium concentration gradient established by principal cells:
if aldosterone present- Na+ into principle cell/plasma
if ADH present- aquaporins allow water to flow into principle cell/plasma

111
Q

Amount of secretion of H+ and absorption of HCO3-/K+ that occurs in late DCT/CD depends on what?

A

Acid-base status of plasma

112
Q

How do type A intercalated cells (A-IC) regulate acid-base balance in late DCT/CD?

A

Very active in regulation of H+, HCO3-, K+ when plasma is acidotic

113
Q

How do type B intercalated cells (B-IC) regulate acid-base balance in late DCT/CD?

A

Very active in regulation of H+, HCO3-, K+ when plasma is alkalotic

114
Q

Mechanism of Type A intercalated cells in acidosis?

A

Cell forms cabonic acid that dissociates into CO3- and H+
–> H+ secreted into lumen (decreases plasma H+, raises plasma pH)
–>HCO3- is reabsorbed into plasma (raises plasma pH, buffers the acidosis)

115
Q

How is hyperkalemia associated with acidosis?

A

Kidneys: type A cells promote potassium reabsorption
Tissues/ECF: H+ flows into cells, K+ flows out of cells into plasma

116
Q

Mechanism of Type B intercalated cells in alkalosis?

A

Cell forms cabonic acid that dissociates into CO3- and H+
–> H+ is reabsorbed into plasma (increases plasma H+, lowers plasma pH)
–>HCO3- is secreted into lumen (decreases plasma bicarb, lowers plasma pH, buffers the alkalosis)

117
Q

How is hypokalemia associated with alkalosis?

A

Kindeys: Type B cells promote K+ secretion

118
Q

How much filtered sodium is reabsorbed in the PCT?

A

67%

119
Q

What inhibits HCO3- reabsorption in the PCT?

A

Carbonic anhydrase inhibitors via the Na+/H+ pathway

120
Q

Is sodium reabsorbed in the descending limb of the loop of Henle?

A

No

121
Q

How much sodium is absorbed in the ascending limb (TAL) of the loop of Henle?

A

25%

122
Q

How much sodium is reabsorbed in Early DCT?

A

5%

123
Q

How much sodium is absorbed in late DCT/CD?

A

3%

124
Q

How much potassium is reabsorbed in the PCT?

A

60-70%

125
Q

Is potassium reabsorbed in the descending limb of the loop of Henle?

A

No

126
Q

How much potassium is absorbed in the ascending limb (TAL) of the loop of Henle?

A

25%

127
Q

Is potassium reabsorbed in early DCT?

A

No

128
Q

Which cells secrete potassium via sodium/potassium pump in the late DCT/CD?

A

Principal cells

129
Q

Which cells have a sum of potassium activity that has less effect compared to principle cells, yet can still alter potassium homeostasis?

A

Intercalated cells: Type A & B

130
Q

Rough rule of thumb for acidosis?

A

Promotes K+ reabsorption (Type A cells)
*Hyperkalemia and acidosis

131
Q

Rough rule of thumb for alkalosis?

A

Promotes K+ secretion (Type B cells)
*Hypokalemia and alkalosis

132
Q

The liver breaks down ammonia (toxic) to what nontoxic product?

A

Urea

133
Q

The kidney uses urea for what?

A

Regulation of concentration gradients in renal medulla necessary for maintaining urine concentration

134
Q

Where is 50% of urea passively reabsorbed?

A

PCT

135
Q

Where is urea secreted?

A

Descending limb of loop of Henle

136
Q

Where is urea reabsorbed, and where does ADH increase permeability of urea?

A

Reabsorbed in late DCT/CD
ADH inc. permeability of urea in CD

137
Q

How much total urea is excreted?

A

30-50% of filtered load

138
Q

What does the BUN test measure?

A

Amount of urea nitrogen in plasma

139
Q

What would a high BUN indicate?

A

Kidney pathology that decreases GFR (causing urea to accumulate in blood)

140
Q

What is azotemia?

A

High nitrogen in the blood

141
Q

What would a low BUN indicate?

A

Liver pathology that decreases urea synthesis

142
Q

What does the BUN/creatinine ratio compare?

A

BUN with serum creatinine

143
Q

Normal BUN/creatinine ratio?

A

Between 10:1 and 20:1

144
Q

What would a high BUN/creatinine ratio indicate?

A

Kidney pathology that decreases GFR or pathologies that decrease blood flow to kidneys
(ex. shock- not enough pressure to push blood through kidneys)

145
Q

How does the BUN/creatinine ratio still appear high when both BUN and creatinine increase?

A

Creatinine will still be secreted into PCT despite low GFR, so BUN will increase “more” than creatinine in blood

Net result: increased BUN/creatinine ratio

146
Q

What would a low BUN/creatinine ratio indicate?

A

Liver pathology or rhabdomyolysis (skeletal damage/necrosis)

146
Q
A
147
Q

In which low BUN/creatinine ratio disease will BUN decrease, while creatinine remains the same?

A

Liver pathology - synthesis of less urea while creatinine is still synthesized at same rate from the muscle

148
Q

In which low BUN/creatinine ratio disease will BUN remain the same, while creatinine increases?

A

Rhabdomyolysis - liver synthesizes same amount of urea while excess muscle breakdown releases excess amounts of creatinine into the plasma

Pathophysiology II Exam 2 Renal (5 decks)

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