Week 1 Flashcards
1
Q
Where are aquaporin 1 channels?
A
Proximal tubule
thin descending limb of loop of Henle
aquaporins allow for reabsorption of water
2
Q
Where does nephron first become impermeable to water?
A
ascending thin limb of loop of Henle
3
Q
Is the DCT permeable to water?
A
no
4
Q
Is the collecting tubule permeable to water?
A
only if ADH is present
5
Q
Where do efferent arteries flow into?
A
vasa recta / peritubular capillaries
these capillaries supply the nephron
6
Q
What is only part of nephron with brush border?
A
proximal tubule
7
Q
What is the thin descending tubule epithelium ?
A
simple squamous, no microvilli
8
Q
What is the thick ascending tubule epithelium ?
A
cuboidal epithelium
lots of tight junctions
low water permeability
9
Q
What structure of nephron has no villi?
A
distal convolute tubule
10
Q
What are 2 types of epithelia cells in collecting tubule?
A
principle cells (few microvilli)
intercalated cells (no cilia! surface micoplicae)
11
Q
List the glomerular capillary filtration barrier from inside out:
A
fenestrate capillary endothelium
glomerular basement membrane
podocyte (visceral epithelial cell)
12
Q
When are the peritubular capillaries called a vasa recta?
A
in a juxtamedullarly glomerulus
13
Q
juxtamedullarly glomerulus
A
located deep within the cortex
loop of henle dips into the medulla
14
Q
What are proximal tubular cells closely associated with? Why?
A
Closely associated with peritubular capillaries so that reabsorbed solute/water can easily go back into bloodstream
15
Q
Is reabsorption of solute in proximal tubule active or passive?
A
mostly active
Na/K/ATPase pump
16
Q
What happens when afferent arteriole is constricted?
A
GFR and RPF decrease so there is no change in filtration fraction
17
Q
What happens when efferent arteriole is constricted?
A
GFR stays the same
RPF decreases
increased filtration fraction (GFR/RPF)
18
Q
What happens to afferent/efferent arterioles in massive fluid loss?
A
afferent arteriole dilates and efferent arteriole constricts
want to maximize RPF/GFR
19
Q
Myogenic response
A
responding to BP / stretch
20
Q
When is RAAS activated?
A
in period of massive volume loss
21
Q
What does RAAS do to arterioles in volume loss?
A
AT2 causes efferent arteriolar constriction
afferent arteriole doesn’t constrict due to counteracting prostaglandin influence
22
Q
Increase NaCl causes macula densa to do what?
A
vasoconstrict afferent arteriole
23
Q
What is tubuloglomerular feedback?
A
macula densa sensing NaCl
24
Q
When are prostaglandins more important?
A
severe volume depletion
25
Where is ADH released from?
the pituitary gland
26
What is primary effect of ADH?
decreased water secretion
27
How much Na+ do we secrete daily?
0.4%
most Na+ is reabsorbed
28
Where does ENAC work?
principal cells of collecting duct
29
What does sodium reabsorption from ENaC cause?
negative potential that leads to secretion of potassium and hydrogen ions (from intercalated cells)
30
What happens to bicarbonate with excess aldosterone production?
increased H+ ion secretion leads to more bicarbonate being added to body
31
Where does aldosterone primarily act?
principal cells of collecting duct
32
When does ANP release increase?
if there is an increase in extracellular fluid volume
33
Where is 2/3 of sodium reabsorbed?
proximal tubule
34
Where is sodium not reabsorbed?
descending thin limb of loop of Henle
35
Where does ADH regulate water reabsorption?
the collecting tubule
36
Where is water flow passive?
in the proximal tubule
37
What is the main release factor for ADH?
plasma osmolarity
38
How do physicians assess extracellular fluid?
physical examination
39
How do physicians assess effective arterial circulating volume? When is this not helpful?
urine studies
not in CHF and cirrhosis
40
What is a good proxy for total body sodium?
Extracellular fluid volume (physical examination)
since sodium is tightly regulated, any increase in sodium will have increase in TBW
41
Angiotensin II effects
constricts both efferent and afferent arteriole
afferent arteriole constriction is counteracted by prostaglandins
efferent arteriole will therefore constrict more
angiotensin ALSO increases sodium reabsorption in the proximal tubule
42
What indicates activation of RAAS?
low urine sodium due to more sodium reabsorption due to activation of RAAS
43
What 2 conditions trigger ADH release?
1) reduced effective arterial volume
2) increased plasma osmolarity
44
Which diuretic commonly causes hyponatremia? Why?
thiazide diuretics
normal medullary osmotics that allows you to reabsorb lots of water without reabsorbing salt
45
Where do thiazide diuretics work?
Na-Cl cotransporter in DCT
46
When can loop diuretics cause hyponatremia?
if the patient is volume depleted
this will lead to high ADH levels being secreted and hyponatremia
47
What can happen with chronic loop diuretic use? What do you do about this?
distal tubule hypertrophy
use a thiazide to help
48
What does blocking aldosterone do?
aldosterone normally secretes K+/H+ and reabsorbs Na+
by blocking aldosterone, you decrease Na+ reabsorption and K+ secretion
49
What do you need to adjust for in CKD with diuretics?
in CKD, less blood is flowing through nephron
therefore, less drug will reach target site
need to increase the threshold dose of a drug
50
What happens to risk of hyperkalemia as CKD progresses?
risk goes up as GFR decreases
51
How can loop and thiazide diuretics cause hypokalemia?
there is increased Na+ flow to distal DCT due to blocking Na+ reabsorption downstream
this leads to increased ENaC reabsorption of Na+ which correspondingly pushes K+ out through ROMK channels
this will lead to more K+ excretion and hypokalemia
52
How do K+ sparing diuretics actually spare potassium?
since they work on the ENaC channels they prevent excretion of K+ through ROMK channels and spare K+
53
Diabetes insipidus
low ADH release leads to low volume
have dilute urine since you aren't retaining as much water (ADH not working)
54
Effects of bicarbonaturia on K+ secretion
Increased bicarb = increased K+ secretion
55
What 2 channels secrete potassium
ROMK
Maxi-K
55
Why do loop diuretics cause hypocalcemia?
by blocking Na-K-2Cl channels they prevent creation of positive gradient that normally drives calcium reabsorption
55
How can carbonic anhydrase inhibitors cause increased potassium secretion?
carbonic anhydrase inhibitors can cause bicarbonaturia
56
Where is ADH produced and secreted from?
produced from anterior hypothalamus
secreted from pituitary
57
What does renin lead to?
secretion of angiotensin II
58
What does angiotensin do?
constricts the efferent arteriole
59
When do you secrete renin?
when there is decreased sodium or water detected by baroreceptors
60
What does low urine sodium tell you?
RAAS is activated and blocking secretion of Na+
means that EACV is low cause RAAS is working
61
What is activated when EACV is low?
RAAS
62
What is activated when EACV is high?
ANA
63
What is a common fluid state in CHF / cirrhosis?
ECV is high but EACV is low
64
Where does angiotensin act on?
proximal tubule
65
Where are aquaporin 2 channels? What puts them there?
principal cells in collecting duct
ADH increases these channels
66
Where are H+ ATPase channels?
intercalculated discs of collecting ducts
secrete H+
67
What does hyponatremia indicate in CHF / cirrhosis?
the disease is advanced
there is low EACV
68
What is the filtration fraction?
GFR / RPF
69
Effects of RAAS on filtration fraction
RAAS increases filtration fraction by constricting the efferent arteriole
this leads to a decrease in RPF with no change in GFR
70
What does hypertonic saline infusion do to RAAS?
decreases RAAS since you don't need more sodium
71
How do diuretics work in theory?
increase secretion of Na+ which decreases ECF
72
What is a risk of carbonic anhydrase inhibitors?
increase bicarb excretion (less bicarb) can lead to acidosis
73
Differences between maxi-K and ROMK?
ROMK is only on principal cells; maxi-K on both types of cells
Maxi-K is flow mediated; ROMK is charge mediated
74
Aldosterone effects on potassium secretion
Increases potassium secretion through increased ENaC
75
Where specifically is carbonic anhydrase found?
on the brush border of PCT
76
What type of diuretic are you more likely to get kidney stones with?
loop diuretics
they decrease Ca2+ cotransport and increase calcium in urine which can cause kidney stones
77
Which type of diuretics can cause hypocalcemia?
loop diuretics
78
When should you give calcium for hyperkalemia?
only if there are associated ECG changes
79
what happens to ICF and ECF with hyptotonic solution?
both volumes increase
80
what happens to ICF volume if isotonic solution is given?
there is no change
no water movement since isotonic
81
what happens to ADH if isotonic solution is given?
ADH responds to changes in osmolarity primarily so there is no change here
82
what happens to RAAS if isotonic solution is given?
RAAS will decrease since you have more EACV
83
What does hypertonic solution do to ADH?
increases ADH since we want to keep more water to balance the increase in solute
84
What are the 3 barriers that regulate flow through the glomerulus?
1) Podocytes
2) Basement membrane
3) Fenestrations in capillaries
85
Where the the juxtaglomerular apparatus? What does it include?
along the distal tubule at vascular pole
includes macula densa, JG cells and extraglomerular mesangial cells
86
How can you determine proximal vs. distal tubules?
Proximal have brush border and are thicker
87
What can thiazide and loop diuretics cause in terms of acid/base ?
alkalosis
88
What does high urine osmolality indicate? What does high urine sodium indicate?
High urine osmolality = ADH active (stopping excretion of water)
High urine sodium = RAAS active (water is being reabsorbed)
89
How do we calculate V when given a single volume?
you normally assume this is a daily urine volume and divide by 1440 minutes in a day
90
How do we define hyponatremia with lab values?
PNa < 135 mEq/L
91
Where can SIADH anatomically arise from?
posterior pituitary or lung problem
92
What drugs can often cause SIADH?
SSRI
93
When do we worry about hyponatremia?
when PNa < 125
at this level, you are going to start seeing intracranial swelling and CNS symptoms
94
What do we worry about when treating hyponatremia?
that we could potentially cause osmotic demyelination syndrome
95
When muscle mass is low, what happens to eGFR if we use creatinine?
overestimated GFR
96
What does estimate of ECF largely come from?
physical exam!
97
What is treatment for hyponatremia caused by polydipsia?
fluid restriction
98
What is treatment for heart failure / cirrhosis hyponatremia?
fluid restriction, loop diuretics, V2 receptor antagonists (-vaptans)*, urea*
*do not use vaptans / urea in cirrhosis
99
What medications can you use for hyerkalemia?
albuterol
insulin / glucose
bicarbonate
potassium binding resins
100
Why do we use urea to treat SIADH?
urea acts as an osmotic diuretic and will increase water secretion
101
Why do we use vaptans in SIADH?
block V2 receptors for ADH
*they are expensive and hepatotoxic*
102
Why do we use loop diuretics in SIADH?
loop diuretics secrete diluted urine which leads to more water than Na+ loss
103
Where is potassium primarily secreted NOT reabsorbed?
cortical collecting duct
104
What 2 factors does ADH primarily EFFECT?
water and urea reabsorption
105
peaked T-wave indicates ...
hyperkalemia
106
prominent U-wave indicates ...
hypokalemia
107
does hypokalemia or hyperkalemia cause a decreased response to ADH?
hypokalemia
108
What are RBC casts in urine associated with?
glomerular basement membrane damage
109
What can raise BUN?
high protein intake
glucocorticoids
110
Is urea clearance more or less than true GFR?
less than true GFR since some is reabsorped
111
What is PAH's relation to GFR? PAH?
approximates RPF
overestimates GFR
112
In a steady state what is true of a solute?
excretion = secretion
113
