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A&P 1 > FINAL EXAM - Lecture 7 > Flashcards

FINAL EXAM - Lecture 7 Flashcards

1
Q

The proximal tubule probably has a ______ metabolic rate

A

High

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2
Q

How much water is reabsorbed in the thin descending LOH?

A

20%

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3
Q

How much water has been reabsorbed by the time it gets to the ascending LOH?

A

65 + 20 = 85%

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4
Q

The distal tubule and collecting duct will _______ when it comes to water.

A

Decide how much to reabsorb

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5
Q

What % of ions are reabsorbed in the TAL?

A

25%

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6
Q

What % of electrolytes have been reabsorbed by the time they reach the distal tubule?

A

65% in proximal tubule + 25% in TAL = 90%

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7
Q

What determines how much solutes will be reabsorbed? By what kind of cells?

A

Late portion of distal tubule and entire collecting duct; principal cells

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8
Q

What determines water reabsorption at the end?

A

ADH

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9
Q

What section also has a high metabolic rate?

A

TAL

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10
Q

What’s the primary way of getting calcium across cell wall into interstitium in distal tubule?

A

Na+/Ca++ exchanger, secondarily will be Ca++ ATPase pumps.

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11
Q

The electrochemical gradient that the NCE runs on, originates from the

A

Na/K ATPase pump

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12
Q

In the distal tubule, the Na/K ATPase pump keeps Na+ intracellular concentration relatively ____, so the ______ can function properly.

A

Low; NCE (it will want sodium to reabsorb from interstitium since Na/K been spitting it out)

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13
Q

If we block the NaCl reabsorption into the distal tubule cells from the lumen (thiazides), what happens to the rest of the pumps?

A

Decreases intracellular sodium, which cause an increase of the NCE (sodium being reabsorbed FROM THE INTERSTITIUM) to make up for the lost sodium, which results in more calcium being reabsorbed.

Helpful for osteoporosis, they may be prescribed thiazides.

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14
Q

If someone is on a thiazides diuretic, they should watch their dietary _______ intake.

A

Calcium

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15
Q

How can we treat someone with chronic kidney stones?

A

Thiazides diuretics, to have less calcium in urine.

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16
Q

When you think of principal cells, think of

A

Aldosterone

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17
Q

When you have more aldosterone, the more ____ we reabsorb from tubular lumen.

A

Sodium. Which will lead to increased water reabsorption.

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18
Q

Aldosterone is a ________

A

Mineralocorticoid

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19
Q

since aldosterone promotes Na+ reabsorption, it will also cause a

A

Increase in potassium excretion into tubular lumen

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20
Q

How exactly does aldosterone affect Na and K levels?

A

Aldosterone directly speeds up the Na/K ATPase pump between the renal interstitium and the distal tubule cells. This promotes movement of K into cell, and Na into the interstitium. In turn, the cell will compensate by absorbing more Na+ from the tubular lumen, and secrete more K+ into the lumen.

End result: decreased serum potassium, increased serum sodium.

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21
Q

How does the potassium specifically leave the cell into the distal tubule lumen?

A

Leaks. Not a channel/pump. But it’s still called secretion.

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22
Q

Two types of K channels in principal cells

A

ROMK and BK

ROMK: Renal outer medullary potassium channel
BK: Big potassium channels

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23
Q

Discuss principal cells in regards to low K excretion, normal K excretion, and high K excretion

A

During low K excretion, ROMK channels are sequestered and BK channels are closed.

During normal K excretion, ROMK channels are in the wall, open, and the BK channels are still CLOSED.

During high K excretion, ROMK channels are in the wall, open, and the BK channels are also OPEN.

Note: BK channels do not sequester (go to middle of cell, away from wall). They just open and close. ROMK channels do not open or close, they just sequester.

24
Q

What mediates the movement of ROMK channels and opening/closing of BK channels, controlling amount of potassium excreted by principal cells?

A

Aldosterone

25
Q

Sodium channel in the cell wall next to distal tubular lumen is also referred to as?

A

ENaC. Epithelial sodium channel. This allows sodium reabsorption from tubular lumen.

26
Q

What drugs block the ENaC?

A

Amiloride, Triamterene

Blocking the sodium channel will indirectly block the Na/K ATPase pump in the renal interstitial side of the cell wall, which decreases the amount potassium coming into cell from renal interstitium, which decreases potassium excretion.

end result: increased serum potassium, decreased serum sodium, water loss.

27
Q

If we have something that reduces Na reabsorption at the earlier parts, that means that more sodium is delivered to later parts of tubule at principal cells. If we increase Na+ to principal cells, then more sodium will be reabsorbed. This results in a faster rate of _____________ pump, so it will result in what?

A

Na+/K+ interstitium; Increased potassium wasting (decreased serum potassium)

28
Q

Most commonly prescribed drug to offset potassium wasting diuretic to save excess potassium loss?

A

Triamterene

29
Q

Aldosterone comes from where?

A

Outermost part of the adrenal gland, called the Zona glomerulosa.

30
Q

What produces cortisol and androgens?

A

Zona fasciculata and Zona reticularis

31
Q

What produces estrogen, and how much?

A

Small amount of estrogen is produced by Zona Fasciculata

32
Q

Where do catecholamines come from?

A

Inner part of adrenal gland, the medulla.

Epi/norepi

33
Q

What is the ratio that the adrenal gland releases epi and norepi?

A

Epi 4 to 1 norepi

34
Q

The higher our potassium levels, the ______ aldosterone secreted from Zona glomerulosa

A

More

35
Q

What else can cause Aldo release?

A

ANG II binding to AT1 receptors found within the Zona glomerulosa

36
Q

The RAAA stands for

A

Renin-Angiotensin-Aldosterone-Axis

37
Q

What enzyme produces aldosterone?

A

Aldosterone synthase

38
Q

Excess cortisol can interact with _____ and result in?

A

Aldosterone receptor because they look similar; hypertension. Because aldosterone receptor is constantly causing fluid reabsorption.

39
Q

How does stress increase blood pressure?

A

Increased cortisol, which will bind to aldosterone receptors, which will increase sodium reabsorption, and water reabsorption.

40
Q

Under normal circumstances, our body has more aldosterone or cortisol floating around?

A

Cortisol

41
Q

Even though there is more cortisol than aldosterone, cortisol gets eaten up by what enzyme specifically in the principal cell?

A

11beta-HSD Type 2(11beta-Hydroxy-steroid-dehydrogenase)

It hydrogenates cortisol. Type 2 is the specific enzyme present in the principal cell.

42
Q

Natural inhibitor of 11beta-HSD type 2? and what is it found in? What is the result on the body?

A

Licorice (real licorice, not candy)

Found in flavoring for smokeless tobacco.

Hypertension (nicotine, AND increased cortisol) and hyperkalemia.

43
Q

As potassium concentration goes up, aldosterone will ____

A

Increase, in order to secrete and excrete the potassium. This increases Na and water reabsorption.

44
Q

Intercalated cells in distal tubule will

A

Deal with acid-base regulation by secreting either hydrogen or bicarb, depending on what’s needed.

45
Q

Type A intercalated cells will secrete

A

H+

46
Q

Type B intercalated cells will reabsorb ___ and secrete ____

A

H+; HCO3-

47
Q

How do Type A intercalated cells secrete their ion?

A

Secrete H+ via Hydrogen-Potassium ATPase pumps, and hydrogen ATPase pump.

The hydrogen ATPase pump is super strong and can dump a lot of H+ into the urine.

48
Q

Intercalated and principal cells are both sensitive to ______ which are both found in the distal tubule and collecting duct.

A

ADH (Vasopressin)

49
Q

V1 receptors are found in the ____, and V2 are found in ______

A

V1 are found in Periphery vessels, causing constriction.

V2 are found in late distal tubule and collecting duct of kidneys.

50
Q

What happens when ADH binds to V2 receptors?

A

ATP turns into cAMP, activating PKA, which phosphorylates vesicles called AQP-2, that moves them to the tubular lumen cell wall, which allows water reabsorption from the tubular lumen.

51
Q

AQP3 and 4 are found where? Are they ADH dependent?

A

Allow water reabsorption into the interstitium, and they are not.

52
Q

Nephrogenic diabetes insipidus

A

Likely has an issue with PKA phosphorylating AQP-2, which results in excessive urination.

53
Q

If there is a problem with ADH secretion, it is considered ______. If there is a problem with the kidney reacting to ADH, it is considered

A

Central Diabetes insipidus; Nephrogenic diabetes insipidus

54
Q

A patient on a massive dose of lithium will cause massive diuresis, from _____. Their lower lumen osmolarity would be around ____.

A

Nephrogenic diabetes insipidus; 50

55
Q

What’s the effect of alcohol on ADH?

A

Decreases ADH released from brain, and impairs kidney to respond to ADH. That’s why it’s a good diuretic.

A&P 1 (36 decks)

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