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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.

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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

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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.

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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.

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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)

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28
Q

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

A

Triamterene

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29
Q

Aldosterone comes from where?

A

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

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30
Q

What produces cortisol and androgens?

A

Zona fasciculata and Zona reticularis

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31
Q

What produces estrogen, and how much?

A

Small amount of estrogen is produced by Zona Fasciculata

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32
Q

Where do catecholamines come from?

A

Inner part of adrenal gland, the medulla.

Epi/norepi

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33
Q

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

A

Epi 4 to 1 norepi

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34
Q

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

A

More

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35
Q

What else can cause Aldo release?

A

ANG II binding to AT1 receptors found within the Zona glomerulosa

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36
Q

The RAAA stands for

A

Renin-Angiotensin-Aldosterone-Axis

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37
Q

What enzyme produces aldosterone?

A

Aldosterone synthase

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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.

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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.

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40
Q

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

A

Cortisol

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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 hypokalemia.

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.

56
Q

Our water control system is via

A

Vasopressin

Dehydration equals high vasopressin levels

57
Q

If someone has a head injury that affected the ______ gland, they would ______

A

Pituitary gland; have decreased vasopressin release and increased urine output

58
Q

Causes of decreased vasopressin (ADH)

A

Low osmolarity, high blood pressure, high blood volume

59
Q

What area monitors for blood volume changes?

A

Low pressure areas in large veins, atria, etc.

60
Q

Where are baroreceptors located?

A

In high pressure areas

61
Q

Osmoreceptors are cell that

A

Sense changes in osmolarity.

62
Q

Where are osmoreceptors in the brain located?

A

In nuclei in the Hypothalamus

63
Q

If we have really salty blood and the osmoreceptors in the hypothalamus detect that, they will

A

Release more vasopressin to retain water because we are dehydrated.

64
Q

The nuclei (collection of cell bodies) that is in the front of the hypothalamus

A

Supraoptic neuron

65
Q

What fraction of our ADH is produced by supraoptic nuclei?

A

5/6th

66
Q

What is the nuclei that produces 1/6th of our ADH?

A

Paraventricular nuclei

67
Q

Why is it called paraventricular nuclei? What ventricle is it near?

A

Para(side)ventricular(each side of THIRD ventricle)

68
Q

Where is ADH delivered after it’s produced in hypothalamus?

A

To the posterior pituitary gland

69
Q

From the pituitary gland, where is ADH delivered?

A

Dumped into blood, pituitary gland has a large vasculature.

70
Q

Another name for the posterior pituitary gland is

A

Neurohypophysis

71
Q

Another name for anterior pituitary gland

A

Adenohypophysis

72
Q

Isotonic solution

A

A solution with an equal osmolarity as the cell its around. No movement of ions and proteins.

73
Q

Hypotonic solution

A

A solution with a low osmolarity, and the cell will absorb water and swell to even the osmolarity in/outside the cell.

74
Q

A swelling osmoreceptor will ____

A

Slow Rate of production of action potentials that are being sent to ADH production centers. Results in Decreased ADH production -> more urine.

A swollen osmoreceptor should occur during hypervolemia.

75
Q

When an osmoreceptor shrinks, the _____.

A

Rate of action potential firing is increased, and increases ADH production, resulting in less urine, and should occur during states of hypovolemia/dehydration.

76
Q

Osmolarity in the proximal tubule should be WHAT in relation to the osmolarity of the plasma?

A

The same. You reabsorb 2/3rds of everything, not picky.

77
Q

In the descending thin limb loop of henle, the osmolarity is _____ than the plasma.

A

Much higher.

78
Q

After the early part of the distal tubule, the osmolarity is entirely dependent upon

A

ADH

79
Q

If we have lots of ADH around beyond the beginning portions of the distal convoluted tubule, what’s going to happen?

A

Lots of water reabsorption.

80
Q

If we NO ADH, our urine osmo will be

A

50

81
Q

What is our max urine osmo when we have boatloads of ADH?

A

1200

82
Q

How does ADH control osmolarity in loop of henle?

A

Vasopressin (in addition to controlling water), it will play a large role in reabsorbing UREA from the tubular fluid.

83
Q

Is urea freely filterable?

A

Yes, and it’s small.

84
Q

How much urea is reabsorbed in proximal tubule? And how is it reabsorbed?

A

It’s inside water, so it’s reabsorbed with the water. About 50% is leftover towards end of proximal tubule.

85
Q

Urea is super important and responsible for our ability to hang onto water via _____ through the ______.

A

Osmosis; aquaporin water channels

86
Q

Urea transporters in walls of collecting duct

A

UT-A1 and UT-A3

87
Q

ADH is the only signaling compound that is capable of influencing _______ without simultaneously influencing ________.

A

water reabsorption; salt reabsorption

88
Q

ANG II and aldosterone will ___________, but not ADH.

A

Cause electrolyte (NaCl) reabsorption ALONG WITH water reabsorption.

89
Q

What is the primary controller of plasma osmolarity?

A

ADH

90
Q

Caffeine will reduce ______ release from _____

A

ADH release from the brain

91
Q

What can happen if you drink caffeine with a high salt intake?

A

Caffeine will reduce ADH secretion from the brain and cause you to urinate, and lack the ability to control your electrolyte balance. If you combine that with a high salt intake, it can result in an elevated plasma sodium concentration.

92
Q

Decreased thirst will be caused by what changes in osmo, blood volume/pressure, ANGII levels, GI?

A

Decreased plasma osmolarity, increased blood volume/blood pressure, decreased Angiotensin II, and gastric distention will all cause decreased thirst levels.

93
Q

Changes that cause increased thirst in relation to these: osmo, blood volume/pressure, ANGII levels, GI?

A

Increased osmo, decreased blood volume/pressure, increased ANGII, dry mouth.

94
Q

Things that will cause decreased ADH? Fluid status and drugs

A

Decreased osmolarity, increased blood volume and blood pressure.

Drugs: alcohol, clonidine, Haloperidol

95
Q

Things that will cause an increase in ADH secretion

A

Increased serum osmo, decreased blood volume/pressure, nausea (anticipation of vomiting and losing fluid), hypoxia (hold onto the volume to deliver oxygen?)

Drugs: Nicotine and morphine

96
Q

If we block aldosterone (spironolactone, or triampterine), what can happen?

A

Increased potassium intake will result in increased serum potassium levels.

97
Q

Increased potassium intake results in increased K+ serum concentration, Which results in ______ which will then _______

A

Increased aldosterone, which will then increase K+ secretion in cortical collecting tubules, and excrete K+ in urine.

98
Q

Changes in osmolarity, urine flow rate, and urinary solute excretion if you drink 1L of H2O? (No solutes at all!)

A

After about 30 minutes to absorb, SLIGHTLY decreased plasma osmo, big decrease in urine osmo, increased urine flow rate (decreased ADH), and very slightly increase solute excretion.

99
Q

How long is the entire process of managing extra liter of water it took in?

A

Within 180 minutes.

100
Q

Why does plasma osmolarity barely change with the 1L of water?

A

Decrease in ADH will allow water to not be reabsorbed, and since ADH can only affect water reabsorption and not NaCl, the kidneys can get rid of the water without affecting the electrolytes much.

101
Q

Normal urine osmolarity in ideal environment?

A

600 mOsm/L

102
Q

If we are taking excess electrolytes, what should our urine osmo be?

A

Greater than 600 mOsm/L

A&P 1 (39 decks)

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