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A&P I (Fall 2022) > Renal Physiology Pt. 2 (Final Exam) > Flashcards

Renal Physiology Pt. 2 (Final Exam) Flashcards

1
Q

What names are given for the cell side that is in contact with the urinary lumen?

A
  • Apical / Tubular / Luminal Side
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2
Q

What is the name given for the side of the cell that is in contact with the interstitium?

A
  • Interstitial Side
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3
Q

What is transcellular reabsorption?

A

Reabsorption occurring through the cell

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4
Q

What is paracellular reabsorption?

A

Reabsorption occurring in-between cells

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5
Q

What mechanism drives the processes of transcellular reabsorption?

A
  • Na⁺ gradient with Secondary Active Transport.
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6
Q

What are the most important transporters in the Proximal Convoluted Tubule?

A
  • Na⁺/Glucose Symporter
  • Na⁺/AminoAcid Symporter
  • Na⁺/H⁺ Antiporter
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7
Q

What ion is reabsorbed by following Na⁺?
By what route is this ion reabsorbed?

A
  • Cl⁻
  • Paracellular Pathway
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8
Q

What molecule follows Na⁺ & Cl⁻ ?

A

H₂O

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9
Q

Movement of _______ is always passive.

A

water

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10
Q

What is bulk flow?

A
  • The flow of H₂O and dissolved substances.
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11
Q

What is the Vᵣₘ of tubular epithelial cells?

A
  • -70mV
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12
Q

What is the brush border?
Where is it located?
What is its purpose?

A
  • Projections out of tubular epithelial cells
  • Located on the tubular lumen side.
  • ↑ surface area
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13
Q

What anatomical component prevents H₂O and electrolyte permeability in between cells?
How does this compare in the proximal tubule?

A
  • Tight junctions
  • Less tight in the PCT.
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14
Q

What is needed for Ca⁺⁺ and Mg⁺⁺ reabsorption?

A
  • Positively charged urinary lumen
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15
Q

How much reabsorption of filtrate occurs in the Proximal Tubule?
What is secreted here?

A
  • 2/3
  • H⁺, organic acids/bases
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16
Q

What two molecules, spoken about in lecture, are highly absorbed in the PCT?
What molecule has no reabsorption in the PCT?
What would occur with this molecule’s luminal concentration as it moves along the tube?

A
  • Glucose & amino acids
  • Creatinine; concentration would increase as the fluid moves down the PCT.
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17
Q

Where does secretion of organic anions & cations occur?
Via what transporters?

A
  • PCT
  • OAT’s & OCT’s
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18
Q

What section of the nephron is primarily responsible for pH regulation?

A
  • PCT
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19
Q

Which transporter is the SGLT?
What does SGLT stand for?

A
  • Na⁺/Glucose Cotransporter
  • Sodium/Glucose Transport Protein
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20
Q

What is the name for the antiporter that moves H⁺s in the PCT?

A
  • NHE (Sodium/Hydrogen Exchanger)
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21
Q

Where are the SGLT, NHE & Na⁺/AA symporter transporters located?

A
  • Apical lumen of the PCT.
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22
Q

What would you expect the ICF concentration of glucose to be in a tubular cell with a healthy SGLT?

A
  • High Concentration of glucose in the ICF.
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23
Q

What GLUT transporter is located in the
S1 segment of the Proximal tubular cells?
What side is this located on?
How does this move glucose and to where?

A
  • GLUT-2
  • Interstitial side
  • Glucose moved to interstitium via facilitated diffusion. (down its concentration gradient)
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24
Q

How much paracellular movement of glucose occurs in the Proximal Tubule? Why?

A
  • None. Glucose is too big to move paracellularly.
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25
Q

What ratio of Na⁺/Glucose is reabsorbed via SGLT2 in the S1 segment of the Proximal Tubule?

A

1:1

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26
Q

What ratio of Na⁺/Glucose is reabsorbed via SGLT1 in the S2/S3 segments of the Proximal Tubule?

A

2Na⁺ : 1Glucose

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27
Q

What occurs with Na⁺ reabsorption when a patient is severely hyperglycemic?

A
  • Na⁺ reabsorption increases (due to co-transporter nature)
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28
Q

What is the mechanism behind a chronically increased GFR with chronic hyperglycemia?

A
  1. ↑Gl reabsorption = ↑Na⁺ reabsorption
  2. Less Na⁺ downstream for Macula Densa.
  3. MD thinks GFR is low and dilates afferent arteriole & constricts efferent arteriole.
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29
Q

What occurs long term to nephrons with hyperglycemia?
What would help prevent this damage?

A
  • Nephron damage from chronically increased GFR from hyperglycemia.
  • ACE Inhibitors or ARBs.
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30
Q

What percentage of glucose reabsorption occurs via the S1 segment of the PCT?
What GLUT transporter is used here?
What sodium/glucose transporter is used on the S1 segment?

A
  • 90%
  • GLUT-2
  • SGLT2
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31
Q

What GLUT transporter is located in the
S2/S3 segment of the Proximal tubular cells?
How much of glucose reabsorption occurs here?
What sodium/glucose transporter is used in the S2/S3 segments?

A
  • GLUT-1
  • 10%
  • SGLT1
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32
Q

What drug inhibits the NHE?
What are the effects of this?

A
  • Acetazolamide
  • ↓Na⁺ reabsorption = H₂O loss & ↓BP.
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33
Q

Where does the majority of urea management occur?
Besides this, what other areas manage urea?

A

-Medullary Collecting Duct via ADH
- Proximal Tubule

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34
Q

What enzyme would facilitate the process in the figure below?

A
  • Carbonic Anhydrase (CA)
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35
Q

Each HCO₃⁻ reabsorbed or produced means less _____.

A

H⁺

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36
Q

What serum glucose is considered normal for A&P class?
At what serum glucose do we exceed to the ability of the kidney to completely reabsorb all filtered glucose?

A
  • 100mg/dL
  • 200mg/dL
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37
Q

At what serum glucose do we meet our transport maximum?
What does this mean?

A
  • 375mg/dL
  • All glucose past this serum level is excreted.
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38
Q

How is filtered load calculated? Give an example with glucose.

A

Filtered Load = VFF (volume of filtered fluid) · [substance]
FL = 1.25dL/min · [100mg/dL glucose]
Filtered Load = 125mg/min

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39
Q

Long-term use of SGLT Inhibitors would have what effect on one’s weight?

A
  • Weight loss would occur
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40
Q

What would SGLT Inhibitors do the glucose transport max and the glucose threshold?

A
  • ↓ Transport max
  • ↓ Threshold
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41
Q

Are SGLT Inhibitors natriuretics? Why or why not?

A
  • Yes; Block Na⁺ & Glucose reabsorption = more Na⁺ later in tube with H₂O following.
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42
Q

What effects would SGLT Inhibitors have on angiotensin? Why?

A

SGLT inhibition = ↑[Na⁺] at macula densa = ↓ Angiotensin.

43
Q

Where is new bicarbonate produced?
What molecule is broken down for this process?
What two molecules are created via this breakdown?

A
  • Proximal Tubular cells
  • Glutamine
  • 2HCO₃⁻ + 2NH₄⁺
44
Q

What makes urine smell?
How is this byproduct of bicarbonate production secreted?

A
  • NH₄⁺
  • Via the Na⁺/NH₄⁺ antiporter.
45
Q

What important urinary buffer (other than HCO₃⁻) was discussed in lecture?
Where does this buffer typically come from?

A
  • PO₄⁻
  • PO₄⁻ comes from bone breakdown.
46
Q

Describe the renin-angiotensin-aldosterone system (RAAS) system?

A
  1. Angiotensinogen → Renin
  2. Renin → Angiotensin 1
  3. Ang 1 → ACE → Ang 2
47
Q

Where is angiotensinogen produced?

A
  • Liver
48
Q

What effect does Angiotensin II have on angiogenesis?
What effect does blockage of angiotensin II have on cancer growth?

A
  • ↑ Angiogenesis
  • ↓ Cancer growth
49
Q

What pumps in the proximal tubule would be affected by angiotensin II activation?

A

Potentiate:
- Na⁺ K⁺ ATPase pump
- NHE pump
- Na⁺ HCO₃⁻ symporter

50
Q

What receptors are used by Ang II in the proximal tubule?
What would occur if this receptor was blocked?

A
  • AT1 receptors
  • Acid/Base Issues
51
Q

What effects would be generated by Ang II in the proximal tubule?

A
  • ↑ Na⁺ reabsorption = ↑ H₂O reabsorption
  • ↑ H⁺ secretion
52
Q

Where is does calcium regulation occur?
By what paths does calcium reabsorption occur?

A
  • Proximal tubule
  • Transcellular & Paracellular
53
Q

How does Ca⁺⁺ get from the proximal tubular cells into the ISF?

A
  • Ca⁺⁺ ATP Pump
  • 3Na⁺/ Ca⁺⁺ Antiporter
54
Q

How does the body respond to hypocalcemia?

A
  • By releasing PTH (parathyroid hormone)
55
Q

What are the three effects of parathyroid hormone?

A
  • ↑ Ca⁺⁺ release from bones
  • ↑ renal Ca⁺⁺ reabsorption
  • ↑ Vitamin D₃ activation
56
Q

In the thin descending portion of the Loop of Henle we have ______% of our total water reabsorption via _______.
What is the mechanism that facilitates this?

A
  • 20% : aquaporins.
  • Increasing ISF concentration.
57
Q

What would cause in a more positive urinary lumen in the Thick Ascending Limb (TAL)?
What would this in turn result in?

A
  • ↑[K⁺] from leaky K⁺ channels
  • ↑ reabsorption of Ca⁺⁺ & Mg⁺⁺ via paracellular reabsorption.
58
Q

What ion transporters are active in the TAL?

A
  • Na⁺, 2 Cl⁻, & K⁺ transporters
59
Q

What do loop diuretics inhibit?
What does this result in?

A
  • Ion transporters of the TAL
  • Loss of ions & less [ ] ISF = H₂O loss
60
Q

What three loop diuretics were mentioned in lecture?

A
  • Furosemide
  • Ethacrynic Acid
  • Bumetanide
61
Q

Which segment is known as the diluting segment?
Why?

A
  • DCT
  • Reabsorption of salts but not H₂O occurs here.
62
Q

What happens if no AQP-2 are activated in the medullary duct?

A
  • No AQP-2 = No urea to ISF = ↑ H₂O loss
63
Q

Where are the juxtaglomerular cells located?
What do these cells release?

A
  • Afferent Arteriole primarily
  • Renin
64
Q

Where is the Macula Densa located?

A
  • Very beginning of the DCT or the end of the TAL
65
Q

What are triggers for Ang II release?

A
  • Hypotension or hyponatremia
66
Q

What mediates afferent arteriole dilation?

A
  • NO release
67
Q

What mediates Efferent arteriole constriction?

A
  • Renin-Ang II
68
Q

What cells produce Renin?

A
  • Granular Cells
69
Q

Where are cations secreted at?
By what method are cations secreted?

A
  • Proximal Tubule
  • C+/H⁺ Antiporter
70
Q

What exogenous drugs (mentioned in lecture) would be secreted via OCT’s?

A
  • Atropine
  • Isoprel
  • Morphine
  • TEA
71
Q

What endogenous compounds would be secreted via OCT’s?

A
  • ACh/Choline
  • Creatinine
  • Monoamines (NE, Serotonin, Dop, Epi, etc)
  • Thiamine
  • Guanidine
  • Histamine
72
Q

What compound is necessary for Anion secretion?

A
  • αKG (αlpha-keto-glutarate)
73
Q

How are anions secreted in the proximal tubule?

A
  1. 3 Na⁺ / αKG Symporter
  2. αKG / A⁻ Antiporter
74
Q

What are examples of endogenous anions that would secreted by OATs?

A
  • Bile Salts
  • Fatty acids
  • Hippurates
  • Hydroxybenzoates
  • Oxalate
  • Prostaglandins
  • Urate
75
Q

What are examples of exogneous anions that would secreted by OATs?

A
  • Acetazolamide
  • Furosemide
  • Penicillin
  • Salicylates
  • Sulfonamides
76
Q

How was penicillin conserved during World War II?

A
  • PAH was given to keep the OAT’s “busy” so that penicillin stuck around longer.
77
Q

What could be said about ADH if a medullary osmolarity of 1200 was noted?
Why would this osmolarity be this high?

A
  • ADH levels would be high.
  • Due to ADH causing Urea to be reabsorbed thus massively increasing medullary ISF concentration.
78
Q

What cells mediate K⁺ levels?
What cells mediate acid/base balance?
Where are both of these cells located?

A
  • Prinicipal Cells
  • Intercalated cells
  • DCT & collecting duct
79
Q

Does PTH have a greater effect in the PCT or the DCT?

A
  • DCT
80
Q

Where is the Na⁺/Cl⁻ symporter located?

A
  • Luminal side of DCT
81
Q

What do thiazide diuretics inhibit?
What is the effect of this on Ca⁺⁺?

A
  • Na⁺/Cl⁻ symporter
  • ↑ Ca⁺⁺ absorption due to better Na⁺ gradient for 3Na⁺/Ca⁺⁺ symporter on interstitial side
82
Q

What is the primary source of salt reabsorption in the DCT?

A
  • Na⁺/Cl⁻ symporter
83
Q

What are the two types of cells in the DCT?
What do each of these regulate?

A
  • Principal Cells - K⁺ regulation
  • Intercalated Cells - acid/base regulation
84
Q

Both intercalated and principal cells are responsive to ______.

A

ADH

85
Q

Diuretic use prior to the DCT (particularly the principal cells) results in greater concentration of what ion in the tubule?

A
  • Na⁺
86
Q

What two ions are reabsorbed in the principal cells?
What ion is lost in the prinicipal cells?

A
  • Na⁺ & Cl⁻
  • K⁺
87
Q

Where does Aldosterone cause its effects?
What does it do?

A
  • Principal cells of the DCT
  • Potentiates Na⁺ K⁺ ATPase pump
  • Increases Na⁺ channels
  • Causes K⁺ loss
88
Q

What drugs inhibit Aldosterone?

A
  • Spironolactone
  • Eplerenone
89
Q

What endogenous molecule can inhibit Aldosterone in high enough concentrations?
What enzyme helps prevent this?
What food can inhibit this enzyme?

A
  • Cortisol
  • 11β-HSD2 Enzyme
  • Licorice
90
Q

What occurs with tubular sodium near principal cells?
What can inhibit this?

A
  • Na⁺ is reabsorbed from the apical lumen via the ENaC (epithelial Na⁺ channel)
  • Amiloride & Triamterene (Na⁺ channel blockers)
91
Q

What is another name for aldosterone receptors?

A
  • Mineralcorticoid Receptors
92
Q

Where is Aldosterone produced?

A

Zona Glomerulosa of the Adrenal Cortex (outermost part of the cortex)

93
Q

What causes Aldosterone to be released?

A
  • Angiotensin II binding to AT1 receptors on the renal cortex.
94
Q

What maintains homeostasis of serum K⁺?

A
  • Aldosterone
95
Q

How is hyperkalemia dealt with using the Renal system?

A
  • Aldo increases K⁺ secretion in Cortical collecting tubules.
96
Q

Where are V2 receptors located?
What is the endogenous ligand for V2 receptors?

A
  • Intercalated cells of the DCT & Collecting Duct.
  • ADH (Vasopressin)
97
Q

What occurs with when ADH binds to V2 receptors in intercalated cells?

A
  • ↑ H₂O reabsorption
  • ↑ Urea reabsorption
98
Q

What structure allows water flow into intercalated cells from the tubular lumen?
What structures allow water flow from the intercalated cells into the ISF?

A
  • Tubular side: AQP-2
  • Interstitial side: AQP-3 & AQP-4
99
Q

What occurs with V1 receptor agonism?

A
  • Vasoconstriction & ↑SVR
100
Q

_________ interferes with the release of ADH from the pituitary gland thus resulting in ____________.

A
  • Ethanol ; diuresis
101
Q

Differentiate AQP-2, AQP-3, & AQP-4.

A
  • AQP-2 - ADH activated, tubular side of intercalated cells.
  • AQP-3, AQP-4 - always present, interstitial side of intercalated cells.
102
Q

What cells deal with acid/base homeostasis in the kidney?
Where are these located?

A
  • Type A & Type B intercalated cells.
  • Located in late DCT, & cortical & medullary collecting duct.
103
Q

Which intercalated cell secretes protons and which reabsorbs protons?

A
  • Type A = Secretion
  • Type B = Reabsorption

A&P I (Fall 2022) (17 decks)

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