Exam 3 Flashcards
(389 cards)
1
Q
4 ways that solute moves across membranes
A
diffusion, facilitated diffusion, active transport, & secondary active transport
2
Q
Describe simple diffusion
A
w/ conc gradient
passive
membrane must be permeable to solute
continues until equilibrium
3
Q
What increases the rate of (simple & facilitated) diffusion
A
larger gradient & a more permeable membrane
4
Q
Ex of simple diffusion
A
paracellular reabsorption of Cl- in late proximal tubule
5
Q
What is the membrane permeable to
A
lipid soluble & sm polar molecules
6
Q
What is the membrane impermeable to
A
charged & lg polar molecules
7
Q
Describe facilitated diffusion
A
w/ conc gradient passive membrane is not permeable to solute utilizes transporters/ pores continues until equilibrium
8
Q
Ex of facilitated diffusion
A
Na+, K+, & Cl- transport via NKCC1 in macula densa to monitor glomerular filtration
9
Q
Describe active transport
A
against conc gradient active transporter moves solute across membrane transporter itself hydrolyzes ATP does not continue until equilibrium
10
Q
Ex of active transport
A
movement of Na+ at basolateral membrane of proximal tubule by Na+K+ATPase
(occurs in other nephron sections)
11
Q
Describe secondary active transport
A
against conc gradient active transporter moves solute across membrane uses potential energy generated by ATP-dependent processes elsewhere in the cell does not continue until equilibrium
12
Q
Ex of secondary active transport
A
movement of glucose & amino acids at the luminal membrane of the proximal tubule
both moved against conc gradient into the cell
energy from Na+ moving w/ conc gradient into the cell via the same transporter
Na+ gradient was established by Na+K+ATPase burnig ATP
13
Q
1 way solvent moves across membrane
A
osmosis
14
Q
Define osmosis
A
movement of water across a semi-permeable membrane from a dilute to a concentrated solution
15
Q
For there to be osmosis, what has to happen
A
whatever solute creates the difference in water cannot move across the membrane
16
Q
What does an ineffective osmole do
A
if membrane is soluble to solute, then
solute diffuses until its equillibrium is met
creates two solutions of equal water conc
17
Q
What does an effective osmole do
A
if membrane is not soluble to solute, then
solute cannot diffuse across the membrane
creates a diffference in water conc to drive osmosis
18
Q
What is molarity/molality used to define
A
conc of a solution (in terms of solute)
19
Q
Molarity/molality is the driving force for what
A
solute
20
Q
Molarity units
A
mol/L
21
Q
Molality units
A
mol/kg
22
Q
What is osmolarity/osmolality used to define
A
conc of a solution (in terms of solvent)
23
Q
Osmolarity/osmality is the driving force for
A
water
24
Q
Osmolarity units
A
conc of osmotically active solute/L
25
Omolality units
conc of osmotically active solute/kg
26
NaCl would equal how many osmoles & why
2 osmoles
| b/c NaCl dissociates into two potentially osmotically active osmoles
27
Water moves in what direction in terms of osmolarity
from low to high osmolarity
28
Tonicity defines what
conc of effective osmoles in a solution
29
Can tonicity be expressed numerically
no, only comparitively
30
A hypertonic solution has what
higher effective osmolarity than another
31
A isotonic solution has what
equal effective osmolarity as another
32
A hypotonic solution has what
lower effective osmolarity than another
33
Location of kidneys
dorsal
slightly posterior in lumbar region
retroperitoneally located
34
Comparison of left vs right kidneys
righty high & tighty
| lefty low & loosy
35
Kidney shape in cats, dogs, sheep, & goats
kidney bean
36
Kidney shape in pigs
squashed w/ poles stretched
37
Kidney shape in equine
larger & heart-shaped
38
Kidney shape in cattle
deeply fissured & scalloped; brain-shaped
39
Components of kidney capsule
collagen membrane w/ smooth muscle (elasticity)
40
Capsule is important for
structural integrity of kidney
41
Hilum is what
cleft where renal artery enters & renal vein/ureter leave
42
Describe cortex (in comparison to medulla)
darker staining
cells have more cytoplasm
more extensive vasculature
43
Describe medulla (in comparison to cortex)
lighter staining
more interstitial fluid
high osmolarity
44
Location of renal pyramid
base in outer cortex
| apex in inner medulla
45
Renal pyramids fuse in some species to form
renal crest
46
Renal papilla is what
apex of renal pyramids
47
Renal pelvis functions as
funnel that collects urine
48
Color & location of renal pelvis
off-white
| at center of kidney
49
Renal pelvis is an extension of what
ureter
50
Parts of nephron found in cortex
```
renal corpuscle
proximal convoluted tubule
proximal straight tubule
(later) part of distal straight tubule
distal convoluted tubule
(earlier) part of collecting duct
```
51
Parts of nephron found in medulla
loop of henle
(earlier) part of distal straight tubule
(later) part of collecting duct
52
What is found in the cortical labyrinth of the cortex
renal corpuscle
proximal convuluted tubule
distal convoluted tubule
53
What is found in the medullary rays of the cortex
proximal straigh tubules
distal straight tubules
collecting ducts
54
What is found in the outer medulla
loops of henle
distal straight tubule
collecting ducts
55
What is found in the inner medulla
collecting ducts
56
Microscopic distal tubule
touches vascular part of glomerulus
| includes macula densa
57
Microscopic afferent/efferent arteriole
cannot differentiate b/w them
| smooth muscle at vascular pole of glomerulus
58
Microscopic glomerulus
bundle of capillaries
| lumens of blood vessels & some RBCs
59
Intraglomerular mesangial cells function
support capillaries
| contractile & phagocytic
60
Extraglomerular mesangial cells function
support capillaries
| renin-angiotensin system
61
Microscope intraglomerular mesangial cells
found inside glomerulus
62
Microscope extraglomerular mesangial cells
found outside glomerulus
| near vascular pole
63
Urinary space function
where filtrate emerges
64
Microscope urinary space
surrounds glomerulus
65
Microscope Bowman's capsule
thin squamous epithelium surrounding glomerulus
66
Parietal layer of Bowman's capsule
does not touch capillaries
67
Visceral layers of Bowman's capsule
touches capillaries
68
Visceral layer of Bowman's capsule is adapted into a layer of
podocytes
| help w/ filtration
69
Urinary pole of renal corpuscle
where proximal tubule leaves
70
Vascular pole of renal corpuscle
where afferent arteriole enters & efferent arteriole leaves
close to distal tubule
71
Secondary processes of podocytes are called
pedicels
72
Pedicels do what structurally
wrap around capillaries
| interdigitate w/ other phagocytes/ pedicels
73
Components of filtration apparatus
fenestrated capillary
basal lamina of visceral layer
slit diaphragm
74
Fenestrated capillary has what that acts as what
pores
| filter/sieve
75
Basal lamina of visceral layer is secreted by
podocytes/pedicels
76
Lamina densa externa & interna are composed of what
laminin, fibronectin, & polyanions
77
Lamina densa rara is composed of what
collagen
78
Slit diaphragm is what & secreted by what
protein sheet full of holes
| podocytes
79
Structure of proximal tubule
tall cuboidal epithelium
thick brush border of microvilli
caniculi
80
Proximal tubule has what features in the cytoplasm of the epithelial cells
many mitochondria
| lysozymes
81
Lysozymes do what
break up what is absorbed
82
Shape & location of nuclei in proximal tubule
spherical
| central & basolateral
83
Function of proximal tubule
active reabsorption
84
Does proximal or distal tubule have a larger diameter
proximal
85
Structure of loop of henle
simple squamous epithelium
| few microvilli
86
Loop of henle has what features in the cytoplasm of the epithelial cells
few mitochondria
87
Descending limb of loop of henle is permeable/impermeable to what
permeable to water
| impermeable to Na+
88
Ascending limb of loop of henle is permeable/impermeable to what
permeable to Na+
| impermeable to water
89
Function of loop of henle
passive reabsorption
90
Structure of distal tubule
low cuboidal epithelium
| minimal brush border of microvilli
91
Distal tubule has what features in the cytoplasm of the epithelial cells
fewer mitochondria
| straight tubule has more mitochondria than convoluted tubule
92
Shape & location of nuclei in distal tubule
oval
| apical
93
How does the permeability of the early & late distal tubule vary
early distal tubule is always impermeable to water
| late distal tubule is permeable to water only w/ a diurectic
94
Function of distal tubule
active reabsorption
95
Does the proximal or distal tubule have stronger reabsorption
proximal tubule
96
Where are collecting tubules found
from outer cortex to renal papillae
97
Features of collecting tubules as they move deeper into the medulla
empty into each other
| increase in diameter
98
Cells of cortical part of collecting duct & their features
principal cells w/ microvilli & mitochondria
| intercalated cells w/ more mitochondria; extend past principal cells
99
Function of principal cells
minimal active reabsorption
100
Function of intercalated cells
active reabsorption
101
Type A intercalated cells function
excrete H+ & resorb HCO3-
| help w/ K+ reabsorption
102
Tybe B intercalated cells function
excrete HCO3- & resorb H+
103
Medullary part of collecting duct has what cells
outer has both principal & intercalated cells
| inner has only principal cells
104
Papillary part of collecting ducts has what cells
only principal cells
105
Collecting ducts are impermeable to what
water
| unless diurectic is present
106
Size of cells in collecting duct in comparison to other parts of the nephron
in b/w proximal & distal tubule
107
Shape & location of nuclei in collecting ducts
oval (large)
| near lumen or central
108
Unique feature of nuclei in collecting ducts
halo
| due to cytoplasm not being dense
109
Do collecting ducts have a brush border
no
110
Function of collecting ducts
varying degrees of active reabsorption
111
Function of juxtaglomerular apparatus
samples tubule constituents & feedbacks onto glomerulus to change filtration rate
112
Macula densa is located where
at junction of straight & convoluted distal tubules
113
The macula densa is a specialized patch of cells that are
densely packed
tall
no basal lamina
114
Extraglomerular mesangial cells do what in relation to the juxtaglomerular apparatus
receive signal from macula densa
| pass signal to juxtaglomerular cells
115
Juxtaglomerular cells are specialized what
smooth muscle cells full of granular renin inclusions
116
Function of ureter
convey urine from kidney to bladder via peristalsis
117
Special epithelium of urinary system is what & has what features
transitional epithelium
| protection & distension
118
Lamina propria is what
fibrous connective tissue covered by mucosa
119
Mucosa serves as a layer b/w what
acidic urine & tissues
120
Mucosa is what when the structure it covers is full
not folded
121
Are there mucus glands in the mucus of the ureter
no
122
Ureter has how many layers of lamina propria
one
123
What are the smooth muscle layers of the ureter
1- outer circular layer
2- inner longitudinal layer
3- near bladder, additional outer longitiduinal layer
124
Structure of adventitia
outer fibrous coat
125
Function of adventitia
elasticity & protection
126
Function of bladder
muscular & elastic bag that stores urine
127
Bladder has how many layers of lamina propria
two
128
What are the smooth muscle layers of the bladder
1- thin inner longitudinal layer
2- thick middle circular layer
3- thin outer longitudinal layer
129
Smooth muscle layers of bladder are collectively called
dextrusor muscle
130
What is the internal sphincter of the bladder
thickening of middle circular layer of dextrusor
| smooth muscle
131
Function of internal sphincter
contracted during 1st phase of micturition
| involuntary
132
What is the external sphincter of the bladder
skeletal muscle
133
Function of external sphincter
voluntary
134
Function of urethra
conveys urine from bladder during voiding
135
Features of urethra lamina propria
large & porous
136
Are there mucus glands in the mucus of the urethra
yes, called glands of Littre
137
What are the smooth muscle layers of the urethra
1- inner circular layer
2- outer longitudinal layer
3- inner longitudinal layer that is lost as urethra leaves the bladder
138
Dominant layer of smooth muscle
circular layer
139
How do fenestrated capillaries filter on the basis of size
hold back RBC & plasma proteins > 3.6 nm in diameter (like albumin)
140
How do fenestrated capillaries filter on the basis of charge
laminin & fibronectin (polyanionic glycoprotein glycocalyx) repel neg molecules
141
How does the lamina rara filter on the basis of size
densa-> holes in nephrin (collagenous protein) let molecules < 2 nm pass easily while molecules > 4 nm are excluded completely
142
How does the lamina rara filter on the basis of charge
interna/externa-> laminin, fibronectin, & heparan sulfate (polyanionic non-collagenous proteins) repel neg charged molecules
143
How does the slit diaphragm filter on the basis of size
holes in nephrin (collagenous protein) let molecules < 2 nm pass easily while molecules > 4 nm are excluded completely
144
How does the slit diaphgram filter on the basis of charge
supporting podocytes (covered in polyanionic glycoportein glycocalyx) repel neg charged molecules
145
The ultrafiltrate is described as being what due to the filtration apparatus
mostly protein free
146
Describe how a neutral molecule/protein would get through the filtration apparatus
large molecules have difficulty crossing due to size
147
Describe how a cationic molecule/protein would get through the filtration apparatus
large molecules have difficulty crossing due to size
| more molecules get through compared to a neutral molecule since the neg charge of the filtration barrier attracts them
148
Describe how an anionic molecule/protein would get through the filtration apparatus
large molecules have difficulty crossing due to size
| less molecules get htrough compared to a neutral molecule since the neg charge of the filtration barrier repels them
149
Some proteins get through the filtration barrier, but how good is the nephron at reabsorbing them
not good
150
A non-functioning kidney would have what distinct clinical sign
protein lost in the urine
151
Name 4 Starling's forces
hydrostatic pressure of capillaries & Bowman's space (denoted w/ P)
oncotic pressure of capillaries & Bowman's space (denoted w/ π)
152
What is oncotic pressure
osmotic pressure caused by colloids
153
Hydrostatic pressure of capillaries (Pc) is due to
(pushes out)
blood pressure in capillaries pushes out
generated by resistance difference b/w afferent & efferent arterioles in combination w/ pressure of blood due to left ventricular contraction
154
Hydrostatic pressure of Bowman's space (Pbs) is due to
(pushes in)
| fluid in Bowman's space pushes against the walls of the glomerulus
155
Oncotic pressure of capillaries (πc) is due to
(pushes in)
| protein in capillaries generate an osmotic pull of fluid into the capillaries
156
Oncotic pressure of Bowman's space (πbs) is due to
(pushes out)
| small amount of protein in Bowman's space that exerts a negligible osmotic pull
157
What is the largest Starling's force that drive filtration
Pc
158
Is filtration higher at the efferent or afferent end
afferent
159
Why does Pc decrease at the efferent end
some energy has been used up
160
Why does πc increase at the efferent end
plasma has left the capillaries
| colloids have stayed
161
If blood can enter glomerulus more easily than it can leave it, then
Pc increases
| GFR increases
162
What causes Pc & GFR to increase
dilated afferent arterioles
| constricted efferent arterioles
163
If blood can leave the glomerulus more easily than it can enter it, then
Pc decreases
| GFR decreases
164
What causes Pc & GFR to decrease
dilated efferent arterioles
| constricted afferent arterioles
165
What is Kf
area available for filtration * permeability of the membrane
166
Heartworm affects Kf how
reduces filtration area
reduced Kf & GFR
kidney failure
167
Changes in Pc result from
systemic hyperextension or pre-renal obstruction
168
What happens to Pc & GFR in acute renal failure
Pc decreases due to impaired renal perfusion
| thus, GFR decreases
169
Relationship b/w Pc on GFR is indirect or direct
direct
170
Relationship b/w πc & Pbs on GFR is indirect or direct
indirect
171
What would affect πc
plasma protein levels increasing (increased πc & decreased GFR)
plasma protein levels decreasing (decreased πc & increased GFR)
172
During liver impairment, what is the effect on πc
πc decreases
| thus, GFR increases
173
Obstructions (uroliths or plugs) do what to Pbs
Pbs increases
| thus, GFR decreases
174
Uroliths or plugs occur can lead to
acute renal failure
175
Autoregulation has what functions
prevents fluctuations in bp to protect the delicate glomeruli from being slammed due to spikes in bp
prevents changes in Pc that would affect GFR by controlling bp in order to control the amount of filtrate sent to the tubules
176
Renal autoregulation works in what range
80-180 mmHg
177
Trigger for myogenic mechanism
fluctuations in bp change transmural pressure in afferent arteriole
178
Function of myogenic mechanism
protective
| prevents damage to glomeruli caused by spiking bp
179
Increased bp causes what response in myogenic mechanism
vasoconstriction of afferent arteriole & decreased blood flow to the glomerulus
180
Decreased bp causes what response in myogenic mechanism
vasodilation of afferent arteriole & increased blood flow to glomerulus
181
Speed of myogenic mechanism
rapid changes (1-2 sec) in response to rapid bp changes
182
Trigger for tubuloglomerular mechanism
fluctuations in bp change GFR, meaning distal tubule fluid composition is altered
183
Function of tubuloglomerular mechanism
regulatory
| prevents a change in GFR
184
Speed of tubuloglomerular mechanism
slow changes (10-12 sec) in response to slower bp changes
185
Steps of tubuloglomerular filtration to reduce GFR when bp is high
1) increased Na+, K+, & Cl- sensed by NKCC2 on apical surface of macula densa
2) macula densa releases ATP and/or adenosine
3) ATP/adenosine activate receptors on extraglomerular mesangial cells
4) increased intracellular Ca2+ in extraglomerular mesangial cells cause same response in afferent arteriole smooth muscle & juxtaglomerular cells
5) afferent arteriole smooth muscle contracts
6) juxtaglomerular cells inhibited from releasing renin
186
Steps of tubuloglomerular filtration to increase GFR when bp is low
1) decreased Na+, K+, & Cl- sensed by NKCC2 on apical surface of macula densa
2) macula densa releases PGE2
3) PGE2 causes afferent arteriole dilation & stimulates juxtglomerular cells to release renin, which then increases angiotensin II
4) angiotensin II in bloodstream
187
As a result of tubuloglomeralr filtration functioning to increase GFR when bp is low, what does angiotensin II in the bloodstream do
- causes systemic vasoconstriction
- preferentially contracts efferent over afferent arteriole
- increases PGE2 production from macula densa
- negatively feedbacks onto contralateral kidney to stop renin release
188
Nephron reabsorption forms what
ultrafiltrate carried in the lumen
189
What is contained in the ultrafiltrate
waste & important molecules
190
Important molecules in tubular fluid moves across the epithelial lining of the nephron & into where
bloodstream via peritubular capillaries
191
Reverse process of reabsorption is
secretion
192
What is secretion
waste sent from blood into nephron
| forms urine
193
Describe the trancellular route
reabsorption through cytoplasm of tubular cells
194
Is trancellular route active or passive transport
active & passive transport
195
Describe the paracellular route
reabsorption b/w tubular cells across tight junctions
196
Is paracellular route active or passive transport
passive transport
197
What is the key molecule for reabsorption
Na+K+ATPase
198
Tonicity of ultrafiltrate from glomerulus/Bowman's space compared to epithelial cells & blood is
isotonic
199
Since ultrafiltrate is isotonic w/ epithelial cells & blood, all transport would need to be active; how does Na+K+ATPase remedy this
generates an electrochemical gradient to allow reabsorption
200
Where is Na+K+ATPase located
basolateral membrane of tubules
201
Describe Na+K+ATPase modality
pumps 3 Na+ out of cell for 2 K+ into cell
| low intracellular [Na+], so this movement is against its gradient
202
Na+K+ATPase allows for reabsorption where (down electrochemical gradient)
luminal membrane of tubules
203
% of what proximal tubule reabsorbs/ secretes
```
Reabsorbs:
67% of filtered water, Na+, & solutes
99% of filtered glucose & AAs
90% of filtered bicarbonate
Does not secrete
```
204
Describe how reabsorption occurs in first half of proximal tubule
1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters via Na+H+ antiporter & Na+ glucose/ AA/ PO4(3-) symporter (luminal membrane)
3) Water follows Na+ down osmotic gradient (luminal membrane)
205
Glucose, AA, & PO4(3-) are moved where by what after the initial reabsorption across the luminal membrane at the first half of the proximal tubule
moved across basolateral membrane by specific transporters & into peritubular capillaries
206
How did the solute movement in the first half of the proximal tubule promote water following Na+ entry
solute movement increased osmolarity inside proximal tubule cells compared to tubular fluid
207
Describe how reabsorption occurs in the second half of proximal tubule
1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters down electrochemical gradient via Na+H+ antiporter
3) Cl- enters down electrochemical gradient via Cl- anion antiporter & Cl- also moves via paracellular route
4) lumen +ve PD drives Na+ movement paracellularly
208
How is Cl- moved on the basolateral membrane of the second half of the proximal tubule
K+Cl- symporter
209
Why is Na+ & Cl- transport encouraged in second half of proximal tubule
reabsorption of water in 1st half concentrated Na+ in 2nd half
H+ & anion leave cell separately, fuse, & diffuse back into cell, effectively recycling themselves for transport to continue
210
After proteins are partially degraded by enzymes in luminal membrane, what happens
reabsorbed by exocytosis
211
Proteins are further degraded by enzymes in lysozymes into AAs & go where
across basolateral membrane
212
Protein reabsorption can become easily saturated, leading to what
proteinuria (protein in urine)
213
% of what loop of henle reabsorbs/ secretes
Reabsorbs:
25% of filtred NaCl (ascending loop)
15% of filtered water (descendng loop)
Does not secrete
214
Active or passive transport in loop of henle
passive
215
% of what distal tubule & collecting duct reabsorb/ secrete
```
Reabsorbs:
7% of filtered NaCl
8-15% of filtered water (w/ diuretic)
Secretes:
K+ & H+
```
216
Describe how reabsorption occurs in the initial part of distal tubule
1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters cell via NKCC1 symporter & Na+H+ antiporter (luminal membrane)
3) +ve transmembrane PD allows cations (Na+, K+, & Ca2+) to move down electrochemical gradient via paracellular route (luminal membrane)
217
Does water follow solutes in initial part of distal tubule
no, not even with ADH
218
How does K+ & Cl- get across basolateral membrane in initial part of distal tubule
transporters
219
What inhibits NKCC1 symporter
loop diuretics
220
Describe how reabsorption occurs in the later part of distal tubule
1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
| 2) Na+ enters cell via Na+Cl- symporter (luminal membrane)
221
Does water follow Na+ in later part of distal tubule
yes, but only w/ ADH
222
What inhibits Na+Cl- symporter
thiazide diuretics
223
Describe how reabsorption occurs in principal cells of collecting ducts
1) Na+K+ATPase generates Na+ gradient (basolateral membrane)
2) Na+ enters cell via Na+ channels
3) K+ leaves through K+ channels
4) Na+ reabsorption generates neg PD that allows Cl- to be absorbed via paracellular route
224
Does water follow N+ in principal cells of collecting duct
yes, but only w/ ADH
225
What inhibits Na+ channels
amiloride diuretics
226
Describe how reaborption occurs in intercalated cells of collecting ducts
secrete H+ & HCO3-
227
How does osmolarity or [Na+] differences play a role in reabsorption in descending limb of loop of henle
osmolarity of tubular fluid is always lower than the osmolarity of interstitia surrounding it so water moves out
228
How does osmolarity or [Na+] differences play a role in reabsorption in ascending limb of loop of henle
[Na+] of tubular fluid is always higher than the [Na+] of interstitia surround it so Na+ moves out
229
Why is the loop of henle described as being a countercurrent multiplier (2 reasons)
1) fluid in one limb moves countercurrent to fluid in the other
2) effect of one limb multiplies effect of the other
230
Example of how descending limb affects ascending limb
water reabsorption in descending limb amplifies Na+ reabsorption in the ascending limb
231
Fluid leaving proximal tubule is
iso-osmotic
232
Fluid leaving loop of henle to distal tubules is
hypotonic
233
Describe how reaborption occurs in loop of henle
1) active reabsorption of Na+ in early distal tubule creates an osmotic gradient, causing water to leave the descending limb
2) medullary interstitium osmolarity increases, so water keeps moving passively out of descending limb
3) at hairpin loop, water reabsorption has concentrated Na+ above interstitial concentration, so a Na+ gradient is formed
4) Na+ passively leaves ascending limb into interstitium, contributes to interstitial osmolarity that allowed water reabsorption in descending limb
5) Na+ reabsorption decreases tubular fluid osmolarity until it is less than the interstitium
234
At the hairpin loop, what is the tonicity difference b/w tubular fluid & interstitium
iso-osmotic
| osmolarity of tubular fluid is equal to the interstitium
235
High tubular osmolarity at hairpin loop is due to
Na+
236
High interstitial osmolarity at hairpin loop is due to
Na+ & urea
237
What does low ADH mean
diuresis -> water expelled
238
What does high ADH mean
antidiuresis -> water retained
239
Stimuli for ADH (3 of them)
1) high ECF osmolarity sensed by shrinking omoreceptors
2) low ECF volume sensed by baroreceptors
3) omoreceptors & baroreptors stimulate thirst center
240
Explain the modality of ADH
increases expression of aquaporins in medullary collecting duct (NOT CORTICAL) & later parts of distal tubule
241
Is it true that there is always some level of ADH present & what does this mean
yes, so nephron sections are always permeable to a degree
242
What does diuresis result in
1) high volume of dilute urine
2) ADH low/ zero
3) water is not reabsorbed into distal tubule or medullary collecting ducts
4) instead, water stays in tubular fluid & is expelled in urine
5) loss of ECF water to reduce ECF volume & increases ECF osmolarity
243
What does antidiuresis result in
1) low volume of concentrated urine
2) water is reabsorbed in distal tubules & collecting ducts
3) retains ECF water to increases ECF volume & decrease ECF osmolarity
244
Urea is constantly produced where
glomerulus
245
Water reabsorption in descending limb of loop of henle causes there to be what relationship b/w [urea] in distal tubule compared to interstitia surrounding it
more urea in distal tubule compared to interstitia
246
What happens to urea in distal tubule & cortical collecting duct
cannot leave
247
What happens to urea in medullary collecting duct
cannot leave without ADH
248
Is urea an effective or ineffective osmole at the collecting duct
ineffective
249
Is urea an effective or ineffective osmole at the loop of henle
effective
250
What is the result of urea being an effective osmole at the loop of henle
increased interstitial [urea] increases interstitial osmolarity around loop
more water than normal is pulled from descending limb
leads to a low volume of concentrated urine (antidiuresis)
251
When urea is added to medullary interstitium, what prevents toxic accumulation
when ADH levels are reduced, less urea accumulates
ascending loop is slightly permeable to urea so it can recycle it
vasa recta is permeable to urea & recycles it
252
Modality of vasa recta
removes water in countercurrent multiplier function from interstitium & keeps Na+ in interstitium
253
What happens in the ascending limb of vasa recta
permeable to Na+ & water
H2O moves down osmotic gradient into ascending limb & is carried from medulla to blood
H2O removed from descending limb of vasa recta & descending limb of loop of henle
254
What happens in the descending limb of vasa recta
permeable to Na+ & water
Na+ circulates from ascending to descending limb
keeps Na+ in medulla to maintain a high interstitial osmolarity
255
Main ion contributor to ECF & main osmole
Na+
256
Higher [Na+] means
higher ECF osmolarity
257
Lower [Na+] means
lower ECF osmolarity
258
Increase in amount of Na+ means
increase in ECF volume
259
Decrease in amount of Na+ means
decrease in ECF volume
260
Kidneys are the only site of ECF Na+ regulation, therefore they are critical in regulating
ECF osmolarity & volume
261
During high ECF osmolarity/ high [Na+], what happens
fluid moves out of ICF (cells shrink)
262
During low ECF osmolarity/ low [Na+], what happens
fluid moves into ICF (cells swell)
263
What is hypernatremia
high ECF [Na+]
| high ECF osmolarity
264
Clinical signs of hypernatremia
rupture of cerebral vessels/ hemmorhage
muscle weakness
behavioral changes/ ataxia
coma -> death
265
Regulation of hypernatremia
omoreceptors shrink, causing increased ADH release & thirst response
266
What is hyponatremia
low ECF [Na+] concentration
| low ECF osmolarity
267
Clinical signs of hyponatremia
cerebral/ pulmonary edema
muscle weakness
incoordination & seizures
268
Regulation of hyponatremia
omoreceptors swell, causing reduced ADH release
269
Is changing Na+ amount the only way to affect ECF volume
no
270
How do the kidneys regulate ECF volume
by changing Na+ amount
271
What is hypovolemia
low ECF volume
| low circulating volume (hypotension)
272
Clinical signs of hypovolemia
hypovolemic shock
| organ damage
273
Regulation of hypovolemia is by
sympathetic nervous system (baroreceptors) & renin-angiotensin system (juxtaglomerular apparatus)
274
Describe regulation of hypovolemia
1) baroreceptors (stretch receptors) sense decreased volume & send signals to the brain
2) sympathetic flow to kidney increases
3) norepinephrine is released
4) stimulates renin release from Juxtaglomerular apparatus to activate renin-angiotensin system
275
What does norepinephrine stimulate during hypovolemia regulation
causes vasoconstriction of efferent tubule more than afferent tubule (increases GFR)
alters Starling's forces to increase Na+ reabsorption in proximal tubule (even though more Na+ is being filtered)
causes juxtaglomerular cells to release renin
276
How does Starling's forces increase Na+ reabsorption in proximal tubule during hypovolemia regulation
since GFR increases, so does Pt (tubules)
since a greater amount of plasma is filtered, less makes it to the capillaries so Pc (capillaries) decreases
since GFR increases, not much protein goes through the filtration barrier so πt (tubules) does not change
since GFR increases, elevated filtration increases protein conc in peritubular capillaries so πc (capillaries) increases
277
Angiotensin II as a result of renin-angiotensin system in hypovolemia does what
constricts efferent arteriole to increase Na+ & H2O uptake
stimulates Na+H+ antiporter to increase Na+ uptake
stimulates ADH release to increase H2O uptake
stimulates aldosterone to increase Na+ uptake
278
Aldosterone is secreted where
from glomerulosa cells of adrenal cortex
279
What does aldosterone stimulate
increased Na+ channels in principal cells of collecting duct
increased Na+K+ATPase
increased NKCC1
280
What is hypervolemia
high ECF volume
| increased capillary hydrostatic pressure (hyperextension)
281
Clinical signs of hypervolemia
ascites & pulmonary edema
282
What is natiuresis
renal excretion of Na+
283
Where are atrial natrioretic peptides synthesized
atrial myocytes
284
Where are brain natiuretic peptides synthesized
cardiac ventricles
285
Regulation of hypervolemia is by
natiruetic peptide release (baroreceptors)
286
Where are baroreceptors found
heart, aorta, & carotid sinus
287
Describe regulation of hypervolemia
1) natiuretic peptide release constricts efferent arterioles & dilates afferent arterioles, which increases GFR, thus increasing Na+ & water load entering tubules
2) inhibits renin release from juxtaglomerular apparatus to prevent renin-angiotensin system (RAS)
3) inhibits ADH release by inhibiting RAS
4) inhibits aldosterone release by inhibiting RAS & acting directly on adrenal cortex
5) inhibits NaCl reabsorption in collecting duct by inhibiting Na+ channels
288
Main ion contributor to ICF
K+
289
Inside cells, function of K+
```
important osmole (maintains cell volume)
cofactor for enzymes
```
290
Outside cells, function of K+
small amount, but critical that it is maintained
291
Where can kidney regulate K+
extracellular only
292
What does the conc gradient of K+ set
resting membrane potential
293
Why does K+ govern resting membrane potential
Na+ channels have low permeability
| K+ channels are leaky
294
Result of leaky K+ channels
inside of cell more neg than outside as K+ follow conc gradient
eventually, inside of cell is so neg that K+ can no longer move out
membrane potential set b/c charge attraction for K+ = conc gradient for K+ moving out of the cell
295
What is hypokalemia
less K+ outside cell
296
Result of hypokalemia
conc gradient for K+ to move out is larger
inside cell gets more neg -> lower resting potential
to reach threshold, excitable cells need more Na+ so it is more difficult to generate AP
297
Symptoms of hypokalemia
muscle weakness, respiratory problems, cardiac arrythmia, & renal dysfunction
298
What is hyperkalemia
more K+ outside cell
299
Result of hyperkalemia
conc gradient for K+ to move out is smaller
inside of cell gets less neg -> higher resting potential
at first, AP is easier to generate
but then Na+ channels are unable to reset b/c the membrane potential is not low enough
excitable cells become unexcitable
300
Symptoms of hyperkalemia
muscle weakness & cardiac dysfunction
301
Describe external K+ homeostasis
K+ from diet must be excreted in urine/ feces
if it does not excrete enough -> hyperkalemia
if it secretes too much -> hypokalemia
302
Where does K+ come from
diet or parenteral fluids
303
Where is K+ lost at
90% via kidney (kaliuresis) & 10% via GI (colon helps when kidney is sick)
304
GI/renal problems can result in
hypokalemia or hyperkalemia
305
Describe internal K+ homeostasis
adjusts for rapid changes in K+ by translocating K+ from ECF to ICF or vice versa
acid base balance plays a role
306
Why is internal K+ homeostasis necessary
kidneys & gut work slowly, so body needs buffers in place to allow these organs to catch up
307
What hormones facilitate translocation of K+ in internal regulation
insulin promotes movement of K+ into cells by stimulating Na+K+ATPase (prevents hyperkalemia)
catecholamines -mainly epinephrine- promote K+ uptake into cells (B2 stimulation of Na+K+ATPase) & out of cells (alpha receptor)
308
How does acid base balance play a role in internal K+ homeostasis
high H+ promotes movement of K+ out of cells to maintain electronegativity & low H+ promotes movement of K+ into cells
309
Why is bicarbonate administered to treat hyperkalemia
reduces H+ & pushes K+ into cells
310
What parts of the nephron determine K+ balance
distal tubule & collecting duct
311
Describe paracellular movement of K+ in proximal tubule
K+ movement in late part of tubule where transepithelial PD become lumen pos & cell junctions are leaky
312
Describe transcellular movement of K+ in proximal tubule
movement facilitated by K-Cl symporter at basolateral membrane & K+ channels at luminal membrane
313
% of K+ that proximal tubule reabsorbs
67%
314
Describe paracellular movement of K+ at distal straight tubule
movement b/c transepithelial PD is lumen pos
315
Describe transcellular movement of K+ at distal straight tubule
movement faciliated by NKCC1 at luminal membrane & K+ channels at basolateral membrane
316
% of K+ that distal straight tubule reabsorbs
20%
317
Principal cells in collecting duct illicit what re K+
K+ secretion
318
How do principal cells in collecting duct cause K+ secretion
1) Na+K+ATPase generates Na+ gradient
2) Na+ enters via Na+ channels to make lumen more neg, causing K+ to want to move into the lumen
3) K+ leaves through K+ channels down gradient
4) Luminal membrane is more permeable than basolateral membrane, so most K+ enters the lumen but some does go back to the serum
319
Alpha intercalated cells in collecting duct illicit what re K+
K+ absorption
320
How do alpha intercalated cells in collecting duct cause K+ absorption
1) H+ leaves through H+ATPase & H+K+ATPase in luminal membrane
2) K+ enters cell via luminal membrane
3) K+ channels at basolateral membrane return K+ to ECF
321
Beta intercalated cells in collecting duct illicit what re K+
reversed, so do not absorb K+ like alpha intercalated cells
322
What are the factors that determine K+ handling
increase in size of conc gradient b/w cell & tubular fluid
tubular flow rate affects secretion
lumen electronegativity
323
Increased plasma [K+] leads to hyperkalemia, so K+ is moved where which causes what
translocated into ICF
this increases K+ gradient in renal cells so K+ is pushed into the lumen
stimulates aldosterone
324
Stimulation of aldosterone during hyperkalemia results in
increase in amiloride sensitive channels, which increases Na+ uptake
neg lumen & pos cell result in K+ secretion into lumen
Na+K+ATPase is stimulated
325
What stimulates aldosterone
hyperkalemia & angiotensin II
326
What inhibits aldosterone
natriuretic peptides
327
Low tubular flow rate decreases K+ secretion, resulting in
K+ persists in tubular fluid (hyperkalemia)
| K+ gradient reduced at luminal membrane
328
High tubular flow rate increases K+ secretion, resulting in
already secreted K+ is washed away (hypokalemia)
| high conc gradient for K+ maintained for secretion
329
Under low flow rate, what increases K+ channel activity (hyperkalemia)
ADH increases K+ channel activity
330
When does ADH act to increase K+ channel activity
occurs when water deprived or in extended periods of antidiuresis
flow rate reduced to conserve H2O
331
What can occur when ADH acts to increase K+ channel activity
hyperkalemia
332
Under high flow rate, what decreases K+ channel activity (hypokalemia)
ADH is low
333
What can occur when ADH does not act to increase K+ channel activity
hypokalemia (K+ wasting)
334
Increased lumen electronegativity does what re K+
increases K+ secretion
335
What increases lumen electronegativity
Na+ reabsorption or presence of ions like SO4, HCO3, or penicillin
336
Decreased lumen electronegativity does what re K+
decrease K+ secretion
337
What are the factors that influence renal K+ handling
```
Na+ intake
Acidosis
Alkalosis
Loop-, Thiazide-, & osmotic diuretics
Amiloride-like diuretics
```
338
How does Na+ intake affect renal K+ handling
dietary Na+ increases tubular [Na+], which increases Na+ reabsorption & increases K+ secretion (low intake does the opposite)
339
What effect does ECF osmolarity have on K+ as a result of Na+ intake
increased ECF osmolarity generates hypokalemia & decreased osmolarity generates hyperkalemia
340
How does acidosis affect renal K+ handling
increases serum [H+] so H+ moves into cells & K+ leaves to maintain electroneutrality
since luminal membrane is not permeable to K+ under acidosis, K+ is dumped into ECF -> hyperkalemia
341
How does alkalosis affect renal K+ handling
decreases serum [H+] so H+ moves out of cells & K+ enters to maintain electroneutrality
luminal membrane not permeable to K+ under alkalosis, so K+ is dumped into ICF -> hypokalemia
342
How does Loop-, Thiazide-, & osmotic diuretics affect renal K+ handling
increase flow rate & [Na+] in collecting duct
| results in increased K+ secretion -> hypokalemia
343
How does Amiloride-like diuretics affect renal K+ handling
inhibit Na+ uptake in collecting duct
this inhibits K+ secretion -> hyperkalemia
(K+ sparing diuretics)
344
Define acid
proton (H+) donor
increases [H+] conc of a soln
low pH
345
Define base
proton (H+) acceptor
decreases [H+] conc of a soln
high pH
346
Normal physiological pH
7.35-7.45
347
Define acidemia
pH < 7.35
348
What is severe acidemia
pH < 7.2
349
Define alkalemia
pH > 7.45
350
What is severe alkalemia
pH > 7.6
351
Define acidosis
processes by which acidemia occurs
352
Define alkalosis
proceses by which alkalemia occurs
353
Simplified equation for partial pressure of CO2
dCO2 -> H+ + HCO3-
354
Is CO2 an acid or base
acid
355
How does a low ventilation rate regulate acid/base balance
increases ECF pCO2 which increases [H+] that can lead to respiratory acidosis
356
How does a high ventilation rate regulate acid/base balance
decreases ECF pCO2 which decreases [H+] that can lead to respiratory alkalosis
357
Equation that represents the relationship b/w lung ventilation rate & acid/base balance
Henderson-Hasselbalch equation
358
Rapid changes of acid/base balance that manipulate pCO2 occur where
lungs & tissues
359
What are strong ions
ions that completely dissociate at a normal physiological pH
360
Strong cations
Na+, K+, Ca2+, & Mg2+
361
Strong anions
Cl-, lactate, & SO4(2-)
362
What does the strong ion difference reflect
in normal plasma, [strong cations] > [strong anions]
363
How does SID decrease & how would this affect ECF
strong anions added or strong cations removed
| ECF neg
364
How does SID increase & how would this affect ECF
strong cations added or strong anions removed
| ECF pos
365
Slow changes of acid/base balance that manipulate SID occur where
kidneys, gut, & tissues
366
If [SID] decreases, ECF is less positive & what happens
pos charge is required for balance
H+ > OH-
metabolic acidosis
367
If [SID] increases, ECF is more positive & what happens
neg charge is required for balance
OH- > H+
metabolic alkalosis
368
What are weak acids
acids that partially dissociate at physiologial pH
369
Ex of weak acids
proteins (albumins & globulins)
| phosphates
370
Eq for weak acids
HA -> H+ + A-
371
What is Atot
Weak acid buffers in a system
372
Eq for Atot
HA + A-
373
If Atot increases, what happens
increased [H+]
| metabolic acidosis
374
If Atot decreases, what happens
decreased [H+]
| metabolic alkalosis
375
Does [H+] determine pH
no, only pCO2, [SID], & Atot determine pH
376
Are the factors determining acid/base balance independent or dependent
independent
377
Kidney goal in acidemic animal
increase ECF [SID]
378
What does kidney do in an acidemic animal
decrease Cl- reabsorption & increase Na+ reabsorption (alkalosis)
379
When kidneys increase ECF [SID] in an acidemic animal, what happens to urinary [SID]
decreases
| urine becomes more acidic
380
What is the kidneys response to urine becoming more acidic
synthesis & secretion of NH4+ to maintain electroneutrality
381
Kidney goal in alkalemic animal
decrease ECF [SID]
382
What does kidney do in an alkalemic animal
decreases Na+ reabsorption & increase Cl- reabsorption (acidosis)
383
When kidneys decrease ECF [SID] in an alkelmic animal, what happens to urinary [SID]
increases
| urine becomes less acidic
384
What is the kidneys response to urine becoming less acidic
synthesis & secretion of NH4+ is suppressed to maintain electroneutrality
385
What allows animals to sense abnormal ECF volume
baroreceptors (stretch receptors) in left atria/pulmonary vessels & in aortic arch/sinus
386
What do baroreceptors in left atria & pulmonary vessels sense
volume change
| on venous side where most of the volume is
387
What do baroreceptors in the aortic arch & sinus sense
pressure changes
on arterial side where most of the pressure is
(more important than venous baroreceptors)
388
If baroreceptors on arterial side stretch, what happens
no ADH is released
389
If baroreceptors on arterial side do not stretch, what happens
ADH is released
