FINAL. Flashcards
1
Q
What are the 3 main functions of the CV system?
A
- transport nutrients to tissues
- transport waste products away from tissues
- transporting hormones: signaling (ex. endocrine system)
2
Q
vascular conductance is the _____ of vascular resistance
A
inverse
3
Q
High conductance = ______ flow
Low conductance = ______ flow
A
high = high
low = low
4
Q
How much blood is found in our veins?
A
64%
5
Q
a system in series will have _____ resistance while a system in parallel will have _____ resistance
A
Series = High
Parallel = Low
6
Q
The greater the cross sectional area, the ______ the velocity of blood flow
A
lower
7
Q
the smaller the cross sectional area, the ___ the velocity of blood flow
A
higher
8
Q
What are the high resistance vessels in the systemic circulation
A
Small arteries and arterioles (mainly arterioles)
9
Q
When measuring blood pressure:
Proximal to the choke point the BP would be _____.
Distal to the choke point the BP would be ______.
A
Proximal: higher
Distal: lower
10
Q
What is it called when we have nice orderly blood flow?
A
laminar flow
11
Q
What is it called when we have disorderly flow..maybe due to a plaque build up.
A
turbulent flow
12
Q
When looking at laminar blood flow, why does the blood in the middle of the tube flow faster?
A
the blood on the outside edges are making contact with the wall which is where the high resistance is
13
Q
How much of our CO goes to the kidneys to be filtered?
A
~22%
14
Q
How can we rearrange ohms law to figure out flow?
A
Flow = delta P / Resistance
15
Q
True/false: If we constrict a vessel to half of its original diameter, we decrease flow by 16 fold
A
true
16
Q
How can we arrange ohms law to solve for resistance?
A
Resistance = Delta P / flow
17
Q
The drop in blood pressure that occurs between large arteries and capillaries is due to what?
A
mainly due to the increase in resistance and NOT due to the face that it has multiple paths to take.
18
Q
if we have decreased total cross sectional area that would cause an _______ in velocity.
A
increase (think aorta)
19
Q
what are capillaries responsible for?
A
exchange of nutrients and waste products
20
Q
blood flow through capillaries is controlled by ______
A
arterioles
21
Q
Why are arterioles good at managing blood flow?
A
bc they have a layer of smooth muscle associated with them
22
Q
true/false: arterioles have two laters of smooth muscle fibers
A
false, roughly four
23
Q
how many capillaries do we have in our body?
A
10+ billion
24
Q
What is the total surface area of all our capillaries combined?
A
500-700 sq meters
25
The blood pressure associated with the arteriole end of the capillaries is _______.
30mmHg
26
The blood pressure associated with the venous end of the capillaries is _______.
10mmHg
27
The average blood pressure associated with the capillaries is _______.
17.3 mmHg
28
Why is the avg blood pressure in the capillaries 17.3 and not 20?
bc it starts small and gets bigger in diameter as it moves towards the venous end
29
Pcap in:
Art end
Avg
Vein end
Art end: 30 mmHg
Avg: 17.3 mmHg
Vein end: 10mmHg
30
Pisf
-3 mmHg
31
Cap oncotic pressure
28 mmHg
32
Isf oncotic pressure
8 mmHg
33
What are the proteins associated with the Cap oncotic pressure
1. Albumin
2. Globulin
3. Fibrinogen
34
What are the proteins associated with the Isf oncotic pressure?
1. proteoglycan filaments
2. Hyaluronic acid
3. collagen
35
The lymphatic system can increase activity by ____
20-40X
36
True/false: If your capillaries become swiss cheese, the lymphatic system will rapidly reuptake the lost proteins.
false. its slow af
37
Kf is the capillary filtration coefficient. What does this look at?
1. permeability
2. surface area
38
In a normal 70 kg patient. How much intracellular fluid do we have?
1/3 of TBW
~14L
39
In a normal 70 kg patient. How much plasma do we have?
1/4-1/5 of the ECF
~3L
40
In a normal 70 kg patient. How much ISF do we have?
3/4-4/5 of the ECF
~11L
41
In a normal 70kg patient. How much Intracellular fluid do we have?
2/3 of TBW
~28L
42
What kind of valves are in the lymphatic system?
one way valves
43
Where do the lymphatics empty?
into the subclavian veins on either side; R lymphatic duct, thoracic duct
44
What is the NFP in a capillary on the arteriole end?
13 mmHg
45
What is the NFP in a capillary on the venous end?
-7 mmHg (net reabsorption pressure = 7 mmHg)
46
What is the NFP in a capillary using the average bp in a cap?
0.3 mmHg (using 17.3)
47
True/false: NaCl is generally small enough to diffuse paracellularly
true
48
MAP in the renal artery
100 mmHg
49
Glomerular capillary pressure
60 mmHg
50
The afferent arteriole is important for
regulating renal blood flow
51
the efferent arteriole is important for
fine tuning GFR
52
If we have an increase in BP what will happen to the afferent arteriole? What will happen to the pressures and GFR?
It will constrict.
-decrease RBF
-decrease Pcap
-decrease GFR
53
If we have a decrease in BP what will happen to the afferent arteriole? what will happen to the pressures and GFR?
It will dilate
-increase RBF
-increase Pcap
-increase GFR
54
Normal GFR
125 mL/min
55
Autoregulation in the nephrons is meant to control what two things?
1. Blood flow
2. Filtration
56
True/False: Autoregulation in the kidney is just as tight as it is in the brain
False
57
If we have constriction of the efferent arteriole, what would that cause?
-decrease RBF
-increase Pcap
-increase GFR
58
If we have dilation of the efferent arteriole what would that cause?
-increase RBF
-decrease Pcap
-decrease GFR
59
What is the oncotic pressure in the afferent art?
28 mmHg
60
what is the oncotic pressure in the efferent art right after glomerular caps?
36 mmHg
61
What is the oncotic pressure in the glomerulus
32 mmHg
62
What is the Ptubule
18 mmHg
63
What is the oncotic pressure in the tubule
0
64
What is the NFP in glomerulus? what favors/opposes filtration?
10 mmHg
favor (Pcap: 60 mmHg)
oppose (Onc Cap: 32 mmHg & Ptubule 18mmHg).
60-18-32= 10
65
How do we find the filtration coefficient
Kf = filtration rate/NFP
Kf = 125mL/min / 10mmHg
Kf = 12.5
66
what is the Pcap at the end of the efferent art?
18mmHg
67
What blood vessel segment has the highest amt of resistance in the kidney?
efferent art
68
How do we know the efferent art has a greater resistance compared to the afferent art
It has a drop in Pcap of 42 mmHg.
afferent art: bp goes from 100 in renal art to 60 in glomerulus (drop of 40)
efferent art: bp goes from 60 in glomerulus to 18 at end of efferent art (drop of 42)
69
Approx ______% of what is filtered gets reabsorbed
99%
70
Oncotic pressure in peritubular caps
32 mmHg
71
Pcap (peritubular cap)
13 mmHg
72
Oncotic ISF (peritubular cap)
15 mmHg
73
Pisf (preitubular cap)
6 mmHg
74
what is the NFP at the peritubular cap? what opposes/favors filtration
-10 mmHg
favor: Pcap 13 mmHg, Onc ISF 15 mmHg
Oppose: Onc CAP 32 mmHg, Pisf 6 mmHg
13 + 15 - 32 - 6 = -10
75
Excretion = what
filtration - reabsorption + secretion
76
If the kidneys decide to filter more fluid at the glomerulus, how would it achieve that?
constriction of efferent art
77
If we have increased filtration at the glomerulus what would happen to the oncotic pressure in glomerulus?
it would increase (become more concentrated)
78
What is normal GFR?
125 mL/min
79
Normal RBF
1100 mL/min
80
normal RPF
660 mL/min
81
normal FF (filtration fraction)
19%
82
How do we find filtration fraction?
FF = GFR/RPF
FF = 125mL/min / 660mL/min
FF = 0.19 (19%)
83
How to we find RBF
its just ~22% of our CO (1100 mL/min)
84
How do we find RPF?
RPF = Plasma % * RBF
RPF = 0.6 * 1100mL/min
RPF = 660 mL/min
(if HCT is 0.4)
85
in response to increased hydrostatic pressure the afferent art will ______
constrict
86
in response to decreased hydrostatic pressure the efferent art will _____
dilate
87
Constriction of either afferent/efferent art will do what to RBF
decrease
88
normal UOP
1mL/min
89
What is an example of something that is filtered and partially reabsorbed
Na
90
Example of something that is filtered and completely reabsorbed
glucose
91
example of something that is filtered and the completely secreted (nothing reabsorbed)
PHA (para aminohippuric acid)
92
what is the innermost layer of the glomerular caps? what is special about this layer
endothelium
has fenestrations
93
what layer in the glomerular caps comes after the endothelium? what is special about this layer
connective tissue called basement membrane. has neg charges to repel things that we dont want to filter like proteins
94
what is the outermost layer in the glomerular caps
epithelium. made up of podocytes used for support due to the high pressure and has slit pores
95
How are podocytes helpful particularly with chronic HTN
prevents swelling of glomerulus
96
how does the kidney handle LT regulation of BP
through RAAS and fluid retention/secretion
97
how does kidney regulate LT pH
short term pH regulator is lungs.
Kidney produces and reabsorbes HCO3 and can also excrete excess protons (H+)
98
LT regulation of RBC by the kidneys
O2 sensor deep in medullary renal interstitum. if pO2 is low erythropoietin is released
99
LT vit D regulation by the kidneys
Vit D is activated by the kidneys, vit d is important for ca reabsorption
100
Drug clearance in kidneys
drugs metabolized in liver and the filtered/secreted by kidneys
101
What do the kidneys have to do with the removal of metabolic waste products
gets rid of them. like nitrogenous compounds (urea)
102
All of the regulatory roles of the kidney is primarily carried out by what?
GFR
103
What are the more superficial nephrons
cortical nephrons
104
what % makes up the cortical nephrons
90-95%
105
what are the deep nephrons
medullary nephrons
106
what % make up the medullary nephrons
5-10%
107
What is the capillary bed that surrounds the tubules of the medullary nephrons?
vasa recta
108
what is special about the vasa recta
has more ascending compared to descending
109
with more split points that exist in the ascending vasa recta, flow velocity will be ______
decreased
110
why is a decrease in velocity in ascending vasa recta helpful?
maintain normal concentration of solutes in the deep medullary interstitum
111
what happens if the velocity in the ascending vasa recta is increased?
ends up washing out the interstitum and then that affects reabsorption
112
True/false: the deep medullary is sensitive to low BP and has limited O2 delivery
true
113
Where do the kidneys sit?
slightly below diaphragm
114
What sits on top of each of the kidneys
adrenal glands
115
The superior lateral side of the right kidney comes into contact with what organ?
liver
116
the right kidney comes into contact with what organs
liver and colon
117
the left kidney comes into contact with what organs
stomach, spleen, pancreas, and descending colon
118
The top lateral side of the left kidney comes into contact with what organ
spleen
119
green
zona glomerulosa
120
where is aldosterone released?
from the zona glomerulosa
121
blue
zona fasciculata
122
pink
zona reticularis
123
yellow
medulla
124
what is released from the adrenal medulla
catecholamines
125
what is released from zona fasciculata and zona reticularis
Glucocorticoids: cortisol and a little bit of estrogen
126
what is the ratio of epi:norepi
4:1
127
blue
minor calyx
128
pink
major calyx
129
contact with liver:
red
liver (hepatic surface)
130
contact with liver:
yellow
colon (right colic flexure surface)
131
contact with liver:
blue
duodenal surface
132
contact with liver:
orange
stomach (gastric surface)
133
contact with liver:
purple
spleen (splenic surface)
134
contact with liver:
pink
pancreas (pancreatic surface)
135
contact with liver:
green
descending colon (descending colic surface)
136
artery & veins:
light blue
interlobular
137
artery and veins:
Green
segmental
138
artery and veins:
purple
arcuate
139
artery and veins:
orange
interlobar
140
pink
renal artery. obvi
141
dark blue
renal vein
(wow you're literally so smart)
142
Name the renal arteries in sequential order starting with the renal artery.
1. renal art
2. segmental art
3. interlobar art
4. arcuate art
5. interlobular art
143
what are the layers of the adrenal cortex. starting from outermost moving inward
1. zona glomerulosa
2. zona fasciculata
3. zona reticularis
144
when the macula densa senses a decrease in Na, _____ is released from the juxtaglomerular cells
renin
145
describe how renin gets converted to Ang II
renin leads to increased angiotensinogen (produced in liver) this leads to angiotensin 1, ang 1 is converted to ang 2 via ACE (angiotensin converting enzyme) that is found in large amounts in the lungs
146
angiotensin 2 primarily constricts the ______ arteriole
efferent
147
what happens as a result of constriction of the efferent arteriole following ang 2 release
increased Pcap in glomerulus
increased filtration
148
what nerve controls the bladder?
Pudendal nerve. coming from S 2, 3 and 4
149
what is renal clearance
the quantity of plasma that is cleared of a substance per measured time (mL/min)
150
what is the normal rate of filtration and rate of reabsorption?
filtration: 125mL/min
reabsorption: 124mL/min
151
Approximately _____ of everything that is filtered is reabsorbed at the PCT
2/3 or 66%
152
When thinking about glucose in a normal healthy individual (without glucose issues) the clearance should equal what?
zero. we aren't clearing the plasma of any glucose
153
if we have a BP of 200, what happens to the afferent art? why would this happen?
it constricts due to autoregulation
154
Kf = what
12.5
155
If we have chronic hypertension and then have a period of super low bp (like 50) what is going to happen
the afferent art will try to dilate to bring glomerular pressure up but if it has been constricting for a long time due to chronic HTN, it might not be able to relax
156
If we have a decrease in GFR we are going to have a ______ in reabsorption
increase. This is because we have slower filtration so its staying in the tubule longer, which would increase absorption.
157
______ affects the efferent constricting/dilating more so than the afferent art
ang 2
158
solutes that are freely filtered but reabsorbed primarily in the PCT will have a ____ concentration in the tubule distal the the PCT
low
159
the PCT can be split into ____ segments. what are they
3.
S1
S2
S3
160
How is glucose reabsorbed in the S1 segment of the proximal tubule. what %.
90% via SGLT 2 pumping 1Na and 1 Glucose. then out the basolateral side via GLUT 2.
Low affinity
161
How is glucose reabsorbed in S2 segment of proximal tubule? what %
10% via SGLT1 requiring 2Na for every 1 glucose. then out basolateral side via GLUT 1
high affinity
162
At what point would we reach a transport maximum for glucose
a serum glucose level of 300 mg/dL
163
we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.
What is the primary response to this?
Increased renin release from JG cells. leading to increased Angiotensin 2.
ultimately constricting the EFFERENT art
164
we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.
What is the secondary response to this?
dilation of the AFFERENT art (likely due to NO release)
165
we have a low BP resulting in a reduction in Pcap in glomerulus resulting in a decrease in GFR which means there will be decreased NaCl making it to macula densa.
What is the tertiary response to this?
Angiotensin 2...when all is said and done and all is right in the world, it will increase the reabsorption of NaCl and the macula densa will be happy again.
166
where is the macula densa
thicky thick ascending limb of the loop of hennessy.
167
almost all drugs will affect the ______ arteriole
afferent.
168
what is the angiotensin receptor that is found in the PCT. where are they located
AT1. on BOTH the basolateral and apical sides
169
on the basolateral membrane, AT1 receptors will do what?
Speed up the rate of the Na/K/ATPase, thereby decreasing intracellular Na
170
What is the most important effect of angiotensin 2 binding to AT1 receptors in the PCT
the increase in speed of the Na/K/ATPase
171
What transporter is affected first as a result of the Na/K/ATPase increasing cycling speed after Ang 2 binds to the AT1 receptor in the PCT on the basolateral membrane
the intracellular Na will be lower therefore the NHE pump would be pumping faster. pumping Na in and H out (into lumen)
172
What transporter is affected second as a result of the Na/K/ATPase increasing cycling speed after Ang 2 binds to the AT1 receptor in the PCT on the basolateral membrane
the Na/HCO3 pump on the basolateral membrane. pumps BOTH Na and HCO3 out into renal interstitum
173
what is transcellular reabsorption
reabsorption via channels within the cell membrane
174
what is paracellular reabsorption
between cells
175
the paracellular space is held together by ______
tight junctions
176
at the PCT, Cl is reabsorbed primarily via _____
paracellular route
177
In the PCT, when does Cl reabsorption happen?
later on. there is little to no Cl reabsorbed in the first half bc its besties with Na so once Na starts to leave, it follows.
178
Urea is found in abundance in the _____
interstitum.
179
what helps promote greater reabsorption in the tubule?
brush border.
180
Brush border increases the surface area by _____
20X
181
In the PCT, the tubular epithelial cells have a membrane potential of _____.
-70mV
182
in the PCT the tubular lumen has a membrane potential of _____
-3mV
183
On average _____ proteins are filtered. Of those, _____ are reabsorbed and ______ are excreted in the urine
1.8g
1.7g
100mg
184
what is the primary reabsorption process for Na in the PCT?
the NHE transporter
185
How is acid base managed in the PCT
the whole ass process with CA.
H binds to HCO3
forming H2CO3
carbonic acid breaks this down to
H20 and CO2
186
Glutamine is an ______ produced in the ______. It is used in the tubular epithelial cells of the PCT to produce _______
amino acid.
liver.
bicarb
187
glutamine is converted stoichiometrically into two compounds, what are they
2 HCO3
2 NH4
188
the 2 NH4 that are produced via the breakdown of glutamine serve what purpose?
act as a urine buffer the avoid free H from floating around in the urine
189
What is another buffer for the urine aside from NH4?
NaHPO4. protons can bind to become NaH2PO4
190
How is Ca reabsorbed in the PCT
via transcellular AND paracellular.
191
what is the apical membrane transcellular route Ca takes in the PCT to be reabsorbed?
just a good old Ca channel. It wants to flow in that bitch due to the charge and the concentration gradient
192
what is the basolateral membrane transcellular route Ca takes in PCT to be reabsorbed
Ca/ATPase
Na/Ca exchanger (3Na for 1Ca)
193
what monitors the Ca level in the ECF?
PTH (parathyroid hormone)
194
if we have low Ca what will 3 things will follow
the PTH will
1. increase Vitamin D3 activation (increasing Ca reabsorption)
2. Increase Ca reabsorption by increasing apical Ca channels
3. Increase osteoclast activity (decrease osteoblast activity)
195
what is the short term and long term storage of Ca
short: SR
long: bones
196
Organic cations are secreted in the PCT via ____
H dependent antiporters.
Cation gets into cell on basolateral side allllll by itself. on apical side the cation is exchanged for 1 H.
197
what are some of the endogenous cations (6)
1. creatinine
2. ACh
3. Choline
4. Histamine
5. Serotonin
6. Epi/norepi
198
what are the organic exogenous cations? (6)
1. atropine
2. isoproterenol
3. morphine
4. procaine
5. quinine
6. tetraethylammonium (thats a mouthful)
199
How are the organic anions secreted in the PCT?
Na-dependent antiporters.
to get into the cell on the basolateral membrane it needs its hand held, unlike the cation.
FIRST. there is a pump on the basolateral membrane that pumps 3Na and 1 aKG into the cell.
THEN the anion can be pumped into the cell (on basolateral membrane) with one of the aKG.
FINALLY it can cross to the tubular lumen all by itself.
200
what is the intermediary that helps anions get tf out?
aKG. alpha ketoglutarate
201
what are some of the organic endogenous anions (6)
1. hippurates
2. bile salts
3. PGE
5. uric acid
6. oxalate
202
what are the organic exogenous anions (4)
1. Furosemide
2. PCN
3. ASA
4. sulfonamides
203
during WW2 alexander fleming found that hippurates added to PCN compound did what?
"competitive secretion". basically if you overwhelm the secretion mechanism with hippurates then you have PCN floating around for longer
204
how much water is reabsorbed in the thin descending loop
20%
205
how much water is reabsorbed in PCT
65%
206
what transporter is in the thin ascending limb
Na/Cl/ATP
207
in the thick ascending limb, Mg and Ca are reabsorbed via paracellular diffusion. this is driven by what?
K has leak channels on both the apical and basolateral sides. the increase in K causes the membrane potential to increase. which will drive those big bitches out.
208
what is the membrane potential for the thick ascending limb
8mV
209
% of ion reabsorption in:
PCT ____
TAL ____
PCT: 65%
TAL: 25%
210
what transporters are in the TAL
Na/K/2Cl (1Na/1K/2Cl)
NHE (1Na/1H)
Na/K/ATPase
(Cl and K channels)
211
what is the highest our osmolarity goes? lowest?
1200.
50.
212
How is Ca reabsorbed in the DCT
apical: Ca channel
basolateral: 3Na/1Ca pump
213
what can influence the rate of reabsorption of Ca on the apical side
PTH
214
thiazides block what?
the Na/Cl symporter in the DCT
215
what happens if we block the Na/Cl symporter in the DCT?
the Na concentration gradient will further be reduced which will increase the Na/Ca exchanger which will increase the rate of reabsorption of Ca
216
How can thiazide diuretics be helpful for patients with osteoporosis?
thiazides block the Na/Cl symporter in DCT. with less Na coming into cell, the Na/Ca exchanger will pick up pace because that Na wants to move down its concentration gradient. this will lead to increased reabsorption of Ca.
217
When I say principal, you say _____
ALDO
218
Aldosterone increases the reabsorption of ______
Na
219
what happens in response to the increased Na reabsorption from aldosterone
it will indirectly increase the reabsorption of H2O.
AND it will result in excess K excretion
220
Aldosterone is released from the adrenal glands, the primary effect is ____. The secondary effect is ______. The third effect is _____.
1. increasing Na/K/ATPase
2. planting additional ENAC (Na coming in)
3. increasing K channels (K leaving)
221
what two drugs inhibit the ENaC channels
triamterene and amiloride
222
_____ is commonly given with triamterene to inhibit K wasting
HCTZ
223
aldosterone R antagonists
1. spironolactone
2. eplerenone
224
Low K excretion:
ROMK is ____
BK is ____
ROMK: sequestered
BK: closed
225
Normal K excretion:
ROMK is ____
BK is _____
ROMK: open
BK: closed
226
High K excretion:
ROMK is ____
BK is _____
ROMK: open
BK: open
227
opening of both ROMK and BK and likely _____ mediated
aldosterone
228
Why does K wasting happen?
inhibit Na reabsorption anywhere upstream to principal cells = increased Na concentration at principal cells.
this leads to increased Na reabsorption which leads to more K excretion due to the Na/K/ATPase working in overdrive
229
Aldosterone is secreted from the zona glomerulosa in response to ______
increased extracellular K
230
How can ang 2 affect aldo release?
there are AT1-R on the adrenal glands and when Ang 2 binds, it induces aldosterone secretion.
231
what is RAAA
renin angiotensin aldosterone axis
232
what is the enzyme in the principal cells that prevent cortisol from binding to the aldo receptors
11 B-HSD Type 2
11 beta-Hydroxysteroid Dehydrogenase type 2
233
What can happen as a result of excess cortisol from a ACTH secreting tumor
the 11 B-HSD type 2 becomes overwhelmed, cortisol binds to the aldo receptors, increasing Na and H2O retention and leading to Hypokalemia
234
How can REAL licorice cause hypokalemia
11 B-HSD is inhibited. cortisol can bind to the aldo receptors, increasing Na and H2O retention and leading to Hypokalemia
235
Aldo effects on high K.
increased aldo release.
increased K secretion
236
Aldo effects on low K.
decreased aldo release
decreased K secretion
237
Type A intercalated cells secrete ____ via _____
Protons (H+).
H/ATP pump AND K/H/ATP
238
Type B intercalated cells secrete ____
HCO3
239
walk through H2O reabsorption in the intercalated cells starting the vaso binding to receptor
AVP (arginine vasopressin) binds to V2. they are Gs. ATP ----->cAMP---->activates PKA----> phosphorylation of AQP2. AQP2 placed on apical membrane allowing H2O to flow in. On basolateral membrane we have AQP3 and 4 that are always open
240
What happens in nephrogenic DI
lack of response to AVP. no AQP2 moving to apical membrane for H2O reabsorption
241
Lithium effects on urine
reduces expression of AQP2. urinate ~20L/day. urine osmolarity can go down to 50 mOsm
242
affects of alcohol regarding ADH.
impairs ADH release from pituitary gland. as well as AVP response by the intercalated cells. thats why we have to pee all the time when we are getting litty for schmidty at Joes
243
High osmolarity will _____ ADH
stimulate ADH release
244
osmoreceptors stimulate two areas within the hypothalamus. what are they
1. supraoptic nucleus
2. periventricular nucleus
245
supraoptic nucleus is located ______. It is responsible for ______ of our ADH release
above the optic nerve.
5/6
246
Periventricular nucleus is located _____. It is responsible for _____ of our ADH release
either side of the 3rd ventricle.
1/6
247
both the supraoptic nucleus and the periventricular nucleus delivery ADH to the _____
posterior part of the ballsack. neurohypophysis
248
osmoreceptors have _____ membranes.
semipermeable
249
If the osmoreceptors are exposed to hypotonic conditions what happens
ADH inhibited.
AP's slow down
250
If osmoreceptors are exposed to hypertonic conditions, what happens
ADH released.
AP's pick up speed
251
How would the baroreceptors stimulate ADH release
if they have slow signaling (d/t low BP)
252
urea is reabsorbed in the collecting duct via
UT-A1 and UT-A3
253
Urea is secreted via ____ back into the tubule in the thin loop of henle
UT-A2
254
Why is ADH the primary controller of osmolarity
it is the only hormone that controls water reabsorption and water reabsorption ONLY.
255
Caffeine can take ADH offline causing _____
increased Na concentrations
256
what can decrease thirst (5)
1. decreased plasma osmolarity
2. increased blood volume
3. increased BP
4. decreased Ang 2
5. gastric distention
257
what can increase thirst (5)
1. increased plasma osmolarity
2. decreased blood volume
3. decreased BP
4. increased Ang 2
5. dryness of mouth
258
what can decrease ADH (4)
1. decreased plasma osmolarity
2. increased blood volume
3. increased blood pressure
4. Drugs (alcohol, clonidine, haloperidol)
259
what can increase ADH (6)
1. increased plasma osmolarity
2. decreased blood volume
3. decreased blood pressure
4. nausea
5. hypoxia
6. drugs (morphine, nicotine)
260
if we chug 1L of water, what happens in regard to:
1. ADH
2. Urine osmolarity
3. plasma osmolarity
4. urine flow rate
5. urinary solute secretion
1. ADH secretion is reduced
2. urine osmolarity drops (becomes more dilute)
3. plasma osmolarity stays nearly the same
4. urine flow rate increases
5. solute secretion remains nearly constant
261
262
In regard to potassium:
Insulin causes____
Hypokalemia
263
In regard to potassium:
Aldosterone causes _____
Hypokalemia
264
In regard to potassium:
Beta-adrenergic stimulation causes _______
Hypokalemia
265
In regard to potassium:
Alkalosis =
Hypokalemia
266
In regard to potassium:
Insulin deficiency (DM) =
Hyperkalemia
267
In regard to potassium:
Aldosterone deficiency =
Hyperkalemia
268
Addisons diseases causes
Aldo deficiency——>hyperkalemia
269
In regard to potassium:
Beta-adrenergic blockade =
Hyperkalemia
270
In regard to potassium:
Acidosis =
Hyperkalemia
271
In regard to potassium:
Cell lysis =
Hyperkalemia
272
In regard to potassium:
Strenuous exercise =
Hyperkalemia
273
In regard to potassium:
Increased ECF osmolarity =
Hyperkalemia
274
ACUTE metabolic alkalosis causes _____ k secretion (increased/decreased)
Increase. Only with acute. Once the body figures out that it’s turning into a basic bitch (bc of the alkalosis) it’s gonna keep the K around.
275
Excretion rate formula
Concentration of substance in urine * urine flow rate
276
Reabsorption rate formula
Filtered load - excretion rate
(Filtered load = GFR * plasma concentration)
(Excretion rate = concentration in urine * urine output)
277
Secretion rate formula
Excretion rate - filtered load
(Filtered load= GFR * plasma concentration)
(Excretion rate = urine concentration * UOP)
