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A/P > Lecture 11/18: Renal Physiology Cont'd > Flashcards

Lecture 11/18: Renal Physiology Cont'd Flashcards

Final (90 cards)

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1
Q

T/F: MD relaxes both the AA & EA

A

T

Selective to AA though

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2
Q

___% of PAH is left in plasma

A

10%

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3
Q

Describe how a selective vs Nonselective vasoconstrictor/dilator can effect GFR

A

Selective: Will effective either the AA or EA more and we can better gauge how GFR will change

Nonselective: You dont know which one is effected more therefore you cant determine how GFR will be exactly effected

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4
Q

Most pressers/dilators are selective to the _____

A

AA

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5
Q

Describe the Angiotensin II Type 1 Receptors

A

AT1

AT1-R binds to ANGII

-Proximal Tubule
-Apical & Basolateral

Speeds up the cycling of Na/K Atpase pump
-Ultimately results in increased reabsorption of Na+ (and water) and Bicarb by speeding up the NHE pump

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6
Q

Describe the Sodium-Hydrogen Exchanger pump

A

NHE

1 Na+ in (tubular cell)
1 H+ out (urine)

-Important in acid/base regulation
-SECRETES a proton into tubular lumen
-Major role in Na reabsorption

-Proximal Tubule
-Apical

Affected by AT1-R; Speeds up based on Na/K ATPase Na+ gradient on basolateral

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7
Q

Describe the Sodium-Potassium ATPase pump

A

Na+/K+ ATPase

3 Na out (Renal ISF)
2 K in (Tubular cell)

-Proximal Tubule
-Basolateral

-Sped up by AT1-R
-Speeds up the NHE

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8
Q

Describe the Sodium-Bicarb Symporter

A

Co-transporter

1 Na+ & THREE (3) Bicarbs in renal ISF

-Proximal Tubule
-Basolateral

Affected by AT1-R; Sped up by the NHE

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9
Q

What pumps do AT1 affect?

A

This is the ANGII receptor

  1. Na/K ATPase <– primary
  2. NHE
  3. Sodium-Bicarb symporter
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10
Q

What are the routes of reabsorption in the PT?

A
  1. Paracellular pathways via osmosis
  2. Trancellular pathways via transporter/channels in the cell wall
  3. Aquaporins (specialized trancellular pathway for water) via osmosis
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11
Q

Describe water reabsorption in the PT

A
  1. Aquaporins
  2. Transcellular pathway: Na+ influenced
  3. Paracellular: dragged with other ions
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12
Q

Describe how chloride is reabsorbed in the PT

A

Paracellular

This is heavily Na+ influenced

Na+ is reabsorbed via the transcellular route (pumps in the cell wall) and pumps positive charges into the renal ISF. These positive charges attract the negative charges on Cl-

Also increased glucose & amino acids influence Na reabsorption

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13
Q

If you have diabetes, what 2 ions will you see an increased reabsorption in? What will this cause?

A

Increase reabsorption of Na (SGLT) & Cl (paracellular route)

This causes a decrease in Na and Cl at the MD –> thinks GFR is low –> releases renin/ANGII –> EA constricts to increase GFR……. you know this

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14
Q

What is osmosis?

A

Passive movement of water from an area of lower osmolarity to a higher osmolarity to equalize osmolarity

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15
Q

What is bulk flow?

A

The process of reabsorption at the PT cap based on the starling capillary forces

Remember NFP = -10 & NRP = 10
This is a high pressure so lots of reabsorption

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16
Q

What is a big portion of the concentrated renal ISF? What is this?

A

Urea

A waste product that assists in concentrating the renal ISF to assist with reabsorption and osmosis

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17
Q

If you’re dehydrated, you would expect your renal ISF to be _________. Why?

A

Very concentrated

Body is trying very hard to conserve water (prevent body from excreting it)

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18
Q

______ assists with osmosis

A

urea

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19
Q

What is the brush border?

A

Brush-looking structure that increases surface area by 20-fold

Increases room for transporters for reabsorption

Located on the apical/luminal side

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20
Q

T/F: Tubular cells are electrically excitable

A

T

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21
Q

What is the charge in the tubular lumen in the Proximal tubule? What attributes to this?

A

-3 mV

Excess Cl-

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22
Q

T/F: Cl- builds up in the PCT. Why?

A

T

Cl- reabsorption lags behind Na+

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23
Q

What part of the PCT is Cl- most absorbed in?

A

2nd half

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24
Q

What happens when proteins are filtered at the GC?

A

A small amount of SMALL proteins can be filtered
Reabsorbed at the PCT ONLY

-1.8g/day filtered
-1.7g/day reabsorbed via endocytosis (pinocytosis) <– this is the max amount
-0.1g/day excreted (this is normal)

After protein is filtered the brush border grabs the protein –> endocytosis –> degrades to amino acids –> reabsorbs

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25
What is the max amount of protein that can be reabsorbed?
1.7g/day
26
T/F: pinocytosis of proteins can happen in the PCT and DCT
F only in the PCT; if it doesnt happen here the protein will be excreted or stuck in tube causing damage
27
About how much protein do we filter per day? Excrete?
1.8g/day 0.1g/day
28
What is the driving forces behind Na reabsorption in the PCT?
1. NHE 2. SGLT 3. Amino acid/Na cotransporter
29
What is the enzyme associate with bicarb formation?
Carbonic Anhydrase
30
Describe the bicarb process
Proton secreted into tubular lumen from NHE pump --> Bicarb forms with it to make carbonic acid --> carbonic acid (H2CO3) + carbonic anhydrase --> Water + CO2 These can freely diffuse across the cell via osmosis/passive diffusion. Once in the cell: Water + CO2 + Carbonic Anhydrase --> Carbonic Acid (H2CO3) --> Bicarb + H+ -Bicarb is reabsorbed via the Na-Bicarb Symporter -H+ is used by the NHE again for the process to start again :)
31
What happens to bicarb if you decrease Na intake?
Decreases **this can cause mild acid/base imbalances** --> acidosis
32
Bicarb formation is dependent on what pump?
NHE
33
Where is CA (carbonic anhydrase) located? What does it do?
-Tethered to the walls & in between cells in the PCT -Breaks down Carbonic Acid H2CO3 to water and CO2 -Tubular cells -promotes formation of carbonic acid from water and CO2
34
What happens to protons if there's no bicard in the tubular lumen?
-Protons attach to the excess ammonia in the urine --> forms Ammonium -Dont want free protons in urine = pain -Ammonium helps buffer Cl-
35
Describe how CA inhibitors work
Inhibit CA in the PCT --> indirectly slows down the NHE pump (Decrease in protons to spin pump) --> less Na reabsorbed & less bicarb reabsorbed Results: Diuretic effects -acidosis
36
Where is glutamine produced?
Liver
37
What does Glutamine do?
PCT -inside tubular cells in combination with Proximal Tubular cell ... Produces NEW bicarb: -- 2 HCO3 and 2 ammonium
38
What is a common side effect we see in people with liver failure?
acid/base imbalances unable to produce sufficient glutamine --> not able to produce new bicarb or ammonium
39
What are the urinary buffers?
-Ammonia/Ammoniun -NaHPO4- (Sodium phosphate) --> NaH2PO4 -Bicarb
40
Describe the Ammonium pump
SECRETES 1 NH4 into tubular lumen for 1 Na reabsorbed into tubular cells -PCT -apical
41
How is Calcium reabsorbed in the PCT?
1. Paracellular: dragged with water/ions 2. Trancellular: -Apical: Ca++ ion channel -Basolateral: Ca++ ATPase & NCX
42
Explain how Ca++ plays a role in acid/base balance
-If you are more acidotic there are more protons in your blood. Those protons will attach to albumin in the blood because they have opposit changes. Causing more free Ca++ to be in the blood. --> More Ca++ able to be filtered -Alkalotic --> more Ca++ binding to albumin --> less Ca++ filtered
43
What detects low Ca++ levels in the blood?
Parathyroid gland
44
How does the parathyroid gland regulate Ca++ levels?
They sense Ca++ is low & release **Parathyroid hormone (PTH)** 1. Increases Vit D activation --> increases the amount of Ca++ absorbed from diet 2. Increases Ca++ reabsorption in kidneys --> increases # of Ca++ channel 3. Stiumlates bone breakdown via osteoclasts --> uses Ca++ store 4. Inhibits activity of osteoblasts --> prevents Ca++ being used to build new bone
45
Our long term Ca++ stores are ______ & short term is _______
Bone Sarcoplasmic Reticulim
46
Differentiate between Osteoblast & osteoclasts
Blasts = bone builder; increases bone density clasts = break down bone
47
What is bone made of?
Calcium Phosphate
48
What is a common disorder we see in people who are chronically hypocalcemic? What does this put them at risk of? What is the Tx for this?
Osteoporosis Bone fractures Tx: Vitamin C with Activated Vitamin D
49
What is an Antiporter?
Pump that secretes organic compounds into the Proximal tubule to be excreted **Location: PT only** Apical/Tubular Lumen
50
What are your endogenous Organic Cations?
**Think neurotransmitters** mostly Ach Creatine choline dopamine epi histamine serotonin NE
51
What are your exogenous organic cations?
**Think heart drugs** isoproteranol atropine procaine quinine tetraethylammonium (TEA) TEE
52
What are the endogenous organic anions?
Bile salts hippurates prostaglandins urate (uric acid) oxalate
53
What are the exogenous organic anions?
**Abx & Diuretics** Furosemide Penicillin Salicyclates (ASA) sulfonamides acetazolamide chlorothiazide
54
How are Organic cations secreted?
An H-Dependent antiporter -Secreted the organic cation into the PCT -Reabsorbs a proton
55
Organic Anions antiporters involve ________
Alpha-Ketoglutarate
56
How are Organic anions secreted?
1. A pump takes 3 Na+ & 1 AlphaKG into the renal ISF from the PT cap 2. That is able to spin the pump that brings in 1 organic anion from the PT cap to the Renal ISF & takes out 1 AlphaKG from the renal ISF 3. Now the antiporter is able to pump the organic anion into the PCT to be excreted
57
How does penicillin stay in the system longer?
Adding a synthetic hippurate This creates competitive inhibition with the antiporters, making penicillin stay in the system longer
58
Explain the history of penicillin
Mold was producing PCN and stopping the growth of bacteria Discovered prior to WWII --> Used during during WWII PCN was leaving the body rapidly --> added hippurate
59
As a rule of thumb, if we dont know how much of something gets reabsorbed at the PCT, its _____
2/3
60
The majority of the loop of henle is _____
thin
61
Describe the Thin Descending Limb
-Fluid is descending into an area w/ a more concentrated renal ISF -Tubular fluid is becoming more concentrated as well Water reabsorption via AQP1 channels **Impermeable to ions**
62
Where is the hairpin turn?
Between the descending and ascending loop of henle
63
Describe the thin ascending limb in the loop of Henle
-Fluid is ascending into an area w/ a more dilute renal ISF -Tubular fluid is becoming more dilute as well Na+/Cl- ATPase (reabsorbs 1Na & 1Cl) **Impermeable to water**
64
____% of ions filtered are reabsorbed ath the thick ascending loop of henle
25%
65
T/F: TAL is permeable to water
F
66
What is the charge in the TAL? What causes this charge? What is the result of this charge?
+8 mV cause: Leak K+ causing a positive charge result: Causes cations to leave the TAL via the paracellular route
67
Which ions are pushed harder via diffusion in the paracellular route? Why?
Mg++ Ca++ They both have a double charge and want to leave even more away from the positive charge
68
Where does acid/base balance happen in the nephron?
TAL PCT Late DCT Collecting tubule
69
What pumps do the TAL have that are neccesary for acid/base balance?
Na/K ATPase NHE
70
Describe the NKCC2 transporter
1 Na+, 1 K+, 2 Cl- cotransporter TAL Apical
71
The ______ plays an important role, along with urea, in concentrating the renal ISF
TAL
72
Where do loop diuretics work? What is the MOA.
TAL inhibit the NKCC2 pump --> This causes the renal ISF to become less concentrated --> losing the ability to reabsorb water --> excrete more urine
73
T/F: Animals that live in the desert can concentrate their renal ISF higher than 1200
T This allows them to reabsorb more water so their body wont excrete it.
74
T/F: urine can be a little more concentrated than the renal ISF
F Urine can only be as concentrated as the renal ISF, not higher
75
What are 3 examples of loop diuretics?
Furosemide Ethacrynic acid bumetanide
76
What helps preserve the osmotic gradient in the loop of henle?
countercurrent blood flow in allows for exchange of solutes & water with distruption of osmotic gradient This is the reason why 1 side is impermeable to water and the other is impermeable to ions
77
Where does PTH influence Ca reabsorption ini the nephron?
PCT DCT
78
What are the pumps associated with Ca++ reabsorption in the DCT?
apical: -Ca++ ion channel -NCC Basolateral: Ca++ ATPase NCX Na/K ATPase
79
The NCX exchanges ___ Na+ ____ the cell for ____ Ca++ _____ the cell
3 Na+ in the cell 1 Ca++ out the cell (renal ISF) **Basolateral**
80
PTH increase Ca++ ion channels on the _____ side of the cell
Apical
81
What pump drives Na reabsorption in the DCT?
NCC (1Na/1Cl)
82
Where do Thiazide diuretics work? What is the MOA.
In the DCT They inhibit the NCC pump --> More Na+ in the tubular lumen & more Ca++ in the renal ISF Results: More Na+ in the tubular lumen --> less water reabsorption --> more water excreted --Increased Ca++ reabsorbed into the renal ISF
83
What medication can help osteoporosis or preventing kidney stones? Why?
Thiazide diuretics Increases reabsorption of Ca++ by inhibiting the NCC pump in the DCT
84
T/F: Thiazide diuretics can get rid of kidney stones
F Can only help prevent
85
The DCT is also sensitive to ______ & ________
ADH Aldosterone (Aldo)
86
Aldo =
Aldosterone
87
Which cells are sensitive to Aldo?
Intercalated & principal cells in the DCT
88
Which cells are sensitive to ADH?
Intercalated cells in the DCT
89
How does Aldo-R work in the DCT?
Speeds up the Na/K ATPase pump which --> 1. Increase K+ secretion 2. Increase Na+ reabsorption
90
Where are Aldo-R located? Why?
Inside intercalated and principal cells Aldo is a cholesterol derivative therefore can cross membranes freely

A/P (33 decks)

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