A&P Final Lecture 5 Notes Flashcards

1
Q

What happens to the creatinine production, and renal excretion (grams/ day) and plasma creatine concentraion once the GFR drop

A

It drops as well,
Due to the disruption in the balance the plasma creatinine concentration must increase

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2
Q

What causes a long term increase in the Plasma creatinine concentration (mg/dl)?

A

-Due to the disruption in the balance the plasma creatinine concentration must increase, over a couple of weeks

-long term and sustained decrease in GFR causes an increases the amount of creatinine production,therefore, renal excretion (grams/ day) gets back to normal

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3
Q

What causes the life span of the remaining nephons to be cut short ?

A

-Due to higher concentration of toxic compounds that are filtered
-The workload of the remain nephrons are increased

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4
Q

What happens to the remaining kidney’s physical form and the plasma creatinine concentration when the other kidney have been removed?

A

the kidney becomes larger
plasma creatinine concentration increase

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5
Q

what should we expect to see in the steady state as the result of some pathology disease of the kidney?

A

-Doubling plasma creatine

-Cutting GFR in half

-Causing and imbalance relationship in the plasma creatine being created and being filtered

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6
Q

Where is most of NBC transporter found within the renal system and what do they transport ?

A

Proximal tubules
Sodium, bicarb

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7
Q

How did the bicarb get into the tubular lumen?

A

filtration

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8
Q

What is the key enzyme that places a role in bring bicarb back into the tubular cell?

A

Carbonic Anhydrase

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9
Q

What is the amino acid use to create to allow the kidney to procduce their ____________ in the kidney?
What is the name (s) and amount of the product produce?

A

Glutamine ( non - essential amino acid)

2 bicarb - that goes back into the renal interstitum
2 NH3 ( ammonia ) - that is transfer out by the NBC transporter to be use as a protons

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10
Q

After the glutamine metabolism what is the name of the transporteror exchanger that moves the waste product into the tubular lumen?

A

Ammonium sodium exchanger

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11
Q

Where are the 3 main places we can metabolize glutamine to produce bicarb and ammonium in the tubule system would be

A

Proximal Tubules (PT) - most important place
Thick ascending limb of the loop of Helen (TAL)
Distal collecting Tubules (DCT)

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12
Q

What is the primary compound that places a large role in regulating the pH in the urine?

A

Phosphate

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13
Q

What role does angiotensin II places on the glomerular feedback system?

A

Angiotensin II places a role in glomerular feedback system that helps regulated our GFR

RAA Axis
1. Renin causes a release of angiotensin I
2. Angiotensin I is converted into angiotensin II by ACE
3. Causing an increase in the amount of aldosterone
4. Release from the adrenal glands

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14
Q

Where witihin the renal circulatory system can angiotensin II effects be seen?

A

-Afferent arterioles

-Efferent arterioles

-Speeding up some of the process in the proximal tubules

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15
Q

What is the name of the receptor that allows Angio II to bind?

A

Angiotensin II type 1 receptor

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16
Q

What is the MOA of Ang II binding to the receptor?

A

speeds up the sodium /potassium ATP ase pump

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17
Q

How do Ang II cause the sodium/ hydrogen exchanger speed increase?

A

Ang II increases the speed up the sodium /potassium ATPase pump

Lowering the concentration of sodium within the cell

Therefore, the sodium / hydrogen causes the exchanger to increase

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18
Q

What affects does angiotensin II have on the renal system?

A

increase GFR
conserve volume when need

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19
Q

What is the steps in the negative feed back loop that allows the kidney to increase volume involving angiotensin II due to a low BP?

A

Low BP

Low GFR

Low Sodium /chloride deliver to the macula Desa

renin release

results Angiotension 2 production

increasing the amount of sodium in the tubule

increasing water

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20
Q

Calcium follows what electrolyte in the paracellular pathway?

A

Chloride

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21
Q

What are the 2 main pathways that calcium take to reenter the proximal tubules?

A

transcellular pathways
paracellular pathways

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22
Q

What percentage of calcium in the plasma is being filtered and why?

A

60% of the calcium that is in the plasma that is actual filtered

Calcium is freely filterable

Complicated factors:
-Calcium has 2 charges
-Hangs out near proteins within the plasma concentration (that has a net negative charge)
- 40 % calcium is hanging around the protein, because protein is to large to be filtered the calcium is never filtered

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23
Q

How is calcium transported out of the proximal tubule and into the Renal insterstitium?

A

Calcium ATPase
Calcium / Sodium exchanger

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24
Q

What is the molecule that helps control calcium

A

parathyroid hormone

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25
Q

What is the active and inactive form of calcium?
where is it activated ?

A

inactive - cholecalciferol
active -1,2,5- cholecalciferol
kidney

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26
Q

What part of the tubules where PTH act on to increase calcium reabsorption

A

Proximal tubule

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27
Q

where are the other 2 places within the system that calcium can be reabsorbed?

A

Ascending thick end of the loop of helen

Distial collective tubules

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28
Q

What is the name of the cell that is stimulated to breakdown the bone by PTH and to what 2 compounds

A

osteoclast,
calcium, and phosphate

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29
Q

What is the name of the cell that is inhibited by PTH to produce bone.

A

osteoblasts

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30
Q

True or false Thin descending LOH is very permeable to ions

A

False

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31
Q

True or false: the osmolarity of the environment deep within the kidney is low ?

A

False, deeper we go the higher the osmolarity (more concentrated the renal interstitium is

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32
Q

20% of the water that was filtered is reabsorbed in what part of the renal tubule

A

Thin Descending LOH

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33
Q

True or false: anything that increases the velocity of fluid flow through the system, increases the urine output

A

True

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34
Q

How would increased blood velocity affect the water reabsorption in the AVD (ascending vesta recta) and how will that affect our urine output ?

A

If the velocity too fast, we cannot absorb the salt from the blood there decreasing water absorption

increasing urine output/ making it more dilute

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35
Q

True or false. The water permeability in the ascending loop of helen is permeability to water.

A

false

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36
Q

Where is the sodium chloride reabsorption pump located in the renal tubule

A

Thick Asending LOH

37
Q

What is unique about the sodium chloride reabsorption pump in the direction and time it is pumping.

A

Pumps in the same direction at the same time moving ions out the tubule

38
Q

the process of the Thick Ascending LOH ion reabsorption is dependent on what?

A

Leaky K+ channels

39
Q

What are the ions reabsorbed at the Thick ascending LOH

A

Na+, K+, 2Cl-, CA++, Mg+

40
Q

What is secreted at the Thick ascending LOH

A

protons, H+

41
Q

What important benefits does the ions that are reabsorbed at the Thick ascending LOH have on the insterstitium?

A

Active reabsorption that takes place at the thick ascending LOH becomes important on renal interstitial osmotic gradient

Making it more concentrated and easier to hang on to the fluids ( water conservation)

42
Q

True or False, Potassium channels can be found on the tubule lumen side of the tutelar cell.

A

true

43
Q

What happens to the tubular lumen potassium is able to reenter back in?

A

portion of potassium goes back out into the tubular lumen, changing the charge of the tubular lumen more positive (8mV)

44
Q

What effect does potassium has reentering the tubular lumen in the Ascending thick LOH?

A

-increase the charge of the tubular lumen to +8mV
-Drives reabsorption of the other positively charge ions

45
Q

How does Mg++, Ca++, and Na+ reenter the renal interstitial fluid from the Ascending thick LOH?
What role does potassium play?

A

Na+, Mg++, Ca++ moves paracellular between the tight junctions (impermeable to water)

Potassium drives the reabsorption of the other positively charge ions by going back out to the Tubular lumen and increasing to +8mV

46
Q

What is the most potent drug that affects the thick ascending LOH?

A

Furosemide
(loop Diurectic)

47
Q

What is the MOA of furosemide at the Thick ascending LOH?

A

Stops reabsorption of ions (Na/K/Cl), will keep more water in tubule, increases urine output

end up diluting concentration of renal interstitium

48
Q

What is the Osmolarity in the proximal tubules?

What happens to the osmolarity has you descend down the proximal tubules?

A

300 mOms
it increases

49
Q

What is the diluting segment in the renal tubule ?
Where is it located within the renal tubules?

A

Diluting segment creates imbalance between osmolarity of tubular fluid compared to intersitium/environment over shoting it to 100mOms

Primarily though Na and Cl pumping in this segment (DCT)

Because reabsorbing salt but not much water

Located:distal convoluted tubules

50
Q

Which transporter or exchanger does most of the work regarding pumping calcium back into the the interstitial fluid ?

In which portion of the renal tubule the transporter or exchanger can be found?

A

Na/Ca exchanger

Disital Convoluted Tubules (DCT)

51
Q

What drug or class of drugs that effects the Na/Cl pump in the distal tubule ?

What is the MOA?

A

Thiazide Diuretic,

-Inhibits sodium and chloride reabsorption at distal tubule
-Would reduce amount of dilution with tubular fluid

52
Q

How do PTH regulate the calcium in the distal tubule?

A

By stimulating calcium reabsorption

-More channels means more calcium reabsorbed from tubular fluid
-Less channels means less calcium reabsorbed and more calcium in the urine
-If want to get rid of calcium, it is filitered and not reabsorb i
-If want to hang on to calcium, it is filitered and reabsorb

53
Q

How do thiazide diuretics affect the Na/ Ca exchanger

A

Results in losing salt and water, increasing urine output

Calcium reabsorption increases( due to the low Na gradient inside the cell —> the Na/ca exchanger increase

Spinning NCE faster results in more calcium being reabsorbed ( causing the PTH reabsorbing more Ca+)

54
Q

Increase in PTH and decrease in Calcium causes what disease to develope

A

osteoporosis

55
Q

What are the 2 cell types that are found at the end of the distal tubule ?

A

principal cells
intercalated cells

56
Q

What is the job of the principle cells

A

control potassium levels in the body

57
Q

What ion channels can be found on the principle cell membrane ?

What side of the tubular cell membrane?

A

** Apical side ** - Tubular side of principle cell
potassium channels
sodium channels

** Basolateral** - interstital side of principle cell
Cloride

58
Q

What is the driving force of the potassium and sodium channel in the distal tubules?

A

The flow of potassium and sodium channels

potassium and sodium is pump in through the Na/K ATPase on the basolateral side of the cell and leaves out through the apical side of cell through individual channels

59
Q

What would happen if the function of the Na/K ATPase pump was increase?

How would that effect the renal interstital space?

A

reabsorb more sodium
excrete more potassium

increase the Na gradient concentration

60
Q

What hormone affects the Na/ K ATPase pump and how do it affect sodium and potassium?

A

Aldosterone helps us conserve sodium and get rid of potassium

61
Q

Which hormone determines how many sodium channels we have on the apical side of prinicple cell?

A

Aldosterone

62
Q

What is an example of a mineralocorticoid derivative

A

Aldosterone

63
Q

Where in the adrenal gland is aldosterone produce?

A

zona glomerulosa
(The outer portion of the adrenal gland called the)

64
Q

What are the names of the 2 inner layers within the adrenal gland ?
what is/ are the compond(s) produce?

What is the name of the medial layer of the adrenal gland?
What is /are the name(s) of the compond(s) produce?

A

**Zona fasciculata
Zona retciularis **
Cortisol
androgens

**medulla **
catecholamines
(NE, EPI, DOP)

65
Q

True or false, A cholesterol derivative that looks similar to aldosterone may cause the body to increase BP and decrease potassium levels.

A

true

66
Q

How do the kidney destroy any cortisol that may enter the principal cell?

A

by using the enyzme ,(11beta -HSD)
11 beta - hydroxysteroid dehydrogenase that specifically destroy cortisol like compounds but do not act on aldosterone

67
Q

True or false, The 11 beta - hydroxysteroid dehydrogenase enzyme is able to completely destroy cortisol even if we are taking medication

A

False

68
Q

Which hormone is released in response to an increase in the plasma potassium concentration?

What is the MOA?

A

-Aldosterone
-increases potassium secretion by stimulating the Na/ K ATPase pump at the distal tubules in the prinicple cells
( early part of cortical collecting duct)

69
Q

What events within the renal tubules can effect the mechanics of fixing an elevated potassium level?

A

anything that blocks sodium reabsorption earlier in the tubular system
(proximal tubules
ascending thin and thick LOH)

70
Q

What will happen if we have more sodium in the renal tubules that reaches the principle cells in the distal collecting duct ( the MOA of most of the diuretic)

How will that effect the Na and K concentration?

A

-large amount of sodium leaking through the sodium channels that we have

-increase large amount of sodium going out of the renal tubules and in to the renal interstitial fluid

-Therefore large amount of potassium will leave out and into the renal tubular lumen ( potassium wasting)

71
Q

What is the MOA for aldosterone - sensitive (antagonist) drug(s)?

What is an example of one

A

Spironolactone
Eplerenenone

blocks the hormone receptor of aldosterone therefore decrease the usage of the Na/K ATPase pump

72
Q

What are the 2nd generation potassium sparing diuretics
What is the MOA in the principle cells in the distal tubule ?

A

Amiloride
Triamterne

blocks the sodium channels in the principle cell decreasing the amount of sodium reabsorbed

73
Q

What is the job of the intercalated cells and where are they located?

A

The cells deal with acid/ base balance by secreting bicarb - secreted
Type B cells

protons ( H+/ NH4+) - selected
Type A cells (more active )

in the later part of the distal tubules early part of the collective ducts

74
Q

What area in the renal tubule that is sensitive to ADH?

A

later part of the distal tubules early part of the collective ducts

75
Q

ADH have receptor(s) on what type of cell(s)

A

principle cells
intercalated cell

76
Q

How do ADH impact the renal system?

A

water permeability
urea reabsorption

77
Q

What are the pumps that are found in the intercalated cell that regulates Hydrogen?

A

Hydrogen - potassium ATPase pump
Hydrogen ATPase Pump

78
Q

What is another abbreviation for ADH?

A

AVP

79
Q

What is the name of the receptor on the principle or intercalated cell that the ADH binds to?

A

V2 - regulator receptor that control water permeability

80
Q

What is the process to allow water reabsorption when AVP binds to V2?

A

-AVP binding to V2 causes
-Gs (subunit to be release)
-releasing AC
-causing ATP —> cAMP
-increasing the activity of protein kinase A (PKA)
-causing protein phosphorylation on the collection of premade aquaporins -2 (located in the tubular side of the cell to allow water to be reabsorbed

81
Q

What happens to the aquaporins -2 when ADH decreases?

A

they move back to their storage pools

82
Q

Which hormone is sensitive in the cortical and medullary collecting tubules

A

AVP

83
Q

What area in the renal tubules concentrates the remaining filtrate before exiting the kidney?

A

collecting ducts: cortical & medullary by the H+ ATPase pump

84
Q

What area in the renal tubular system will be the final determinant of the urinary osmolarity?

A

collecting ducts: cortical & medullary

85
Q

Which hormone or compond is the only compound or hormone that can change water reabsorb?

A

AVP

86
Q

high volume output witin the renal tubules = AVP levels ________
low volume output within the renal tubules = AVP levels _________

A

low
high

87
Q

What part or region of the brain regulates the amount of ADH release to the kidneys?

what is the MOA?

A

by the osmorecepters located in the hypothalamus
it looks at the blood osmolarity and talks to the posterior lobe in the pituitary gland to increase or decrease the amount of ADH being release

88
Q

How do the osomoreceptor determine when to increase release of ADH?

A

if the environment surrounding the osomoreceptor is very salty then the water will leave the cell causing it to shrink little bit until the internal osmolarity matches the environment

89
Q

How do the osomoreceptor determine to reduce release of ADH?

A

if the environment surrounding the osomoreceptor is diluted then the water will move in the cell causing it to enlarge little bit until the internal osmolarity matches the environment