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Z-Advanced A&P I > Final Exam - Renal 3 > Flashcards

Final Exam - Renal 3 Flashcards

1
Q

Describe angtiotensin II effects on the proximal tubule?

A

Binds to AT I receptors causing:
1. Increase in activity of Na/K ATPase, decreasing [Na+] inside the cell
2. This drives the increase in the NHE transporter, because now Na+ has a greater gradient to enter the cell
3. Increases activity of Na+/HCO3 co-transporter, driven by [HCO3-] intracellularly

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2
Q

Why is paracellular reabsorption prominent in the PCT?
What compound travels by this route and how?

A

The tight junctions are fairly wide, allowing easy passage of solutes.
Cl- and Ca++
Cl- follows the positve charge of the Na+ ion reabsorption. Ca++ follows water reabsorption.

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3
Q

What is bulk flow?

A

They movement of filtrate into the paratubular capillaries set up the capillary starling forces

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4
Q

What drives the movement of water into the PT capillaries?

A

The highly concentrated renal interstitum drives osmosis of water. The primary solute responsible for the renal interstitum osmolarity is urea.

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5
Q

Where is the brush border found and what is its function?

A

Found on luminal side of PCT cells, they are long extensions that increase the surface area of the cells 20x allowing placement of the many transporters.

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6
Q

What is the PCT cell membrane potential? What does this drive?
What is the PCT lumen membrane potential? What causes it?

A

-70mV, promotes Na+ reabsorption
-3mV, caused by dissolved solutes (Na+, K+, primarily Cl-)

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7
Q

Describe Na+ and Cl- concentration as they move through the PCT?

A

Na+ concentrations stay the same throughout the tubule because it’s reabsorption follows water reabsoprtion.
Cl- ion reabsorption is delayed, causing its concentration to increase along the tubule until enough Na+ ions have been reabsorped then Cl- follows it.

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8
Q

How much protein is filtered each day in a healthy patient?
How much is reabsorped? How is it reabsorped?

A

1.8g filtered (mostly peptides, few albumin)
1.7g reabsorped
Reabsoped by tubular cells only in the PCT via endocytosis(pinocytosis) where the proteins are broken down to amino acids to be recycled (this process cannot be sped up)

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9
Q

What is the primary way Na+ is reabsorped in the PCT?

A

The NHE

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10
Q

Explain acid-base balance in the PCT?

A

The NHE secretes a H+ into the tubule lumen with each cycle. This H+ can bond with HCO3- to create carbonic acid. Carbonic acid dissociates into CO2 + H2O, both of which freely cross the tuble cell membrane. Once inside the cell, CO2 and H20 combine again forming carbonic acid, which dissociates into HCO3- and H+. HCO3- can then be reabsorped and H+ secreted again via the NHE.

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11
Q

Describe the role of carbonic anhydrase?

A

Found intracellularly and on the luminal wall. Speeds up the conversion of carbonic acid. Can either break down carbonic anhydrase into CO2 and H2O or create carbonic anhydrase from CO2 and H2O. The direction is driven by the reactants available (HCO3- and H+, or CO2 and H2O)

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12
Q

What are the effects of carbonic anhydrase inhibition?

A

Decreases the speed of the NHE, reducing H+ in the tubule, preventing HCO3- reabsorption, causing HCO3- loss in the urine leading to acidosis. Also, prevents Na+ reabsorption, causing decreased H2O reabsorption leading to diuresis and decreased BP.

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13
Q

Where does glutamine come from?
What is it’s role in the PCT?

A

Produced by the liver; patient’s in liver failure have difficulty with acid base balance.
Broken down into 2 HCO3- and 2 NH4+ in the tubular cells.

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14
Q

What is ammonium’s role in the tubules?

A

NH4+ is a urinary buffer because H+ can bind to NH3 (ammonia) and be excreted as NH4+

We don’t want protons being excreted unbound because it would be very damaging to the tubules and urinary tract

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15
Q

What role does phosphate play in the PCT?

A

Uriniary buffer, combines wih H+ in the tubule and then excreted.

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16
Q

How is calcium reabsorped in the PCT?

A
  1. Via paracellular route by following water
  2. From lumen via transcellular route by Ca++ channels, To renal interstitum via Ca++ ATPase and NCX.
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17
Q

What can reduce calcium filtration and reabsorption?

A

Calcium can be more protein bound if blood pH is more basic, preventing it from being filtered/reabsorbed.

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18
Q

What are the 3 ways PTH increases calcium levels?

A

The parathyroid gland releases PTH when calcium is low. PTH causes: 1) increased Vitamin D activation, increasing intestinal Ca reabsorption. 2) Increased renal calcium reabsorption 3) Increased Ca release from bones

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19
Q

How does PTH cause Ca release from the bones?
How is this related to osteoporosis?

A

Increases osteoclast activity, which breaks down bones (Ca + PO4).
Decreases activity of osteoblasts which build bones from Ca and PO4

In osteoporosis there is chronically low Ca levels. So PTH is very active inhibiting bone building and promote bone break down. This causes the bones to become porous overtime.

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20
Q

How are organic cations secreted by the PCT?

A

Leave the PT capillaries and are in the renal interstitum. The cation enters the cell via specialized transporter and moves into the lumen via cation proton anti-porter. Cations are H+ dependent transport.

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21
Q

How are organic anions secreted by the PCT?

A

Alpha-ketoglutarate (aKG) is uptaken into tuble cells with 3 Na+ creating a high concentration of aKG inside the cell. A different transporter can exchange aKG for the organic anion bringing it into the cell. Once in the cell, it its moved into the lumen by an anion transporter.
Anion transport is Na+ dependent.

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22
Q

What are some endogenous organic cations?

A
  • ACh
  • Creatinine
  • Dopamine
  • Epinephrine
  • Histamine
  • Serotonin
  • Norepinephrine
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23
Q

What are some exogenous organic cations?

A
  • Atropine
  • Isoproternol
  • Morphine
  • Procaine
  • Quinine
  • TEA
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24
Q

What are some endogenous organic anions?

A
  • Bile salts
  • Hippurates
  • Oxalate
  • Prostaglandins
  • Urate
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25
Q

What are some exogenous organic anions?

A
  • Furosemide
  • Penicillin
  • Salicylates
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26
Q

Why was penicillin given with hippurates?

A

Penicillin is heavily secreted in the kidneys. Hippurates use the same secretion transporter as penicillin. Giving enough hippurate would competitively inhibit the transporter allowing PCN levels to remain at a higher level in the body.

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27
Q

What occurs in the descending limb of the loop of Henle?

A

Water reabsorption occurs because the filtrate is descending into medulla where the renal interstitum has a increasingly high osmolarity.

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28
Q

What occurs in the thin ascending limb of the loop of henle?

A

Impermeable to water
Na+/Cl- ATP transporters here are reabsopring Na+ and Cl- from the filtrate

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29
Q

Describe cation reabsorption in the thick ascending loop of henle?

A

Still impermeable to water.
Cations can be reabsorped via paracellular routes. Ca++ and Mg++ reabsorption is driven by K+ leaking from tubular cells that create a tubule membrane potential of +8mV.

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30
Q

What transporters are present at the apical side of the thick ascending loop of henle?
Why are these important?

A

NHE
NKCC2
K+ leak channels
Responsible for generating the highly concentrated renal interstitum.

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31
Q

Why is furosemide the most powerful diuretic?

A

Furosemide inhibits the NKCC2
This decreases the concentration of the renal interstitum, causing decreased water reabsorption, increasing diuresis.

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32
Q

What is the most concentrated the renal interstitum can be?
What compouds make up the osmolarity?

A

1200 mOsm
Dissolved ions and urea

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33
Q

What would it mean if the urine concentration was 1200 mOsm?

A

It would mean that the body is trying to conserve water by removing as much water as possible from the urine.

34
Q

What drives urine osmolarity?

A

The concentration of the renal interstitum.
The urine concentration will match the renal interstitum concentration because water will be reabsorbed via osmosis until interstitum and lumen to have the same concentration.

35
Q

How does PTH increase Ca reabsorption in the kidney?

A

PTH increases the number of Ca channels in the lumen of the distal tubule.

36
Q

What transporter is at the distal tubule?
What drugs inhibit it?

A

Na/Cl transporter
Thiazides

37
Q

What cells are sensitive to aldosterone and ADH in the distal tubule?

A

Principal cells: Aldosterone and ADH
Intercalated cells: ADH

38
Q

What effects does aldosterone have at the principal cells?

A

Aldosterone can enter the cell can bind to the ALDO receptor intracellularly bc aldosterone is a cholesterol derivative.
Binding causes increase in the Na+/K+ pump, lowering the intracellular Na+ which increases the activity of Na+ channels. This increases Na+ reabsoprtion which increases H2O reabsporption. This also results in increased K+ secretion.

39
Q

How much of the filtered water is reabsorped in the thick descending loop of henle?
How much of the total water has been reaborped by this point?

A

20%
85% (65% filtered in the PCT)

40
Q

How much of the filtered ions are reabsorped in the thick ascending loop of henle?

A

25%

41
Q

Where is the last place in the nephron that solutes and water can be reabsorped?

A

The collecting duct via principal and intercalated cells

42
Q

What two areas of the nephron have the highest metabolic rate?

A
  • The PCT and the thick ascending limb of the loop of henle
  • Lots of reabsorption occuring via transporters here (requires energy)
43
Q

How is calcium primarily transported from distal tuble cells to the interstitum?
What drives this pump?

A
  • NCX
  • The Na+/K+ ATPase pump
44
Q

Describe how a thiazide diuretic can increase calcium reabsorption?
When would this be useful?

A

Thiazides inhibit the Na+/Cl- pump in the DCT
This reduces Na+ entry into the cell, and reduces the activity of the Na+/K+ ATPase. The decreased intracellular concentrations of Na+ causes an increased gradient for for Na+ entry from the interstitum.
This increases Na+ entry via NCX which in turn increases calcium reabsorption

Useful in osteoporosis and preventing kidney stones (reduces calcium build up in the urine)

45
Q

What class of drug is aldosterone?

A

Mineralcorticoid

46
Q

What are the effects of aldosterone on the number Na+ and K+ channels at the apical wall of principal cells?

A
  • Increases the number of ENaC channels
  • Increases number of K+ channels by increasing their placement on the wall by ROMK and by opening BK channels (Big Potassium) which are normally closed.
47
Q

What drugs inhibit ENac channels?
What are it’s effects?

A
  • Amiloride and triamterene
  • Decreased Na+ entry via ENaC which also results in decreased secretion of K+
48
Q

What drug is an aldosterone antagonist?
What are it’s effects?

A
  • Spirinolactone
  • Blocks the effects of aldosterone which decreases the Na+/K+ ATPase, and decreases Na+ and water reabsorption and K+ secretion (potassium sparing).
49
Q

Describe the process of how upstream diuretics cause potassium wasting?

A

Upstream diuretics block the reabsorption of Na+ and or Cl-. This causes there to be an increased amount of Na+ that arrives at the principal cells. The increased concentration of Na+ increases the rate of it’s reabsorption via ENaC channels. Because the Na+/K+ ATPase is responsible for moving Na+ from the prinicipal cells to the interstitum, its increased cycling increases the entry of K+ and its secretion into the tubule.

50
Q

What is 1?
What is produced here?

A
  • Zona glomerulosa of adrenal gland
  • Aldosterone
51
Q

What is 2 and 3?
What is produced here?

A
  1. Zona fasciculata of adrenal gland
  2. Zona reticularis of adrenal gland
    Cortisol and androgens

GFR (Glomerulosa, Fasciculata, Reticularis)

52
Q

What class is cortisol in?
Why is it called this?

A
  • Glucocorticoid
  • Helps maintain glucose levels
53
Q

What is 4?
What is produced here?
How much?

A
  • Medulla of adrenal gland
  • Epinephrine and Norepinephrine
  • 4:1; Epi:Norepi
54
Q

What causes release of aldosterone from the zona glomerulosa?

A
  • Increased potassium levels
  • Angtiotensin II binding to AT I receptors
55
Q

What enzyme produces aldosterone in the zona glomerulosa?

A

Aldosterone synthase

56
Q

Why does taking steroids cause hypertension and hypokalemia?

A

Many of the steroid compounds in the body have a very similar structure. Two of these are aldosterone and cortisol. Steroids increase cortisol levels and because cortisol looks a lot like aldosterone, it can bind to the aldo receptor when in high amounts, causing the same effects as aldosterone (Increased Na+ and H2O reabsorption = increased BP, and increased K+ secretion)

57
Q

How do our bodies prevent cortisol form binding to aldo receptors at baseline?
What natural compound inhibits this?

A

The enzyme 11ꞵ-HSD Type II (hydroxysteroid dehydrogenase)
Found in principal cells and destroys cortisol
Licorice - found as a flavoring in tabacco

58
Q

What is the role of intercalated cells in the DCT?
How is this accomplished?

A
  • Acid-Base balance
  • Type A cells: secrete H+ via H+/K+ ATPase and Hydrogen ATPase pump (reduces Acidosis)
  • Type B cells: reabsorp H+ and secrete HCO3- (reduces Bases)
59
Q

Where does vasopressin bind on principal and intercalated cells?
Describe it’s effects?

A
  • V2 receptors
  • Activates Gs, adenylyl cyclase, activating cAMP which activates PKA, causing phosphorylation of AQP-2 channels which moves them to luminal surface where they allow water reabsorption
60
Q

What are the different aquaporins in intercalated and principal cells?
Where are they?
What are they dependent on?

A

AQP-3 and AQP-4 on basolateral membrane, always present
AQP-2 on apical membrane, dependent on vasopressin

61
Q

What is nephrogenic DI?
What can cause this?
What would their urine osmolarity be?

A
  • Cellular dysfunction in ability to respond to vasopressin
  • Lithium therapy; causes very dilute urine in high quantities
  • EtOH
  • 50 mOsm
62
Q

What is central DI?
What can cause this?

A
  • Problem with the release of ADH from pituitary gland
  • EtOH
63
Q

What are the diluting segments?
Why are they called this?

A

Thin and thick asecending limb of loop of henle and begining of DCT
They are relatively impermeable to water, but lots of solutes are reabsorped causing a reduction in the tubule fluid osmolarity (dilution)

64
Q

What receptors controls vasopressin levels?

A
  • Osmoreceptors
  • Barorecptors (sense volume in venous side and pressure in arterial side)
65
Q

What are the two cell bodies where osmo and baro receptors synapse?
Where is their location?
What is their function?

A
  • Supraoptic neuron- sits above above pituatary gland in hypothalamus- 5/6th of vasopressin release
  • Paraventricular neuron - on the sides of the 3rd ventricle in the hypothalamus - 1/6th of vasopressin release
66
Q

What is 1?

A

Posterior lobe of pituitary gland also called the neurohypophysis

67
Q

What is 2?

A

Anterior lobe of pituitary gland also called the adenohypophysis

68
Q

Describe ADH release from the pituitary gland?

A

ADH produced in the hypothalamus descends a pathway that empties into the posterior lobe of the pituitary gland which is highly vascularized and enters the circulation.

69
Q

How do osmoreceptors cause changes in ADH?

A
  • Osmoreceptors swell when osmolarity is low, causing a decreased firing of AP to the hypothalamus, reducing ADH release
  • Osmoreceptors shrink when osmolarity is high, causing an increase in AP firing to the hypothalamus, increasing ADH release
70
Q

Why is the osmolarity in the PCT the same as the plasma?

A

Because there is an equal amount of solutes and water being reabsorbed causing the concentration to remain the same.

71
Q

Describe the osmolarity in the descending and ascending loop of henle?

A
  • The descending loop of hele becomes progesively more concentrated due to water loss driven by the osmolarity of the renal interstitum.
  • The ascending loop of henle is impermeable to water, becoming less concentrated as Na+ and Cl- are being reabsorbed, diluting the tubular fluid.
72
Q

What determines the osmolarity of our urine?

A
  • The amount of ADH
  • More ADH causes more water resabsorption, leaving solutes in the tubule, increasing urinary concentration
  • Less ADH means less water reabsorption, more water in the tubule, and more dilute urine
73
Q

What is the lowest our urine osmolarity can be?

A

50 mOsm

74
Q

How does ADH control the osmolarity in the loop of henle?

A

ADH causes increased reabsorption of urea from the collecting duct via UT-A1 and UT-A3, increasing the osmolarity of the renal interstitum, increasing the amount of water reabsorped from the loop of henle, which increases tubular solute concentrations.

The descending loop of henle will match renal interstitum concentration due to osmosis of water.

75
Q

What is the primary controller of our plasma osmolarity?
What natural compound inhibits it?

A
  • ADH- it is able to change rate of water reabsorption without changing electrolyte levels
  • Caffeine
76
Q

What are some things that decrease thirst?

A
  • Decreased plasma osmolarity
  • Increased blood volume
  • Increased blood pressure
  • Decresed angiotensin II
  • Gastric distention
77
Q

What things increase thirst?

A
  • Increased plama osmolarity
  • Low blood pressue
  • Low blood volume
  • Increased angiotensin II
  • Dryness of the mouth
78
Q

What decreases ADH?

A
  • Decreased plasma osmolarity
  • Increased blood volume
  • Increased blood pressure
  • Alcohol
  • Haldol
  • Clonidine
79
Q

What increases ADH?

A
  • Increased plasma osmolarity
  • Decreased blood volume and pressure
  • Nausea (anticipated loss of volume)
  • Morphine
  • Nicotine
80
Q

What is normal urine osmolarity?

A

600 mOsm, although it changes with fluid intake

81
Q

Desribe the effects of drinking 1L of distilled water on urine and plasma osmolality, urine flow rate, urine solute excretion, and ADH levels?

A
  • Initially when we intake the water we will have a small dip in plasma osmolarity (dilution), this immediately causes decrease in ADH secretion
  • The reduction in ADH temporarily increases our urine flow rate until enough fluid has been excreted to return plasma osmolarity to normal
  • Urine osmolarity decreases as well due to the increased water excretion, until plasma osmolarity is normal
  • Reduced ADH causes more water to be removed but doesn’t affect number of solutes, keeping urine solutes normal.
82
Q

What regulates plasma K+ levels?

A

Aldosterone

Z-Advanced A&P I (12 decks)

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