Renal Module II Flashcards
1
Q
The glomerulus filters everything into Bowman’s space except what?
A
RBC/WBC, most proteins & fats
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
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
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
5
Q
How much reabsorption happens in the PCT?
A
60-90% of everything that was filtered
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
7
Q
What is secreted by the PCT?
A
Creatinine
Urea, ammonia
H+
Meds/drugs
Uric acid
8
Q
Are there any significant dilute/concentration changes in the PCT?
A
No
9
Q
What does the descending limb of the loop of Henle reabsorb?
A
Water
10
Q
What does the descending limb of the loop of Henle secrete?
A
Urea (plays role in urine concentration gradients)
11
Q
Are there any significant dilute/concentration changes in the descending limb of the loop of Henle?
A
Yes, concentrates tubular fluid
12
Q
What does the thick ascending limb of the loop of Henle reabsorb?
A
Sodium, potassium, chloride
13
Q
What does the thick ascending limb of the loop of Henle secrete?
A
Nothing
14
Q
Are there any significant dilute/concentration changes in the thick ascending limb of the loop of Henle?
A
Yes, dilutes tubular fluid
15
Q
What does the early DCT segment reabsorb?
A
Sodium, calcium
16
Q
What does the early DCT segment secrete?
A
Nothing
17
Q
Are there any significant dilute/concentration changes in the early DCT segment?
A
Yes, dilutes tubular fluid
18
Q
What does the late DCT segment reabsorb?
A
Water, sodium, bicarbonate, urea
19
Q
What does the late DCT segment secrete?
A
H+, potassium, ammonia
20
Q
Are there any significant dilute/concentration changes in the late DCT segment?
A
Yes, concentrates tubular fluid
21
Q
What is the central force in driving PCT reabsorption?
A
Sodium/potassium pump: actively pumps sodium from PCT cell into plasma
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
23
Q
PCT reabsorbs how much glucose & amino acids?
A
100%
24
Q
PCT reabsorbs how much bicarbonate?
A
80-90%
25
PCT reabsorbs how much water, sodium, potassium, and chloride?
65%
26
PCT reabsorbs how much urea?
50%
27
Pathway for PCT to reabsorb water?
Na+ concentration gradients formed by active sodium/potassium pump promote water diffusion (osmosis) into bloodstream
28
What structures of the PCT cell allow for osmosis of H2O into the PCT cell/plasma?
Aquaporins
29
What further promotes ion reabsorption in the PCT?
Increased concentration of tubular fluid
30
How does the PCT create Na+ concentration gradients?
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
31
How do lipid-soluble substances diffuse across the PCT membrane?
transcellular route
32
How do various ions (Cl-, Ca2+, and K+) and urea diffuse across PCT membrane?
paracellular route
33
What is the major regulator of extracellular fluid volume (ECF)?
NaCl balance
34
Early PCT pathway for sodium reabsorption?
Sodium reabsorption is coupled with many filtrates (glucose, amino acids, etc.), and H+ secretion
35
Late PCT pathway for sodium reabsorption?
Sodium is reabsorbed w/ chloride as NaCl, also reabsorbed coupled w/ H+ scretion
36
What influences Na+ reabsorption in the PCT?
Hormones
37
What are the stimuli which increase NaCl reabsorption in the PCT?
Angio II, endothelin, smpathetics
38
What are the stimuli which decrease NaCl reabsorption in the PCT?
Natriuretic peptides (ANP, BNP, etc.)
39
What is necessary for reabsorption of bicarb in the PCT?
Na+/H+ exchange
40
Pathway for Bicarb reabsorption in the PCT?
-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
41
What inhibits bicarbonate reabsorption in the PCT?
Diuretics (carbonic anhydrase inhibitors)
42
What happens in the PCT if diuretics present?
-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
43
Diuretics effect on acid-base balance?
Potential disruption due to plasma bicarb decreasing/becoming more acidic and urine bicarb increasing/becoming more alkaline
44
How is glucose reabsorbed in the PCT?
-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
45
Glucose transport in the PCT is limited by what?
of available cotransport carriers
46
What happens to the PCT if there is too much glucose in the plasma/hyperglycemia?
PCT cannot keep up with reabsorption and "glucose dumping" begins to occur
47
What are SGLT2 inhibitors?
Hypoglycemic medications that inhibit reabsorption of glucose to treat diabetes
48
What is the secondary benefit of SGLT2 inhibitors?
Antihypertensive benefit: inhibit sodium reabsorption/promote natriuresis and diuresis
49
What is the glucose transport maximum in the PCT?
Maximum rate a substance can be transported across PCT cell wall
50
What plasma glucose levels correspond with transport maximum of glucose in the PCT?
350 mg/dL
51
What is the glucose renal threshold (diabetes/hyperglycemia)?
Plasma values when glucose first appears in the urine (glucose dumping)
52
At what plasma glucose levels does glucose dumping begin to occur in urine?
180-200 mg/dL
53
What does the PCT secrete?
H+, small amount of creatinine, urea, ammonia/ammonium, meds/drugs, uric acid
54
How much H+ is secreted by the PCT?
Large amounts of H+ ions secreted when reabsorbing bicarbonate
55
How is there no net loss of H+ ions from the PCT?
The H+ ions get recycled
56
When does H+ secretion/excretion occur?
"Later" in the cells of the late DCT segment/collecting duct
57
How is creatinine formed?
Metabolic breakdown of creatinine phosphate in muscle, produced by body at a predictable rate
58
How is creatinine filtered through the glomerulus?
Freely
59
Is creatinine reabsorbed in the nephron?
No
60
How much creatinine is secreted in the PCT?
A small amount
61
How is ammonia/ammonium secreted by the PCT?
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
Ammonium is eventually excreted from the nephron as part of what?
Acid-base regulation
63
What is acute tubular necrosis (ATN)?
Nephron obstruction due to cell damage of PCT and other regions of nephron (may lead to necrosis if severe)
64
What is acute tubular necrosis (ATN) caused by?
-Ischemia (hypotension/hypovolemic states)
-Toxins (drugs such as aminoglycosides, sulfa drugs, acyclovir, etc.)
-Endotoxins (myoglobin and hemoglobin
-Sepsis
65
What do ischemia/toxins cause in ATN?
Acute kidney injury (cell damage to PCT and other regions)
Breakdown of epithelial cells-->form casts/possible nephron obstruction
66
Urinalysis for ATN?
Muddy brown appearing urine from casts of epithelial cells
67
Treatment for ATN?
Focused on underlying cause, prognosis dependent on underlying condition
68
Loop of Henle has a critical role in what?
Regulating urine concentration
69
How does the descending loop of Henle concentrate the filtrate?
Reabsorbs water & leaves behind electrolytes in descending loop lumen
*osmolarity of tubular fluid increases as it descends in loop
70
How does the thick ascending loop (TAL) of Henle dilute the filtrate?
Reabsorbs sodium & other electrolytes
*osmolarity of tubular fluid decreases in the TAL
71
Urine concentration in the PCT?
300 mOsm
72
Urine concentration in the start of the loop of Henle?
300 mOsm
73
Urine concentration in the descending portion of the loop of Henle?
Gradual increase to 1,200 mOsm at the bottom
74
Urine concentration in the thick ascending portion (TAL) of the loop of Henle?
Gradual decrease to 100-200 mOsm
75
Urine concentration in the early DCT segment?
Continues to dilute: 100 mOsm
76
Urine concentration in the late DCT segment?
Begins to concentrate: 150 mOsm
77
Urine concentration in the start of the collecting duct?
150 mOsm
78
Finished urine concentration in the collecting duct?
Concentrated: 1,200 mOsm
or
Diluted: 100-200 mOsm
*dependent on the body's needs
79
Is the descending limb permeable to water?
Yes - allows water to be reabsorbed, but not sodium/other electrolytes
80
What reabsorption does the narrow portion of the ascending limb of the Loop of Henle?
Passive sodium/chloride reabsorption
81
What does the thick ascending limb (TAL) of the loop of Henle reabsorb?
Na+, Cl-, K+ and other electrolytes (HCO3-, Ca2+, Mg+)
82
What is Na+ co-transported with in the thick ascending limb (TAL) of the loop of Henle?
Chloride (Cl-) and K+
83
What does co-transport of Na+/Cl-/K+ create in the TAL of the loop of Henle?
Electrical potential gradient that promotes passive diffusion of Na+, K+, Ca2+, Mg2+
84
The TAL reabsorbs how much of filtered sodium/filtered bicarb?
25% of sodium
20% of bicarb
85
Is the TAL of the loop of Henle permeable to water?
No - water remains in the TAL lumen and osmolarity decreases/dilutes as fluid ascends
86
What do loop diuretics inhibit?
Na+/K+/Cl- co-transport in the TAL
Also inhibit calcium reabsorption
87
Reduced sodium reabsorption in the TAL due to loop diuretics promotes what?
Diuresis, Natriuresis, Potassium excretion (potential for hypokalemia)
88
What can be used to offset potassium loss in the TAL?
Potassium sparing diuretics or potassium supplementation
89
What is a potential risk of loop diuretics inhibiting Ca2+ reabsorption?
Hypocalcemia
90
What can be used as a potential treatment for hypercalcemia ?
Loop diuretics and IV saline fluids
(Loop diuretics inhibit Ca2+ absorption)
91
Is the early segment of the DCT permeable to water/sodium?
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
How much filtered sodium is absorbed in the early segment of the DCT?
~5%
93
How is sodium transported in the early DCT?
From lumen to DCT cell by NaCl co-transport mechanism
94
How much filtered calcium is absorbed in the early DCT?
~10%
95
What stimulates calcium reabsorption in the early DCT?
PTH and estrogen
96
What do thiazide diuretics inhibit?
Na/Cl co-transport in the early DCT,
promote diuresis and natriuresis
97
What can thiazide diuretics potentially cause?
Hypercalcemia (disrupt calcium reabsorption), Hypokalemia, metabolic alkalosis
98
How can thiazide diuretics potentially cause hypokalemia and metabolic alkalosis?
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
What may be used w/ thiazide diuretics to offset potassium loss?
K+ sparing diuretics
100
How do K+ sparing diuretics work?
Inhibit K+/Na+ exhange in late DCT/CD --> less K+ secretion and less sodium reabsorption
101
Functions of the late DCT/CD?
-Regulate final urine conc. (urea resorption, Na+/water resorption)
-Regulate acid-base homeostasis
-Regulate potassium homeostasis
102
Two types of cells in late DCT/CD?
Principal cells and intercalated cells
103
Role of principal cells in late DCT/CD?
Reabsorb sodium and water, secrete potassium
104
Role of Type A intercalated cells (A-IC) in late DCT/CD?
During acidosis: secrete H+ ions and reabsorb HCO3- and K+
*maintenance of acid-base homeostasis
105
Role of Type B intercalated cells (B-IC) in late DCT/CD?
During alkalosis: reabsorb H+ ions and secrete HCO3- and K+
*maintenance of acid-base homeostasis
106
What stimulates principal cells of late DCT/CD to reabsorb sodium and secrete potassium? How?
Aldosterone
Stimulates Na+/K+ pump to:
-transport sodium from DCT/CD cells into bloodstream
-transport potassium from bloodstream into DCT/CD cells
107
What can inhibit aldosterone and therefore inhibit K+ secretion/Na+ reabsorption from principle cells in the DCT/CD?
K+ sparing diuretics
108
What stimulates principal cells of late DCT/CD to reabsorb water?
ADH
109
What are aquaporins? What is the effect of ADH on aquaporins?
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
Water reabsorption in late DCT/CD is regulated by what?
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
Amount of secretion of H+ and absorption of HCO3-/K+ that occurs in late DCT/CD depends on what?
Acid-base status of plasma
112
How do type A intercalated cells (A-IC) regulate acid-base balance in late DCT/CD?
Very active in regulation of H+, HCO3-, K+ when plasma is acidotic
113
How do type B intercalated cells (B-IC) regulate acid-base balance in late DCT/CD?
Very active in regulation of H+, HCO3-, K+ when plasma is alkalotic
114
Mechanism of Type A intercalated cells in acidosis?
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
How is hyperkalemia associated with acidosis?
Kidneys: type A cells promote potassium reabsorption
Tissues/ECF: H+ flows into cells, K+ flows out of cells into plasma
116
Mechanism of Type B intercalated cells in alkalosis?
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
How is hypokalemia associated with alkalosis?
Kindeys: Type B cells promote K+ secretion
118
How much filtered sodium is reabsorbed in the PCT?
67%
119
What inhibits HCO3- reabsorption in the PCT?
Carbonic anhydrase inhibitors via the Na+/H+ pathway
120
Is sodium reabsorbed in the descending limb of the loop of Henle?
No
121
How much sodium is absorbed in the ascending limb (TAL) of the loop of Henle?
25%
122
How much sodium is reabsorbed in Early DCT?
5%
123
How much sodium is absorbed in late DCT/CD?
3%
124
How much potassium is reabsorbed in the PCT?
60-70%
125
Is potassium reabsorbed in the descending limb of the loop of Henle?
No
126
How much potassium is absorbed in the ascending limb (TAL) of the loop of Henle?
25%
127
Is potassium reabsorbed in early DCT?
No
128
Which cells secrete potassium via sodium/potassium pump in the late DCT/CD?
Principal cells
129
Which cells have a sum of potassium activity that has less effect compared to principle cells, yet can still alter potassium homeostasis?
Intercalated cells: Type A & B
130
Rough rule of thumb for acidosis?
Promotes K+ reabsorption (Type A cells)
*Hyperkalemia and acidosis
131
Rough rule of thumb for alkalosis?
Promotes K+ secretion (Type B cells)
*Hypokalemia and alkalosis
132
The liver breaks down ammonia (toxic) to what nontoxic product?
Urea
133
The kidney uses urea for what?
Regulation of concentration gradients in renal medulla necessary for maintaining urine concentration
134
Where is 50% of urea passively reabsorbed?
PCT
135
Where is urea secreted?
Descending limb of loop of Henle
136
Where is urea reabsorbed, and where does ADH increase permeability of urea?
Reabsorbed in late DCT/CD
ADH inc. permeability of urea in CD
137
How much total urea is excreted?
30-50% of filtered load
138
What does the BUN test measure?
Amount of urea nitrogen in plasma
139
What would a high BUN indicate?
Kidney pathology that decreases GFR (causing urea to accumulate in blood)
140
What is azotemia?
High nitrogen in the blood
141
What would a low BUN indicate?
Liver pathology that decreases urea synthesis
142
What does the BUN/creatinine ratio compare?
BUN with serum creatinine
143
Normal BUN/creatinine ratio?
Between 10:1 and 20:1
144
What would a high BUN/creatinine ratio indicate?
Kidney pathology that decreases GFR or pathologies that decrease blood flow to kidneys
(ex. shock- not enough pressure to push blood through kidneys)
145
How does the BUN/creatinine ratio still appear high when both BUN and creatinine increase?
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
What would a low BUN/creatinine ratio indicate?
Liver pathology or rhabdomyolysis (skeletal damage/necrosis)
146
147
In which low BUN/creatinine ratio disease will BUN decrease, while creatinine remains the same?
Liver pathology - synthesis of less urea while creatinine is still synthesized at same rate from the muscle
148
In which low BUN/creatinine ratio disease will BUN remain the same, while creatinine increases?
Rhabdomyolysis - liver synthesizes same amount of urea while excess muscle breakdown releases excess amounts of creatinine into the plasma
